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Impairment of hematopoietic function. a) Comparison of changes in CD34 + , b) Comparison of changes in CFU-GM, c) Comparison of changes in BFU-E, d) Comparison of changes in <t>CXCL12,</t> e) Comparison of changes in EPO, f) Comparison of changes in TPO. Note: 'a' indicates P < 0.05 compared with T0, 'b' indicates comparison with T1, and 'c' indicates P < 0.05 compared with the IV group at the same time.

Cxcl12, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 87 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sdf+1+mab310/Human%2FMouse+CXCL12%2FSDF-1+Antibody/pmc12967180-81-13-33
Average 94 stars, based on 87 article reviews

cxcl12 - by Bioz Stars, 2026-09

94/100 stars

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1) Product Images from "Randomized controlled trial of intraosseous access vs. intravenous access in traumatic hemorrhagic shock: Effects on inflammation, hematopoiesis, and coagulation"

Article Title: Randomized controlled trial of intraosseous access vs. intravenous access in traumatic hemorrhagic shock: Effects on inflammation, hematopoiesis, and coagulation

Journal: Journal of Medical Biochemistry

doi: 10.5937/jomb0-58956

Figure Legend Snippet: Impairment of hematopoietic function. a) Comparison of changes in CD34 + , b) Comparison of changes in CFU-GM, c) Comparison of changes in BFU-E, d) Comparison of changes in CXCL12, e) Comparison of changes in EPO, f) Comparison of changes in TPO. Note: 'a' indicates P < 0.05 compared with T0, 'b' indicates comparison with T1, and 'c' indicates P < 0.05 compared with the IV group at the same time.

Techniques Used: Comparison

other:

Article Title: CYP4A in tumor-associated macrophages promotes pre-metastatic niche formation and metastasis
Article Snippet: Neutralizing antibodies against TGF-β (MAB7346), VEGF (AF-493) and SDF-1 (MAB310) were purchased from R&D Systems.

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Journal: Journal of Medical Biochemistry

Article Title: Randomized controlled trial of intraosseous access vs. intravenous access in traumatic hemorrhagic shock: Effects on inflammation, hematopoiesis, and coagulation

doi: 10.5937/jomb0-58956

Figure Lengend Snippet: Impairment of hematopoietic function. a) Comparison of changes in CD34 + , b) Comparison of changes in CFU-GM, c) Comparison of changes in BFU-E, d) Comparison of changes in CXCL12, e) Comparison of changes in EPO, f) Comparison of changes in TPO. Note: 'a' indicates P < 0.05 compared with T0, 'b' indicates comparison with T1, and 'c' indicates P < 0.05 compared with the IV group at the same time.

Article Snippet: The following indicators were analyzed: IL-1β (DLB50), IL-6 (D6050B), IL-10 (D1000B), HMGB1 (IC1690G), CXCL12 (MAB310), EPO (DEPRU0), and TPO (BAF288): These markers were quantified using enzyme-linked immunosorbent assay (ELISA) with commercially available kits (R&D Systems).

Techniques: Comparison

Fig. 5 CXCL12 regulates CD8+ T-cell infiltration after SAH. A: Representative flow cytometric profiles of CD8+ and CD4+ T cells from the cerebral cortex across different groups. The gating strategy is provided in Supplementary Data 1. B: Immunofluorescence staining for CD8+CXCR4+ cells around the cerebral cortex across different groups. Scale bar = 50 μm. C-D: Quantification of CD8+ and CD4+ T cells (n = 6). E: Quantification of CD8+CXCR4+ cells (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. **p < 0.01, ****p < 0.0001. ns indicates no significance (p > 0.05)

Journal: Journal of neuroinflammation

Article Title: Single-cell sequencing reveals intracranial microvasculature-derived CXCL12 promotes CD8 + T-cell infiltration and blood-brain barrier dysfunction after subarachnoid hemorrhage in mice.

doi: 10.1186/s12974-025-03444-0

Figure Lengend Snippet: Fig. 5 CXCL12 regulates CD8+ T-cell infiltration after SAH. A: Representative flow cytometric profiles of CD8+ and CD4+ T cells from the cerebral cortex across different groups. The gating strategy is provided in Supplementary Data 1. B: Immunofluorescence staining for CD8+CXCR4+ cells around the cerebral cortex across different groups. Scale bar = 50 μm. C-D: Quantification of CD8+ and CD4+ T cells (n = 6). E: Quantification of CD8+CXCR4+ cells (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. **p < 0.01, ****p < 0.0001. ns indicates no significance (p > 0.05)

Article Snippet: Administration of a CXCL12 neutralizing antibody, the CXCR4 antagonist AMD3100, or recombinant CXCL12 protein To intervene in CXCL12-CXCR4 signaling, the mice were intravenously administered a CXCL12 neutralizing antibody (MAB310-100, R&D Systems, Shanghai, China).

