cxcl11 polyclonal antibody  (Proteintech)

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

Article Title: Herbal Medication, Macmoondong Decoction, Attenuates LPS-Induced COPD in Small Airways via TGF- β , CCL-2, and CXCL1

doi: 10.1155/2020/6413491

Figure Lengend Snippet: Macmoondong decoction dose-dependently suppressed the DNA expression of TGF- β , CCL-2, CXCL1, and CXCL11. (a) The DNA expression of TGF- β in the macmoondong decoction-treated groups was lower than that in the Spiriva treatment group; in addition, a dose-dependent suppression was observed. (b) The change in DNA expression of CCL-2 was similar to the pattern in TGF- β . (c) Macmoondong decoction effectively downregulated the DNA expression of CXCL1; the pattern of changes was very similar to that of TGF- β . (d) Compared with the changes in other genes, such as TGF- β , CCL-2, and CXCL1, small changes were observed, but macmoondong decoction effectively suppressed the DNA expression of CXCL11. Each bar represents the mean ± SD ( N = 8). ∗ P < 0.05 vs. control group; ∗∗ P < 0.01 vs. control group; $ P < 0.05 vs. COPD induction group; $$ P < 0.01 vs. COPD induction group; # P < 0.05 vs. Spiriva treatment group; # P < 0.05 vs. Spiriva treatment group.

Article Snippet: The slides were incubated with normal serum to block nonspecific binding and then incubated for 1 h with primary antibodies (1 : 100 to 1 : 200 dilutions) to TGF- β (MBS462142, MyBioSource), CCL-2 (PAB16617, Abnova, Taipei, Taiwan), CXCL1 (PAB8798, Abnova), and CXCL11 (bs-2552R, Bioss).

Techniques: Expressing

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

Article Title: Herbal Medication, Macmoondong Decoction, Attenuates LPS-Induced COPD in Small Airways via TGF- β , CCL-2, and CXCL1

doi: 10.1155/2020/6413491

Figure Lengend Snippet: Macmoondong decoction dose-dependently suppressed the expression of TGF- β , CCL-2, CXCL1, and CXCL11. (a) In the 1500 mg/kg macmoondong decoction treatment group, the expression of TGF- β was lower than that in the Spiriva treatment group, and dose-dependent inhibition was observed. (b) Macmoondong decoction significantly inhibited the expression of CCL-2 in a dose-dependent manner, and in the 1500 mg/kg macmoondong decoction treatment group, the suppression of CCL-2 was more effective than that in Spiriva treatment. (c) Macmoondong decoction dose-dependently downregulated the expression of CXCL1. (d) Similar to the changes in CXCL1, macmoondong decoction exerted dose-dependent suppression. (e) The positively stained cell counts for TGF- β , CCL-2, CXCL1, and CXCL11. Each bar represents the mean ± SD ( N = 8). # P < 0.05 vs. control group; ∗∗ P < 0.01 vs. control group; $ P < 0.05 vs. COPD induction group; $$ P < 0.01 vs. COPD induction group; # P < 0.05 vs. Spiriva treatment group; ## P < 0.01 vs. Spiriva treatment group.

Article Snippet: The slides were incubated with normal serum to block nonspecific binding and then incubated for 1 h with primary antibodies (1 : 100 to 1 : 200 dilutions) to TGF- β (MBS462142, MyBioSource), CCL-2 (PAB16617, Abnova, Taipei, Taiwan), CXCL1 (PAB8798, Abnova), and CXCL11 (bs-2552R, Bioss).

