Abstract
Abstract Type 2 innate lymphoid cells and microbiota play crucial roles in type 2 immune response which is associated with asthma. In this study, we applied an OVA-induced allergic asthma model to examine the treatment of LGG and antibiotics-induced microbiome depletion to analyze the relationship between the microbes and ILC2. We found that pretreatment of LGG before sensitization in mice reduced the numbers of inflammatory cell from bronchoalveolar lavage fluid, inhibited the levels of IL-5 and IL-13 and ameliorated pulmonary inflammation as well as mucus secretion. Additionally, LGG significantly inhibited the induction of KLRG1+ILC2. 16SrDNA sequencing results indicated that asthmatic mice had a lower gut microbiome diversity and abundance compared with control mice. While LGG treatment improved microbial diversity. Notably, inflammatory cells were significantly decreased in different regions of jejunum, ileum and colon in LGG treated asthmatic mice. On the other hand, depletion of intestinal microbiota with antibiotics obviously increased the number of KLRG1+ILC2 from intestinal lamina propria and induced the mucus hypersecretion in the lower respiratory tract. Moreover, intestinal microbial depletion strengthened the pulmonary inflammatory and induction of KLRG1+ILC2 in asthmatic mice. Furthermore, pretreatment of LGG didn’t inhibit the pulmonary inflammation in asthmatic mice with depletion of intestinal microbiota. These findings uncovered a close crosstalk between ILC2 and pulmonary inflammatory, suggesting intestinal microbiota might be a primary determinant for the development of asthma, thus provided additional evidence for the strain treatment on allergic asthma in the future.
Published Version
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