Techniques: Immunofluorescence, Staining, Saline, Control, Recombinant

Fig. 6 CXCL12 regulates CD8⁺ T-cell cytotoxicity and brain edema. A: Western blot analysis showing granzyme B and perforin expression in the cerebral cortex of the sham, saline, CXCL12 Ab, CXCL12, and CXCL12 + AMD3100 groups. B, C: Quantification of granzyme B (n = 5) and perforin expression (n = 6). D: Measurement of brain water content in the bilateral cerebral hemispheres and cerebellum across groups (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. *p < 0.05, ***p < 0.001, ****p < 0.0001. ns indicates no significance (p > 0.05)

Journal: Journal of neuroinflammation

doi: 10.1186/s12974-025-03444-0

Figure Lengend Snippet: Fig. 6 CXCL12 regulates CD8⁺ T-cell cytotoxicity and brain edema. A: Western blot analysis showing granzyme B and perforin expression in the cerebral cortex of the sham, saline, CXCL12 Ab, CXCL12, and CXCL12 + AMD3100 groups. B, C: Quantification of granzyme B (n = 5) and perforin expression (n = 6). D: Measurement of brain water content in the bilateral cerebral hemispheres and cerebellum across groups (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. *p < 0.05, ***p < 0.001, ****p < 0.0001. ns indicates no significance (p > 0.05)

Techniques: Western Blot, Expressing, Saline, Control, Recombinant

Fig. 9 Neutralizing CXCL12 promoted neurobehavioral recovery in mice after SAH. A: Representative electron microscopy images showing ultrastructural changes in the brain cortex after SAH. Yellow arrows indicate mitochondrial damage, and red arrows indicate myelin damage. Scale bar = 2 μm. B: Representative images of the open field test. C: Quantification of the G ratio (n = 4). D: Quantification of movement trajectory distances (n = 6). E: Beam balance scores measured across groups (n = 6). F: Modified Garcia score measured across groups (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Journal: Journal of neuroinflammation

doi: 10.1186/s12974-025-03444-0

Figure Lengend Snippet: Fig. 9 Neutralizing CXCL12 promoted neurobehavioral recovery in mice after SAH. A: Representative electron microscopy images showing ultrastructural changes in the brain cortex after SAH. Yellow arrows indicate mitochondrial damage, and red arrows indicate myelin damage. Scale bar = 2 μm. B: Representative images of the open field test. C: Quantification of the G ratio (n = 4). D: Quantification of movement trajectory distances (n = 6). E: Beam balance scores measured across groups (n = 6). F: Modified Garcia score measured across groups (n = 6). Saline refers to the vehicle-treated control group; CXCL12 refers to the group treated with recombinant CXCL12 protein; CXCL12 Ab indicates the group treated with a CXCL12 neutralizing antibody; and CXCL12 + AMD3100 represents the group cotreated with recombinant CXCL12 and the CXCR4 antagonist AMD3100. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Techniques: Electron Microscopy, Modification, Saline, Control, Recombinant

Fig. 10 Schematic illustration of the present study. After SAH (red arrow), endothelial cells and pericytes secrete CXCL12 (yellow arrow), facilitating the infiltration of CD8+ CXCR4+ T cells into the brain parenchyma (green arrow). These infiltrating T cells release perforin and granzyme B (purple arrow), inducing endothelial cell apoptosis and exacerbating BBB disruption. Blocking CXCL12-mediated T-cell infiltration with CXCL12 antibodies or AMD3100 (a CXCR4 antagonist, blue arrow) preserves BBB integrity and promotes neurological outcomes after SAH

Journal: Journal of neuroinflammation

doi: 10.1186/s12974-025-03444-0

Figure Lengend Snippet: Fig. 10 Schematic illustration of the present study. After SAH (red arrow), endothelial cells and pericytes secrete CXCL12 (yellow arrow), facilitating the infiltration of CD8+ CXCR4+ T cells into the brain parenchyma (green arrow). These infiltrating T cells release perforin and granzyme B (purple arrow), inducing endothelial cell apoptosis and exacerbating BBB disruption. Blocking CXCL12-mediated T-cell infiltration with CXCL12 antibodies or AMD3100 (a CXCR4 antagonist, blue arrow) preserves BBB integrity and promotes neurological outcomes after SAH