Techniques: Expressing, Inhibition, Staining

Journal: Frontiers in Pharmacology

Article Title: CXCR7 Antagonism Reduces Acute Lung Injury Pathogenesis

doi: 10.3389/fphar.2021.748740

Figure Lengend Snippet: Kinetics of the expression of CXCR3/CXCR4 and its ligands in the BAL of LPS-challenged DBA/1 mice. ALI was induced by nebulized LPS inhalation in male DBA/1 mice. Control mice inhaled NaCl 0.9% ( n = 12 mice; all time points were pooled). (A) LPS inhalation increased protein concentrations of the CXCR3 ligands CXCL9, CXCL10, and CXCL11, measured in the BAL 5, 24, 48, and 72 h following LPS challenge, compared with control mice. Results are expressed as mean ± SEM ( n = 8 mice per time point). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus control mice using Student t -test. (B) Representative gating strategy for CXCR3 + myeloid and lymphoid cells. (C) CXCR3 expression on BAL lymphoid and myeloid-infiltrating cells. Results are expressed as mean ± SEM of the mean fluorescence intensity (MFI) of CXCR3 obtained for each LPS-challenged mouse ( n = 7–8 mice per time point) corrected by the MFI obtained in the fluorescence minus one (FMO) controls for CXCR3. Negative MFI values were set to 0. The complete gating strategy for lymphoid and myeloid cells is illustrated in . (D) Proportion of CXCR3 + lymphoid and myeloid cells expressed as percentages (mean ± SEM) of the CD45 + CD11b − and CD45 + CD11b + parent population, respectively, in the BAL (see gating strategy in ) ( n = 7–8 mice per time point). (E) Time course of BAL CXCR3 + lymphoid and myeloid cell infiltrates. Results are expressed as absolute counts in the BAL (mean ± SEM). ** p < 0.01, *** p < 0.001, **** p < 0.0001 using Student t -test versus control mice. (F) LPS inhalation increased protein concentrations of the CXCR4 ligand CXCL12, measured in the BAL 5, 24, 48, and 72 h following LPS nebulization compared with control mice. Results are expressed as mean ± SEM ( n = 7–8 mice per time point). ** p < 0.01, **** p < 0.0001 versus control mice using Student t -test. (G) Representative gating strategy for CXCR4 + myeloid and lymphoid cells. (H) CXCR4 expression on BAL lymphoid and myeloid-infiltrating cells. Results are expressed as mean ± SEM of the MFI of CXCR4 obtained for each LPS-challenged mouse ( n = 7–8 mice per time point) corrected by the MFI obtained in the FMO controls for CXCR4. Negative MFI values were set to 0. The gating strategy for lymphoid and myeloid cells is illustrated in . (I) Proportion of CXCR4 + lymphoid and myeloid cells expressed as percentages (mean ± SEM) of the CD45 + CD11b − and CD45 + CD11b + parent population, respectively, in the BAL (see gating strategy in ) ( n = 7–8 mice per time point). (H) Time course of BAL CXCR4 + lymphoid and myeloid cell infiltrates. Results are expressed as absolute counts in the BAL (mean ± SEM) ( n = 7–8 mice per time point). ** p < 0.01, *** p < 0.001, **** p < 0.0001 using Student t -test versus control mice.

Article Snippet: Recombinant murine CXCL11 (250-29; Peprotech, Cranbury, NJ, United States) was used as a standard, and Fluor-labeled anti-mouse CXCL11 polyclonal antibody (AF572; R&D Systems) was used as the detection antibody.

Techniques: Expressing, Control, Fluorescence

Journal: Frontiers in Pharmacology

Article Title: CXCR7 Antagonism Reduces Acute Lung Injury Pathogenesis

doi: 10.3389/fphar.2021.748740

Figure Lengend Snippet: Antagonism of CXCR7 increases plasma CXCL11 and CXCL12 levels and decreases CXCR3 + and CXCR4 + BAL infiltrates post LPS challenge. ALI was induced by nebulized LPS inhalation, and DBA/1 mice were treated with vehicle (LPS-vehicle, black bars) or ACT-1004-1239 (LPS-ACT-1004-1239, 100 mg/kg, red bars) orally, twice daily, 1 h prior to LPS challenge. Control mice received vehicle 1 h prior to NaCl 0.9% inhalation (NaCl-vehicle, white bars; n = 12 mice, pool of all time points). Protein concentrations of CXCL11 and CXCL12 in the plasma and lung tissue and BAL flow cytometry of immune infiltrates were performed 24, 48, and 72 h after challenge ( n = 6–8 mice per time point). Time course of CXCL11 protein concentration in the plasma (A) and lung tissue (B) . Chemokine concentrations are expressed in pg/ml (plasma) or pg/lung homogenate (mean ± SEM). ** p < 0.01, *** p < 0.001 versus LPS-vehicle-treated animals or # p < 0.05, ### p < 0.001 versus NaCl-vehicle-treated control mice using Student t -tests. Time course of BAL CXCR3 + lymphoid (C) and myeloid (D) infiltrates. Results are expressed as absolute cell counts in the BAL (mean ± SEM). * p < 0.05, **** p < 0.0001 versus LPS-vehicle-treated animals or ### p < 0.001, #### p < 0.0001 versus NaCl-vehicle-treated control mice using Student t-tests. Time course of CXCL12 concentration in the plasma (E) and lung tissue (F) . Chemokine concentrations are expressed in ng/ml (plasma) or ng/lung homogenate (mean ± SEM). **** p < 0.0001 versus LPS-vehicle-treated animals or # p < 0.05, ### p < 0.001 versus NaCl-vehicle-treated control mice using Student t-tests. Time course of BAL CXCR4 + lymphoid (G) and BAL CXCR4 + myeloid (H) infiltrates. Results are expressed as absolute counts in the BAL (mean ± SEM). * p < 0.05, ** p < 0.01, using Student t-test versus LPS-vehicle-treated animals or ### p < 0.001, #### p < 0.0001 versus NaCl-vehicle-treated control mice using Student t-tests.

