Social defeat stress aggravates asthma airway inflammation through neutrophils.
Level 5 - mechanism / opinion, no new human data
Animal experimental study with no human data
PubMed 41197683 · doi:10.1016/j.bbi.2025.106174
What was done
Murine models of asthma were subjected to a social defeat stress (SDS) intervention. Researchers compared wild-type mice, neutropenic mice (Csf3 -/-), and NETosis-impaired mice (Padi4 -/-) to evaluate the roles of neutrophils and neutrophil extracellular trap (NET) formation. Transcriptomic analysis was also performed.
What was found
The abstract reports no numerical values, percentages, or effect sizes. Social defeat stress aggravated airway hyperresponsiveness, inflammation, and remodeling in murine asthma models. These effects were attenuated in neutropenic (Csf3 -/-) mice, exacerbated in neutrophilic mice, and mitigated in NETosis-deficient (Padi4 -/-) mice. Transcriptomic analysis revealed that stress enhanced NETs formation.
Why it matters
This paper identifies neutrophil recruitment and NETosis as mechanistic pathways through which psychosocial stress exacerbates asthma pathology in mice, pointing to potential therapeutic targets.
Limits
The study was conducted entirely in mice, so findings may not translate directly to human asthma or psychosocial stress. The abstract reports no sample size (n is not given) and provides no numerical data, effect sizes, or confidence intervals.
Cited by
- supports Psychosocial stress increases the severity of asthma symptoms and lung inflammation.