Techniques: Disruption, Blocking Assay

The neutralising of SDF‐1 mitigates hepatic IR via promoting hepatocyte lipophagy in T2DM mice. The mice were assigned into normal, T2DM, T2DM + SDF‐1 neutralising antibody (1 mg/kg, intrahepatic injection), T2DM + SDF‐1 neutralising antibody +3‐MA (30 mg/kg, intrahepatic injection), and T2DM + MET (250 mg/kg/day, oral administration) groups. (A) The experimental flow was shown. (B) Hepatocyte marker albumin (green) and SDF‐1 (red) were labelled in mouse liver tissues. (C) The co‐localization of albumin and SDF‐1 was analysed. (D) Fasting blood insulin levels were detected. (E) Fasting blood glucose levels were detected. (F) HOMA‐IR was calculated. (G) The liver index was analysed. (H) Representative images of mouse livers were shown. (I) Liver oil red O staining was shown. (J) The autophagy marker LC3 (green) was labelled in mouse liver tissues. (K) The puncta LC3 per cell was analysed. ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05，## p < 0.01，### p < 0.001 versus T2DM group. ** p < 0.01 versus T2DM + SDF‐1 neutralising antibody group. The n.s. stood for no significance.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: The neutralising of SDF‐1 mitigates hepatic IR via promoting hepatocyte lipophagy in T2DM mice. The mice were assigned into normal, T2DM, T2DM + SDF‐1 neutralising antibody (1 mg/kg, intrahepatic injection), T2DM + SDF‐1 neutralising antibody +3‐MA (30 mg/kg, intrahepatic injection), and T2DM + MET (250 mg/kg/day, oral administration) groups. (A) The experimental flow was shown. (B) Hepatocyte marker albumin (green) and SDF‐1 (red) were labelled in mouse liver tissues. (C) The co‐localization of albumin and SDF‐1 was analysed. (D) Fasting blood insulin levels were detected. (E) Fasting blood glucose levels were detected. (F) HOMA‐IR was calculated. (G) The liver index was analysed. (H) Representative images of mouse livers were shown. (I) Liver oil red O staining was shown. (J) The autophagy marker LC3 (green) was labelled in mouse liver tissues. (K) The puncta LC3 per cell was analysed. ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05，## p < 0.01，### p < 0.001 versus T2DM group. ** p < 0.01 versus T2DM + SDF‐1 neutralising antibody group. The n.s. stood for no significance.

Article Snippet: The mice were assigned into normal, T2DM, T2DM + SDF1 neutralising antibody (MAB310, R&D Systems, USA; 1 mg/kg/day, intrahepatic injection), T2DM + SDF1 neutralising antibody +3‐Methyladenine (3‐MA; autophagy inhibitor; HY‐19312, MedChemExpress, USA; 30 mg/kg/day, intrahepatic injection), T2DM + metformin (MET; S5958, Selleck, USA; 250 mg/kg/day, once a day from week 4 to week 6 of HFHSD feeding, oral administration) groups.

Techniques: Injection, Marker, Staining

SDF‐1 expression and release increase in PA‐treated hepatocytes. The hepatocytes were divided into normal and PA (0.5 mmol/L for 24 h) groups. (A) SDF1 protein levels in hepatocytes were detected by Western blot. (B) SDF‐1 relative protein levels were analysed. (C) SDF‐1 protein levels in hepatocyte culture supernatant were measured by ELISA. ** p < 0.01, *** p < 0.001 versus normal group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: SDF‐1 expression and release increase in PA‐treated hepatocytes. The hepatocytes were divided into normal and PA (0.5 mmol/L for 24 h) groups. (A) SDF1 protein levels in hepatocytes were detected by Western blot. (B) SDF‐1 relative protein levels were analysed. (C) SDF‐1 protein levels in hepatocyte culture supernatant were measured by ELISA. ** p < 0.01, *** p < 0.001 versus normal group.

Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

SDF‐1 inhibits lipophagy in PA‐treated hepatocytes via CXCR4, rather than CXCR7. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody (1 μg for 24 h), PA + AMD3100 (10 μM for 24 h), and PA + ACT‐1004‐1239 (6 nM for 24 h) groups. (A) LC3, p62 and ATG7 protein levels in hepatocytes were detected by Western blot. (B–D) LC3, p62 and ATG7 relative protein levels were analysed. (E) The co‐localization of the autolysosome (red) and the LD (green) in hepatocytes, indicated the induction of lipophagy (yellow). (F) The co‐localization of autolysosome and LD was analysed. (G) The LD inside the hepatocytes was visualised by oil red O staining. ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05, ## p < 0.01 versus PA group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: SDF‐1 inhibits lipophagy in PA‐treated hepatocytes via CXCR4, rather than CXCR7. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody (1 μg for 24 h), PA + AMD3100 (10 μM for 24 h), and PA + ACT‐1004‐1239 (6 nM for 24 h) groups. (A) LC3, p62 and ATG7 protein levels in hepatocytes were detected by Western blot. (B–D) LC3, p62 and ATG7 relative protein levels were analysed. (E) The co‐localization of the autolysosome (red) and the LD (green) in hepatocytes, indicated the induction of lipophagy (yellow). (F) The co‐localization of autolysosome and LD was analysed. (G) The LD inside the hepatocytes was visualised by oil red O staining. ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05, ## p < 0.01 versus PA group.

