Gut-derived memory γδ T17 cells exacerbate sepsis-induced acute lung injury in mice.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 39112475.
- Also identified by DOI 10.1038/s41467-024-51209-9 and PMC identifier 11306781.
- Licence recorded as CC BY-NC-ND.
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Abstract
Sepsis is a critical global health concern linked to high mortality rates, often due to acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). While the gut-lung axis involvement in ALI is recognized, direct migration of gut immune cells to the lung remains unclear. Our study reveals sepsis-induced migration of γδ T17 cells from the small intestine to the lung, triggering an IL-17A-dominated inflammatory response in mice. Wnt signaling activation in alveolar macrophages drives CCL1 upregulation, facilitating γδ T17 cell migration. CD44<sup>+</sup> Ly6C<sup>-</sup> IL-7R<sup>high</sup> CD8<sup>low</sup> cells are the primary migratory subtype exacerbating ALI. Esketamine attenuates ALI by inhibiting pulmonary Wnt/β-catenin signaling-mediated migration. This work underscores the pivotal role of direct gut-to-lung memory γδ T17 cell migration in septic ALI and clarifies the importance of localized IL-17A elevation in the lung.
Medical subject headings
- Sepsis
- Acute Lung Injury
- Interleukin-17
- Cell Movement
- Lung
- Mice, Inbred C57BL