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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Methanobrevibacter smithii activates immune microenvironment of intestinum tenue in a mouse model
Mengli Jin1, Jiandong Hu1, Chong Tian2
1Core Laboratory, Tianjin Beichen Hospital, Tianjin, 300400, China.
Abstract:
In this investigation, we systematically evaluated the immunomodulatory mechanisms of Methanobrevibacter smithii within the intestinal mucosal immune system using a murine oral gavage model. Flow cytometric analysis revealed that M. smithii administration significantly augmented TNF-α, IL-22, and IL-17 production in three key lymphocyte populations: group 3 innate lymphoid cells (ILC3s), CD4 + T cells, and CD8 + T cells. Notably, while the frequency of CD4 + T cells exhibited a reduction in the treatment cohort, CD8 + T cell proportions remained unchanged. Crucially, our comprehensive profiling demonstrated stable GM-CSF expression across all analyzed immune cell subsets. Although comparable activation patterns were observed in both ILC3s and T cell populations, multivariate analysis failed to identify linear correlations between their cytokine expression profiles. These findings demonstrate that Methanobrevibacter smithii actively modulates mucosal immunity through dual activation of innate (ILC3s) and adaptive (CD4+/CD8 + T cells) immune compartments, while highlighting the existence of non-redundant regulatory mechanisms within the intestinal immune ecosystem that merit further mechanistic exploration.
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