Techniques: Western Blot, Staining

SDF‐1/CXCR4 inhibits lipophagy in PA‐treated hepatocytes via activating AKT/mTOR pathway. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody, PA + AMD3100, PA + MK‐2206 2HCl (10 μM for 24 h), and PA + XL388 (100 nM for 24 h) groups. (A) P‐AKT, AKT, p‐mTOR and mTOR protein levels in hepatocytes were detected by Western blot. (B, C) P‐AKT and p‐mTOR relative protein levels were analysed. In Figure , ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05, ## p < 0.01 versus PA group. The hepatocytes were divided into PA + SDF‐1 neutralising antibody, PA + SDF‐1 neutralising antibody + SC79 (4 μg/mL for 24 h), PA + SDF‐1 neutralising antibody + MHY1485 (5 μM for 24 h), PA + AMD3100, PA + AMD3100 + SC79 and PA + AMD3100 + MHY1485 groups. (D) LC3, p62 and ATG7 protein levels in hepatocytes were detected by Western blot. (E–G) LC3, p62 and ATG7 relative protein levels were analysed. (H) The co‐localization of the autolysosome (red) and the LD (green) in hepatocytes, indicated the induction of lipophagy (yellow). (I) The co‐localization of autolysosome and LD was analysed. (J) The LD inside the hepatocytes was visualised by oil red O staining. In Figure , ** p < 0.01, *** p < 0.001 versus PA + SDF‐1 neutralising antibody group. ## p < 0.01, ### p < 0.001 versus PA + AMD3100 group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: SDF‐1/CXCR4 inhibits lipophagy in PA‐treated hepatocytes via activating AKT/mTOR pathway. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody, PA + AMD3100, PA + MK‐2206 2HCl (10 μM for 24 h), and PA + XL388 (100 nM for 24 h) groups. (A) P‐AKT, AKT, p‐mTOR and mTOR protein levels in hepatocytes were detected by Western blot. (B, C) P‐AKT and p‐mTOR relative protein levels were analysed. In Figure , ** p < 0.01, *** p < 0.001 versus normal group. # p < 0.05, ## p < 0.01 versus PA group. The hepatocytes were divided into PA + SDF‐1 neutralising antibody, PA + SDF‐1 neutralising antibody + SC79 (4 μg/mL for 24 h), PA + SDF‐1 neutralising antibody + MHY1485 (5 μM for 24 h), PA + AMD3100, PA + AMD3100 + SC79 and PA + AMD3100 + MHY1485 groups. (D) LC3, p62 and ATG7 protein levels in hepatocytes were detected by Western blot. (E–G) LC3, p62 and ATG7 relative protein levels were analysed. (H) The co‐localization of the autolysosome (red) and the LD (green) in hepatocytes, indicated the induction of lipophagy (yellow). (I) The co‐localization of autolysosome and LD was analysed. (J) The LD inside the hepatocytes was visualised by oil red O staining. In Figure , ** p < 0.01, *** p < 0.001 versus PA + SDF‐1 neutralising antibody group. ## p < 0.01, ### p < 0.001 versus PA + AMD3100 group.

Techniques: Western Blot, Staining

SDF1/CXCR4/AKT/mTOR pathway‐inhibited lipophagy promotes PA‐induced hepatocyte IR. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody, PA + SDF‐1 neutralising antibody +3‐MA (10 mM for 24 h), PA + AMD3100, PA + AMD3100 + 3‐MA, PA + MK‐2206 2HCl, PA + MK‐2206 2HCl + 3‐MA, PA + XL388 and PA + XL388 + 3‐MA groups. (A) The glucose content of the medium was measured. (B) Glucose consumption by hepatocytes was analysed. ** p < 0.01 versus normal group. ## p < 0.01 versus PA group. @ p < 0.05 versus PA + SDF‐1 neutralising antibody group. $ p < 0.05 versus PA + AMD3100 group. % p < 0.05 versus PA + MK‐2206 2HCl group. & p < 0.05 versus PA + XL388 group.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: SDF1/CXCR4/AKT/mTOR pathway‐inhibited lipophagy promotes PA‐induced hepatocyte IR. The hepatocytes were divided into normal, PA, PA + SDF‐1 neutralising antibody, PA + SDF‐1 neutralising antibody +3‐MA (10 mM for 24 h), PA + AMD3100, PA + AMD3100 + 3‐MA, PA + MK‐2206 2HCl, PA + MK‐2206 2HCl + 3‐MA, PA + XL388 and PA + XL388 + 3‐MA groups. (A) The glucose content of the medium was measured. (B) Glucose consumption by hepatocytes was analysed. ** p < 0.01 versus normal group. ## p < 0.01 versus PA group. @ p < 0.05 versus PA + SDF‐1 neutralising antibody group. $ p < 0.05 versus PA + AMD3100 group. % p < 0.05 versus PA + MK‐2206 2HCl group. & p < 0.05 versus PA + XL388 group.

