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Effect of reconstitution of clodronate‐treated mice with littermate control or Cotl1 −/‐ alveolar macrophages on HDM‐induced pulmonary immune cell accumulation. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with WT or Cotl1 −/‐ AMs and treated with HDM. On day 23, mice were sacrificed, and lung tissue single‐cell suspensions were prepared and analyzed by flow cytometry. B) Frequencies of IRF5 + M1 macrophages, CD206 + M2 macrophages, and IL‐10 + M2‐like macrophages among the CD45 + CD11c + CD11b − F4/80 + population ( n = 6). C) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). D) Frequencies of <t>CRTH2</t> + cells among the macrophage population ( n = 6). E) Frequencies of CRTH2 + cells among the basophil population ( n = 6). F) Frequencies of CRTH2 + cells among the eosinophil population ( n = 6). G) Frequencies of CRTH2 + cells among the ILC2 population ( n = 6). H) Frequencies of CRTH2 + cells among the mast cell population ( n = 6). I) Frequencies of CRTH2 + cells among the Th2 cell population ( n = 6). Data shown in (B), (C), and (E)‐(I) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following one‐way ANOVA for (B), (C), and (E–I). p < 0.05 was considered statistically significant.
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Effect of reconstitution of clodronate‐treated mice with littermate control or Cotl1 −/‐ alveolar macrophages on HDM‐induced pulmonary immune cell accumulation. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with WT or Cotl1 −/‐ AMs and treated with HDM. On day 23, mice were sacrificed, and lung tissue single‐cell suspensions were prepared and analyzed by flow cytometry. B) Frequencies of IRF5 + M1 macrophages, CD206 + M2 macrophages, and IL‐10 + M2‐like macrophages among the CD45 + CD11c + CD11b − F4/80 + population ( n = 6). C) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). D) Frequencies of <t>CRTH2</t> + cells among the macrophage population ( n = 6). E) Frequencies of CRTH2 + cells among the basophil population ( n = 6). F) Frequencies of CRTH2 + cells among the eosinophil population ( n = 6). G) Frequencies of CRTH2 + cells among the ILC2 population ( n = 6). H) Frequencies of CRTH2 + cells among the mast cell population ( n = 6). I) Frequencies of CRTH2 + cells among the Th2 cell population ( n = 6). Data shown in (B), (C), and (E)‐(I) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following one‐way ANOVA for (B), (C), and (E–I). p < 0.05 was considered statistically significant.
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Effect of reconstitution of clodronate‐treated mice with littermate control or Cotl1 −/‐ alveolar macrophages on HDM‐induced pulmonary immune cell accumulation. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with WT or Cotl1 −/‐ AMs and treated with HDM. On day 23, mice were sacrificed, and lung tissue single‐cell suspensions were prepared and analyzed by flow cytometry. B) Frequencies of IRF5 + M1 macrophages, CD206 + M2 macrophages, and IL‐10 + M2‐like macrophages among the CD45 + CD11c + CD11b − F4/80 + population ( n = 6). C) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). D) Frequencies of CRTH2 + cells among the macrophage population ( n = 6). E) Frequencies of CRTH2 + cells among the basophil population ( n = 6). F) Frequencies of CRTH2 + cells among the eosinophil population ( n = 6). G) Frequencies of CRTH2 + cells among the ILC2 population ( n = 6). H) Frequencies of CRTH2 + cells among the mast cell population ( n = 6). I) Frequencies of CRTH2 + cells among the Th2 cell population ( n = 6). Data shown in (B), (C), and (E)‐(I) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following one‐way ANOVA for (B), (C), and (E–I). p < 0.05 was considered statistically significant.

