Shenzhen University's latest Nature article subverts the precise medical perspective

Researchers from the School of Medicine, School of Medicine, Shenzhen University, and the University of Massachusetts Medical School published a paper entitled "Nitric oxide prevents a pathogen-permissive granulocytic inflammation during tuberculosis", which subverts the traditional understanding of the role of nitric oxide in preventing tuberculosis. A new discovery of innovative mechanisms for nitric oxide in anti-tuberculosis provides an important direction and potential target for further precise definition of host susceptibility to tuberculosis.

The research was published in the May 15 issue of Nature Microbiology. The author of the article was Professor Chen Xinchun from Shenzhen University and Professor Christopher Sessatti from the University of Massachusetts Medical School.

Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis infection that seriously endangers human health. Nitric oxide (NO) plays an important role in the host against Mycobacterium tuberculosis. It is traditionally believed that host macrophages induce nitric oxide synthase (iNOS) to produce nitric oxide by directly killing tuberculosis, thereby protecting the host's lung inflammation.

In this study, however, the researchers found that nitric oxide first inhibits the replication of tuberculosis by inhibiting neutrophil inflammation in the host lung. This discovery subverts the traditional understanding of the role of nitric oxide in the fight against tuberculosis. Using mouse animal models, the researchers found that iNOS knockout mice can produce large amounts of interleukin IL-1β after infection with tuberculosis.

And 12/15 lipoxygenase, which recruits a large number of neutrophils to the lung tissue, creating a nutrient-rich pathogen-permissive granulocytic inflammation that promotes tuberculosis Bacterial replication.

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