Techniques:

The role and mechanism of SDF‐1 in hepatic IR were displayed. Up‐regulated SDF1 binds to its receptor CXCR4 and CXCR7 on hepatocytes following PA treatment. SDF‐1/CXCR4 signalling, not SDF‐1/CXCR7 signalling, inhibits lipophagy in hepatocytes via activating the phosphorylation of AKT and mTOR1 to promote PA‐induced IR. The blockade of SDF‐1/CXCR4/AKT/mTOR signalling‐induced lipophagy alleviates IR in PA‐treated hepatocytes.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Stromal Cell Derived Factor‐1 Promotes Hepatic Insulin Resistance via Inhibiting Hepatocyte Lipophagy

doi: 10.1111/jcmm.70352

Figure Lengend Snippet: The role and mechanism of SDF‐1 in hepatic IR were displayed. Up‐regulated SDF1 binds to its receptor CXCR4 and CXCR7 on hepatocytes following PA treatment. SDF‐1/CXCR4 signalling, not SDF‐1/CXCR7 signalling, inhibits lipophagy in hepatocytes via activating the phosphorylation of AKT and mTOR1 to promote PA‐induced IR. The blockade of SDF‐1/CXCR4/AKT/mTOR signalling‐induced lipophagy alleviates IR in PA‐treated hepatocytes.

Techniques: Phospho-proteomics

( A – C ) Eight- to 10-month-old ( n = 5) C57BL/6N mice were infected with 1000, 2000, or 5000 PFU SARS2-N501Y MA30 . Weight ( A ), survival ( B ), and lung infectious virus titers ( C ) are shown. Data are representative of 3 independent experiments. Data in A and C are mean ± SEM. LOD, limit of detection. u.d., undetected. * P < 0.05 by 1-way ANOVA with Tukey’s multiple comparisons in C . ( D – H ) Middle-aged C57BL/6N mice (8–10 months old, n = 5) were infected with 1000, 2000, or 5000 PFU SARS2-N501Y MA30 virus. ( D and F ) The number of neutrophils in peripheral blood ( D ) and lung ( F ) of infected ( n = 8) and control mice ( n = 5) was determined by flow cytometry at the indicated time points. Data are mean ± SEM and are representative of 3 independent experiments. ( E and G ) The correlation between the fold increase in peripheral blood ( E ) or lung-derived ( G ) neutrophils and weight change of SARS2-N501Y MA30 –infected mice ( n = 8) on day 5 after infection is shown. Data are representative of 3 independent experiments. ( H ) Infiltration of neutrophils (arrows) in lungs of mock- or SARS2-N501Y MA30 –infected (5000 PFU) mice. Images are representative of 3 independent experiments. Arrows: PMNs. ( I – M ) Eight- to 10-month-old C57BL/6N mice were infected with 5000 PFU SARS2-N501Y MA30 and treated with PBS, α-Ly6G antibody, or isotype control (IC, isotype Ig) ( n = 15 mice/group). Experimental setup ( I ), weight ( J ), survival ( K ), lung histopathology ( L ), and infectious virus titers ( M ) are shown. Data in J and M are mean ± SEM. Data in K are a summary of 3 independent experiments. Data in L are representative images and a summary of 2 independent experiments (data are mean ± SEM) ( n = 9). ** P < 0.01 by Student’s t-test. Scale bars: 25 μm ( H ) and 430 μm ( L ).

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Figure Lengend Snippet: ( A – C ) Eight- to 10-month-old ( n = 5) C57BL/6N mice were infected with 1000, 2000, or 5000 PFU SARS2-N501Y MA30 . Weight ( A ), survival ( B ), and lung infectious virus titers ( C ) are shown. Data are representative of 3 independent experiments. Data in A and C are mean ± SEM. LOD, limit of detection. u.d., undetected. * P < 0.05 by 1-way ANOVA with Tukey’s multiple comparisons in C . ( D – H ) Middle-aged C57BL/6N mice (8–10 months old, n = 5) were infected with 1000, 2000, or 5000 PFU SARS2-N501Y MA30 virus. ( D and F ) The number of neutrophils in peripheral blood ( D ) and lung ( F ) of infected ( n = 8) and control mice ( n = 5) was determined by flow cytometry at the indicated time points. Data are mean ± SEM and are representative of 3 independent experiments. ( E and G ) The correlation between the fold increase in peripheral blood ( E ) or lung-derived ( G ) neutrophils and weight change of SARS2-N501Y MA30 –infected mice ( n = 8) on day 5 after infection is shown. Data are representative of 3 independent experiments. ( H ) Infiltration of neutrophils (arrows) in lungs of mock- or SARS2-N501Y MA30 –infected (5000 PFU) mice. Images are representative of 3 independent experiments. Arrows: PMNs. ( I – M ) Eight- to 10-month-old C57BL/6N mice were infected with 5000 PFU SARS2-N501Y MA30 and treated with PBS, α-Ly6G antibody, or isotype control (IC, isotype Ig) ( n = 15 mice/group). Experimental setup ( I ), weight ( J ), survival ( K ), lung histopathology ( L ), and infectious virus titers ( M ) are shown. Data in J and M are mean ± SEM. Data in K are a summary of 3 independent experiments. Data in L are representative images and a summary of 2 independent experiments (data are mean ± SEM) ( n = 9). ** P < 0.01 by Student’s t-test. Scale bars: 25 μm ( H ) and 430 μm ( L ).

