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A gut commensal protozoa remotely shapes a lung niche for asthma-promoting eosinophils.

Burrows, K.; Ngai, L.; Chiaranunt, P.; Cao, E.; Streutker, C.; Forde, B.; O'Mahony, L.; Mortha, A.

2022-03-27 immunology
10.1101/2022.03.25.485893 bioRxiv
Show abstract

The gut microbiome influences chronic inflammation of the airways via the gut-lung axis. However, causal connections between microbes and their host, including the underlying mechanisms for this phenomenon remain largely unknown. Here, we show that colonization with the gut commensal protozoa, Tritrichomonas musculis (T.mu), remotely shapes the lung immune landscape and exacerbates allergic airway inflammation. We demonstrate that colonization with T.mu mediates the T and B cell-dependent accumulation and activation of inflammatory group 2 innate lymphoid cells in the lungs to constitute a tripartite immune network that serves as a niche for lung eosinophils. Animals colonized with T.mu show severely exacerbated allergic inflammation in the airways and reveal a new protozoan-driven gut-lung axis that remotely shapes the lung immune network to potentiate chronic pulmonary inflammation. One-Sentence SummaryA gut microbe exacerbates asthma severity by promoting lung eosinophilia through a tripartite lymphocyte immune network.

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