Fig. 4: CRHPVN activation limits neutrophil effector functions during ALI.
From: Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve–neutrophil axis
a Schematic diagram of the experimental procedures in CRH-IRES-Cre mice. Created in BioRender. Liu, T. (2025) https://BioRender.com/p48gmjd. b Volcano plot of DEGs identified from neutrophil RNA sequencing data between control mice and hM3Dq mice subjected to ALI. c Bar graph of KEGG pathway enrichment analysis from neutrophil RNA sequencing data between control mice and hM3Dq mice treated with LPS. d Representative flow cytometry plots and analysis of neutrophil phagocytosis activity of PBS-treated, LPS-treated control, and LPS-treated hM3Dq mice (n = 6 mice per group). e Representative flow cytometry plot and analysis of neutrophil ROS production of PBS-treated, LPS-treated control, and LPS-treated hM3Dq mice (n = 6 mice per group). f Representative images of NETs in lung tissues of PBS-treated, LPS-treated control, and LPS-treated hM3Dq mice. Scale bar: 20 μm. g Quantitative analysis of the percentage of CitH3+ neutrophils (n = 4 mice per group). Significance was determined by the 1-way ANOVA with Tukey’s post-hoc multiple comparisons test. Each dot represents an individual mouse. The data are presented as mean ± SEM. All experiments were repeated three times, yielding similar results. Source data are provided as a Source data file. ALI acute lung injury, CRH corticotropin-releasing hormone, LPS lipopolysaccharide, MFI mean fluorescence intensity, NETs neutrophil extracellular traps, DEGs differentially expressed genes, PVN paraventricular nucleus, ROS reactive oxygen species.