Article Snippet: For α-CXCL12 treatment, mice were treated on days 2 and 4 after infection with 0.2 mL PBS, or 25 or 100 mg/kg α-CXCL12 (clone MAB310, R&D Systems) or its isotype Ig (mouse IgG1, clone MAB002, R&D Systems).

Techniques: Infection, Virus, Control, Flow Cytometry, Derivative Assay, Histopathology

( A ) Weights of mice infected with 500 PFU IAV-PR8 ( n = 6), 500 PFU MERS MA ( n = 6), or 5000 PFU SARS2-N501Y MA30 ( n = 8) measured on day 5 after infection. ( B and C ) Correlation between plasma CXCL12 concentration and fold change in peripheral blood neutrophils ( B ) and LDNs ( C ) in IAV-PR8–, MERS MA -, and SARS2-N501Y MA30 –infected mice on day 5 after infection. ( B ) R = 0.04474 ( P = 0.6874) (IAV-PR8), 0.02521 ( P = 0.7639) (MERS MA ), and 0.5072 ( P = 0.0475) (SARS2-N501Y MA30 ). ( C ) R = 3.492 × 10 –6 ( P = 0.9972) (IAV-PR8), 0.4028 ( P = 0.1759) (MERS MA ), and 0.9547 ( P < 0.0001) (SARS2-N501Y MA30 ). Data are representative of 2 independent experiments. Mock- ( D ), SARS2-N501Y MA30 –infected (5000 PFU) ( E ), or IAV-PR8–infected (500 PFU) ( F ) middle-aged C57BL/6N mice (8–10 months old, n = 5/group), or MERS MA -infected (500 PFU) hDPP4 -KI mice ( G ) were treated with 0.5 mg/kg body weight of MERS (EMC)-NTD-Fc, SARS-2 (N501Y)-RBD-Fc, or SARS-2 (ancestral)-RBD-Fc in 0.5 mL PBS by i.v. injection on days 2 and 4 after infection. Mice were euthanized on day 5 after infection and abdominal aortas were harvested. The expression of CXCL12 in endothelial cells was determined by intracellular staining via flow cytometry. Data are representative of 2 independent experiments. ( H and I ) SARS2-N501Y MA30 –infected (5000 PFU) mice were treated with SARS2 (N501Y)-RBD-Fc ( n = 8) or control MERS (EMC)-NTD-Fc ( n = 5). Survival ( H ) and endothelial cell expression of CXCL12 ( I ) were determined. **** P < 0.01 by 1-way ANOVA with Tukey’s multiple comparisons. Data are mean ± SEM and are representative of 2 independent experiments. mpk, mg/kg body weight.

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Figure Lengend Snippet: ( A ) Weights of mice infected with 500 PFU IAV-PR8 ( n = 6), 500 PFU MERS MA ( n = 6), or 5000 PFU SARS2-N501Y MA30 ( n = 8) measured on day 5 after infection. ( B and C ) Correlation between plasma CXCL12 concentration and fold change in peripheral blood neutrophils ( B ) and LDNs ( C ) in IAV-PR8–, MERS MA -, and SARS2-N501Y MA30 –infected mice on day 5 after infection. ( B ) R = 0.04474 ( P = 0.6874) (IAV-PR8), 0.02521 ( P = 0.7639) (MERS MA ), and 0.5072 ( P = 0.0475) (SARS2-N501Y MA30 ). ( C ) R = 3.492 × 10 –6 ( P = 0.9972) (IAV-PR8), 0.4028 ( P = 0.1759) (MERS MA ), and 0.9547 ( P < 0.0001) (SARS2-N501Y MA30 ). Data are representative of 2 independent experiments. Mock- ( D ), SARS2-N501Y MA30 –infected (5000 PFU) ( E ), or IAV-PR8–infected (500 PFU) ( F ) middle-aged C57BL/6N mice (8–10 months old, n = 5/group), or MERS MA -infected (500 PFU) hDPP4 -KI mice ( G ) were treated with 0.5 mg/kg body weight of MERS (EMC)-NTD-Fc, SARS-2 (N501Y)-RBD-Fc, or SARS-2 (ancestral)-RBD-Fc in 0.5 mL PBS by i.v. injection on days 2 and 4 after infection. Mice were euthanized on day 5 after infection and abdominal aortas were harvested. The expression of CXCL12 in endothelial cells was determined by intracellular staining via flow cytometry. Data are representative of 2 independent experiments. ( H and I ) SARS2-N501Y MA30 –infected (5000 PFU) mice were treated with SARS2 (N501Y)-RBD-Fc ( n = 8) or control MERS (EMC)-NTD-Fc ( n = 5). Survival ( H ) and endothelial cell expression of CXCL12 ( I ) were determined. **** P < 0.01 by 1-way ANOVA with Tukey’s multiple comparisons. Data are mean ± SEM and are representative of 2 independent experiments. mpk, mg/kg body weight.