Article Snippet: Recombinant murine CXCL11 (250-29; Peprotech, Cranbury, NJ, United States) was used as a standard, and Fluor-labeled anti-mouse CXCL11 polyclonal antibody (AF572; R&D Systems) was used as the detection antibody.

Techniques: Clinical Proteomics, Control, Flow Cytometry, Protein Concentration, Concentration Assay

Journal: Frontiers in Pharmacology

Article Title: CXCR7 Antagonism Reduces Acute Lung Injury Pathogenesis

doi: 10.3389/fphar.2021.748740

Figure Lengend Snippet: Treatment with ACT-1004-1239 dose-dependently increases plasma CXCL11 and CXCL12 levels and reduces BAL T cell and inflammatory macrophage infiltrates in the LPS-induced ALI/ARDS model. Vehicle (Veh; black bars) or ACT-1004-1239 (10, 30, or 100 mg/kg; bars with different shades of red) was given orally, twice daily, starting 1 h prior to LPS nebulization, for a total of six administrations. Control mice (white bars) were challenged by NaCl nebulization and received vehicle administrations. Plasma CXCL11 (A) and plasma CXCL12 levels (B) 72 h after LPS or NaCl challenge. Results are expressed as mean + SEM ( n = 10–25 mice per treatment-LPS groups and n = 4–5 mice for control group). * p < 0.05, **** p < 0.0001 versus vehicle-treated LPS-challenged mice, using one-way ANOVA test followed by Dunnett’s multiple comparisons test. Total BAL T cell (C) and BAL inflammatory macrophage counts (D) 72 h after LPS challenge. Results are expressed as mean ± SEM with n = 11–23 mice per treatment-LPS groups and n = 3 for controls. ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus vehicle-treated LPS-challenged mice, using one-way ANOVA test followed by Dunnett’s multiple comparisons test.

Article Snippet: Recombinant murine CXCL11 (250-29; Peprotech, Cranbury, NJ, United States) was used as a standard, and Fluor-labeled anti-mouse CXCL11 polyclonal antibody (AF572; R&D Systems) was used as the detection antibody.

Techniques: Clinical Proteomics, Control

Journal: Frontiers in Pharmacology

Article Title: CXCR7 Antagonism Reduces Acute Lung Injury Pathogenesis

doi: 10.3389/fphar.2021.748740

Figure Lengend Snippet: Summary of pathological role of CXCR7 and potential benefit of CXCR7 antagonism during ALI/ARDS. (A) CXCR7 functions predominantly as a scavenger receptor for its two ligands: the interferon-inducible chemokine CXCL11 and the constitutive chemokine CXCL12. Binding of its ligands leads to internalization of the CXCR7–ligand complex and ligand degradation. CXCL11 and CXCL12 also bind and activate the signaling chemokine receptors CXCR3 and CXCR4, respectively. The CXCR3/CXCR4/CXCR7 axes play an important role in lung inflammation. CXCR7 scavenging activity tightly regulates the extracellular levels of its ligands, facilitating the establishment and maintenance of CXCL11/12 chemokine concentration gradients and CXCR3 + /CXCR4 + cell migration from the blood to the inflamed lung. In addition, increased CXCR7 expression in the inflamed lung has been reported to be associated with breathing pattern alteration and endothelial barrier dysfunction. (B) CXCR7 antagonism with the CXCR7 antagonist ACT-1004-1239 exhibits immunomodulatory effects: by blocking the scavenging activity of the receptor and consequently increasing CXCL11 and CXCL12 plasma concentrations, chemokine gradients are disrupted, inhibiting CXCR3 + and CXCR4 + cell migration to the inflamed lung. In addition, treatment with ACT-1004-1239, by increasing plasma CXCL12 and/or by direct inhibition of CXCR7 signaling, ameliorates ALI-induced breathing pattern alteration and endothelial barrier dysfunction.

Article Snippet: Recombinant murine CXCL11 (250-29; Peprotech, Cranbury, NJ, United States) was used as a standard, and Fluor-labeled anti-mouse CXCL11 polyclonal antibody (AF572; R&D Systems) was used as the detection antibody.

Techniques: Binding Assay, Activity Assay, Concentration Assay, Migration, Expressing, Blocking Assay, Clinical Proteomics, Inhibition