PloS one · 2025
The role of gut leakage and immune cell miss-homing on gut dysbiosis-induced lung inflammation in a DSS mice model.
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Eladham Mariam Wed, Sharif-Askari Narjes Saheb, Sekar Priyadharshini, Mdkhana Bushra, Selvakumar Balachandar, Al-Sheakly Baraa Khalid Salah, Sharif-Askari Fatemeh Saheb, Hachim Ibrahim, Halwani Rabih
Аннотация
BACKGROUND: Inflammatory Bowel Disease (IBD), encompassing Crohn's disease and ulcerative colitis, affects millions globally, with extraintestinal manifestations (EIMs) occurring in 25-40% of patients. Among these, respiratory complications are of particular concern, yet the immunologic and physiologic mechanisms underlying gut-lung interactions remain poorly understood. The gut-lung axis (GLA) describes bi-directional communication between the gut and lungs, where microbial dysbiosis in the gut can drive lung inflammation and immune dysregulation.
METHODS: Mice were treated with 4% DSS for 7 days to induce colitis. Gut permeability, tight junction protein expression, lung inflammation, immune cell trafficking, and microbial translocation were assessed through histology, qPCR, flow cytometry, and GFP-tagged fecal microbiome experiments.
RESULTS: DSS treatment led to significant disruption of the gut barrier, with upregulation of gut leakage markers and downregulation of tight junction proteins. Lung inflammation was characterized by elevated IL-17, neutrophil infiltration, and airway hyperresponsiveness. Flow cytometry revealed mis-homing of gut-primed immune cells (α4β7+ and CCR9 + CD4+) to the lungs and tracking bacteria via GFP- tagged fecal microbiome confirmed microbial translocation from the gut to the lungs which may contribute to lung inflammation.
CONCLUSION: Disrupted gut integrity facilitates microbial translocation and immune cell mis-homing, contributing to lung inflammation. These results provide new insights into how gut dysbiosis influences respiratory inflammation.
METHODS: Mice were treated with 4% DSS for 7 days to induce colitis. Gut permeability, tight junction protein expression, lung inflammation, immune cell trafficking, and microbial translocation were assessed through histology, qPCR, flow cytometry, and GFP-tagged fecal microbiome experiments.
RESULTS: DSS treatment led to significant disruption of the gut barrier, with upregulation of gut leakage markers and downregulation of tight junction proteins. Lung inflammation was characterized by elevated IL-17, neutrophil infiltration, and airway hyperresponsiveness. Flow cytometry revealed mis-homing of gut-primed immune cells (α4β7+ and CCR9 + CD4+) to the lungs and tracking bacteria via GFP- tagged fecal microbiome confirmed microbial translocation from the gut to the lungs which may contribute to lung inflammation.
CONCLUSION: Disrupted gut integrity facilitates microbial translocation and immune cell mis-homing, contributing to lung inflammation. These results provide new insights into how gut dysbiosis influences respiratory inflammation.