Techniques: Infection, Clinical Proteomics, Concentration Assay, Injection, Expressing, Staining, Flow Cytometry, Control

( A ) Peripheral blood samples from 6 SARS-CoV-2–infected survivors were collected longitudinally during hospitalization, as described previously . Concentrations of plasma CXCL12 and peripheral blood LDNs were measured. Black dotted line: Average plasma CXCL12 of healthy donors. Red dotted line: Average LDNs of healthy donors. ( B ) Correlation between concentration of plasma CXCL12 and percentage of peripheral blood LDNs analyzed by repeated measures correlation (with log transformation to Ln to meet linear assumption). R = –0.5437174 ( P = 0.003374754). ( C ) Peripheral blood samples from 9 SARS-CoV-2–infected deceased patients were collected at multiple time points during hospitalization, as described previously . Concentrations of plasma CXCL12 and peripheral blood LDNs are shown. Black dotted line: Average CXCL12 of healthy donors. Red dotted line: Average LDNs of healthy donors. ( D ) Correlation between concentration of plasma CXCL12 and percentage of peripheral blood LDNs analyzed by repeated measures correlation (with log transformation to Ln to meet linear assumption). R = –0.01767992 ( P = 0.9184839).

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Figure Lengend Snippet: ( A ) Peripheral blood samples from 6 SARS-CoV-2–infected survivors were collected longitudinally during hospitalization, as described previously . Concentrations of plasma CXCL12 and peripheral blood LDNs were measured. Black dotted line: Average plasma CXCL12 of healthy donors. Red dotted line: Average LDNs of healthy donors. ( B ) Correlation between concentration of plasma CXCL12 and percentage of peripheral blood LDNs analyzed by repeated measures correlation (with log transformation to Ln to meet linear assumption). R = –0.5437174 ( P = 0.003374754). ( C ) Peripheral blood samples from 9 SARS-CoV-2–infected deceased patients were collected at multiple time points during hospitalization, as described previously . Concentrations of plasma CXCL12 and peripheral blood LDNs are shown. Black dotted line: Average CXCL12 of healthy donors. Red dotted line: Average LDNs of healthy donors. ( D ) Correlation between concentration of plasma CXCL12 and percentage of peripheral blood LDNs analyzed by repeated measures correlation (with log transformation to Ln to meet linear assumption). R = –0.01767992 ( P = 0.9184839).

Article Snippet: The binding capability of α-CXCL12 antibodies (clone MAB310 and MCX120) was determined by ELISA using reagents and standard samples included in the ELISA Kit (MCX120, R&D Systems).

Techniques: Infection, Clinical Proteomics, Concentration Assay, Transformation Assay

( A ) The correlation between the concentration of plasma CXCL12 and the fold change in peripheral blood CD4 + and CD8 + T cells, immature neutrophils, degranulated neutrophils, and LDNs in SARS2-N501Y MA30 –infected mice (5000 PFU) on day 5 after infection ( n = 8). R = 0.003954 ( P = 0.8824) (CD4 + T cells), 0.0006628 ( P = 0.9518) (CD8 + T cells), 0.1851 ( P = 0.2873) (immature neutrophils), 0.02186 ( P = 0.7268) (degranulated neutrophils), and 0.9547 ( P < 0.0001) (LDNs). Data are representative of 3 independent experiments. ( B ) Expression of CXCR4 by peripheral blood CD4 + and CD8 + T cells, and neutrophil subsets of mice infected with SARS2-N501Y MA30 on day 5 after infection. ( C ) Expression of intracellular CXCL12 in CD45 – CD31 + CD54 + vascular endothelial cells on day 5 after infection. ( D ) Summary of CXCL12 expression (mean fluorescence intensity, MFI) in peripheral blood cell subsets and endothelial cells, n = 5. Data are representative of 2 independent experiments and are mean ± SEM. ** P < 0.01 by 1-way ANOVA with Tukey’s multiple comparisons. ( E ) RNA (right y axis) and protein (left y axis) CXCL12 levels in homogenates of bone marrow harvested from SARS2-N501Y MA30 –infected mice were determined at the indicated time points by RT-qPCR and ELISA, respectively. n = 4. Data are representative of 2 independent experiments.