Journal: Advanced Science

Article Title: Coactosin‐Like Protein Reduces Prostaglandin D 2 Production in Alveolar Macrophages and Alleviates Allergic Airway Inflammation

doi: 10.1002/advs.202501673

Figure Lengend Snippet: Effect of reconstitution of clodronate‐treated mice with littermate control or Cotl1 −/‐ alveolar macrophages on HDM‐induced pulmonary immune cell accumulation. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with WT or Cotl1 −/‐ AMs and treated with HDM. On day 23, mice were sacrificed, and lung tissue single‐cell suspensions were prepared and analyzed by flow cytometry. B) Frequencies of IRF5 + M1 macrophages, CD206 + M2 macrophages, and IL‐10 + M2‐like macrophages among the CD45 + CD11c + CD11b − F4/80 + population ( n = 6). C) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). D) Frequencies of CRTH2 + cells among the macrophage population ( n = 6). E) Frequencies of CRTH2 + cells among the basophil population ( n = 6). F) Frequencies of CRTH2 + cells among the eosinophil population ( n = 6). G) Frequencies of CRTH2 + cells among the ILC2 population ( n = 6). H) Frequencies of CRTH2 + cells among the mast cell population ( n = 6). I) Frequencies of CRTH2 + cells among the Th2 cell population ( n = 6). Data shown in (B), (C), and (E)‐(I) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following one‐way ANOVA for (B), (C), and (E–I). p < 0.05 was considered statistically significant.

Article Snippet: Antibodies for CLP (10781‐1‐AP), HPGDS (22522‐1‐AP), mPGES‐2 (10881‐1‐AP), CRTH2 (25264‐1‐AP), and β‐actin (60008‐1‐lg) were purchased from Proteintech (Hubei, China).

Techniques: Control, Liposomes, Injection, Flow Cytometry

AMs from Cotl1 −/− mice confer exacerbated airway inflammation via CRTH2. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with Cotl1 −/‐ AMs. Mice were challenged with HDM and treated with OC000459 . On day 23, mice were euthanized, and lung tissue was analyzed. B) The levels of Th2 cytokines (IL‐4, IL‐5, and IL‐13) in lung tissue extracts were determined by ELISA ( n = 6). C,D) Representative lung samples stained with (C) H&E and (D) PAS ( n = 6). Scale bar: 50 µm. E) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). Data shown in (B–D) were presented as mean ± SD, and data shown in (E) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following two‐way ANOVA for (B), and Tukey's multiple comparisons test following one‐way ANOVA for (C–E). p < 0.05 was considered statistically significant.

Journal: Advanced Science

Article Title: Coactosin‐Like Protein Reduces Prostaglandin D 2 Production in Alveolar Macrophages and Alleviates Allergic Airway Inflammation

doi: 10.1002/advs.202501673

Figure Lengend Snippet: AMs from Cotl1 −/− mice confer exacerbated airway inflammation via CRTH2. A) WT mice received clodronate liposomes to deplete endogenous AMs. After 72 h, the mice were intranasally injected with Cotl1 −/‐ AMs. Mice were challenged with HDM and treated with OC000459 . On day 23, mice were euthanized, and lung tissue was analyzed. B) The levels of Th2 cytokines (IL‐4, IL‐5, and IL‐13) in lung tissue extracts were determined by ELISA ( n = 6). C,D) Representative lung samples stained with (C) H&E and (D) PAS ( n = 6). Scale bar: 50 µm. E) Frequencies of IL‐4 + Th2 cells among the CD4 + population, CD49b + basophils among the IgE + population, Siglec‐F + eosinophils among the CD45 + CD11c + population, Sca‐1 + KLRG1 + ILC2 cells among the CD45 + CD25 + Lin − population, and CD117 + mast cells among the IgE + population ( n = 6). Data shown in (B–D) were presented as mean ± SD, and data shown in (E) were presented as median ± interquartile range. p values were assessed using Tukey's multiple comparisons test following two‐way ANOVA for (B), and Tukey's multiple comparisons test following one‐way ANOVA for (C–E). p < 0.05 was considered statistically significant.

Article Snippet: Antibodies for CLP (10781‐1‐AP), HPGDS (22522‐1‐AP), mPGES‐2 (10881‐1‐AP), CRTH2 (25264‐1‐AP), and β‐actin (60008‐1‐lg) were purchased from Proteintech (Hubei, China).

Techniques: Liposomes, Injection, Enzyme-linked Immunosorbent Assay, Staining