
장내 미생물 균총 불균형은 Nos2 발현 증가를 통해 폐 내 Mycobacteria 집락화를 증가시킨다.


coremsg

Increasing researches reveal gut microbiota was associated with the development of tuberculosis. How to prevent or reduce Mycobacterium tuberculosis colonization in the lungs is a key measure to prevent tuberculosis. However, the data on gut microbiota preventing Mycobacterium colonization in the lungs were scarce. Here, we established the clindamycin-inducing intestinal microbiome dysbiosis and fecal microbial transplantation models in mice to identify the effect of gut microbiota on the colonization of Mycobacterium in the mouse lungs and to explore its potential mechanisms. The results showed that clindamycin treatment altered the diversity and composition of the intestinal bacterial and fungal microbiome, weakened the trans-kingdom network interactions between bacteria and fungi, and induced gut microbiome dysbiosis in the mice. Gut microbiota dysbiosis increases intestinal permeability and enhances the susceptibility of Mycobacterium colonization in the lungs of mice. The potential mechanisms were gut microbiota dysbiosis altered the lung transcriptome and increased Nos2 expression through the “gut-lung axis”. Nos2 high expression disrupts the intracellular antimicrobial and anti-inflammatory environment by increasing the concentration of NO, decreasing the levels of ROS and Defb1 in the cells, and resulting in promoting Mycobacteria colonization in the lungs of mice. The present study raises a potential strategy for reducing the risks of Mycobacteria infections and transmission by regulating the gut microbiome balance.

### Competing Interest Statement

The authors have declared no competing interest.

Intestinal microbiome dysbiosis increases Mycobacteria pulmonary colonization in mice by regulating the Nos2-associated pathways

장내-미생물-균총-불균형이-nos2-관련-경로를-조절하여-마우스의-폐-내-mycobacteria-집락화를-증가시킨다


장내 미생물 균총 불균형이 Nos2 관련 경로를 조절하여 마우스의 폐 내 Mycobacteria 집락화를 증가시킨다
