Abstract
Abstract Acute Respiratory Distress Syndrome (ARDS) is a clinical syndrome characterized by an intense host inflammatory response to an infectious, non-infectious, or extrapulmonary insult. It is associated with the development of lung damage, the rapid onset of severe respiratory and organ failure. Neutrophils and lymphocytes have been shown to accumulate in the airways. However, the mechanisms that lead to this aberrant inflammation and the nature of the lymphocyte subsets involved in the recruitment of neutrophils to the lung and in their activation are not yet clearly defined. Using a unique mouse model of virus-induced ARDS that recapitulates the histopathology observed in patients with ARDS, we hypothesized, that the inflammation observed in ARDS is the result of (i) a defective regulatory Foxp3+CD4+ T cell population (T-reg), and (ii) an imbalance in the modulation of T-regs and the proinflammatory TH17 population. Therefore, we evaluated the presence of Foxp3+CD4+ T-regs in the lungs and BAL fluid of infected mice. We observed a difference in the phenotype of the regulatory T cell population in the lungs at different stages of the disease from progression to recovery in our virus-induced ARDS model. We concluded that the inflammation observed in our model, does not result from the absence of regulatory T cells, but may result from an impairment of the function of the Foxp3+CD4+ regulatory T cells, which may contribute to the uncontrolled inflammation observed in ARDS.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call