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Figure Lengend Snippet: ( A ) The correlation between the concentration of plasma CXCL12 and the fold change in peripheral blood CD4 + and CD8 + T cells, immature neutrophils, degranulated neutrophils, and LDNs in SARS2-N501Y MA30 –infected mice (5000 PFU) on day 5 after infection ( n = 8). R = 0.003954 ( P = 0.8824) (CD4 + T cells), 0.0006628 ( P = 0.9518) (CD8 + T cells), 0.1851 ( P = 0.2873) (immature neutrophils), 0.02186 ( P = 0.7268) (degranulated neutrophils), and 0.9547 ( P < 0.0001) (LDNs). Data are representative of 3 independent experiments. ( B ) Expression of CXCR4 by peripheral blood CD4 + and CD8 + T cells, and neutrophil subsets of mice infected with SARS2-N501Y MA30 on day 5 after infection. ( C ) Expression of intracellular CXCL12 in CD45 – CD31 + CD54 + vascular endothelial cells on day 5 after infection. ( D ) Summary of CXCL12 expression (mean fluorescence intensity, MFI) in peripheral blood cell subsets and endothelial cells, n = 5. Data are representative of 2 independent experiments and are mean ± SEM. ** P < 0.01 by 1-way ANOVA with Tukey’s multiple comparisons. ( E ) RNA (right y axis) and protein (left y axis) CXCL12 levels in homogenates of bone marrow harvested from SARS2-N501Y MA30 –infected mice were determined at the indicated time points by RT-qPCR and ELISA, respectively. n = 4. Data are representative of 2 independent experiments.

Techniques: Concentration Assay, Clinical Proteomics, Infection, Expressing, Fluorescence, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

( A – D ) Experimental setup ( A ), survival ( B ), lung histopathology ( C ), and infectious viral titers ( D ) of 8- to 10-month-old C57BL/6N mice infected with 1000 PFU SARS2-N501Y MA30 followed by treatment with α-CXCL12 antibody or its isotype control (IC, isotype Ig). Data in B are a summary of 4 independent experiments ( n = 20). Data in C are representative images and a summary of 2 independent experiments ( n = 10, samples harvested on day 5 after infection). Data in D are mean ± SEM ( n = 8) and are a summary of 2 independent experiments. LOD, limit of detection. Scale bar: 430 μm. ( E – G ) Experimental setup ( E ), numbers of total neutrophils/LDNs ( F ), and CFSE-stained neutrophils/LDNs ( G ) identified in peripheral blood, lung, and bone marrow (BM) after treatment with α-CXCL12 antibody or IC ( n = 5). Data are mean ± SEM and are representative of 2 independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001 by t-test in F and G . ( H and I ) Experimental setup ( H ) and survival ( I ) of 8- to 10-month-old C57BL/6N mice infected with 1000 PFU SARS2-N501Y MA30 followed by treatment with α-CXCL12 antibody and α-Ly6G antibody or IC. Data in I are a summary of 2 independent experiments ( n = 8).

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Figure Lengend Snippet: ( A – D ) Experimental setup ( A ), survival ( B ), lung histopathology ( C ), and infectious viral titers ( D ) of 8- to 10-month-old C57BL/6N mice infected with 1000 PFU SARS2-N501Y MA30 followed by treatment with α-CXCL12 antibody or its isotype control (IC, isotype Ig). Data in B are a summary of 4 independent experiments ( n = 20). Data in C are representative images and a summary of 2 independent experiments ( n = 10, samples harvested on day 5 after infection). Data in D are mean ± SEM ( n = 8) and are a summary of 2 independent experiments. LOD, limit of detection. Scale bar: 430 μm. ( E – G ) Experimental setup ( E ), numbers of total neutrophils/LDNs ( F ), and CFSE-stained neutrophils/LDNs ( G ) identified in peripheral blood, lung, and bone marrow (BM) after treatment with α-CXCL12 antibody or IC ( n = 5). Data are mean ± SEM and are representative of 2 independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001 by t-test in F and G . ( H and I ) Experimental setup ( H ) and survival ( I ) of 8- to 10-month-old C57BL/6N mice infected with 1000 PFU SARS2-N501Y MA30 followed by treatment with α-CXCL12 antibody and α-Ly6G antibody or IC. Data in I are a summary of 2 independent experiments ( n = 8).

Techniques: Histopathology, Infection, Control, Staining

Journal: The Journal of Clinical Investigation

Article Title: CXCL12 ameliorates neutrophilia and disease severity in SARS-CoV-2 infection

doi: 10.1172/JCI188222

Techniques: Infection, Clinical Proteomics, Concentration Assay, Injection, Expressing, Staining, Flow Cytometry, Control

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