Mycobacterium tuberculosis Rv3435c gene regulates inflammatory cytokines and is involved in lung injury and mycobacterial survival in mice
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Updated: Jul 12, 2026

A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection
Published on: October 5, 2015
Xin-Yue Liu1, Dan-Ni Li1, Kun Shi2
1College of Animal Science and Technology, Jilin Agricultural University, Changchun, China.
Abstract:
Mycobacterium tuberculosis enters the body through the respiratory tract, produces and releases virulence proteins through a variety of mechanisms, regulates the host immune mechanism through a variety of ways, and then survives in the body for a long time. These depend on virulence genes encoded by Mycobacterium tuberculosis. Previous studies found that the Rv3435c gene of Mycobacterium tuberculosis is highly conserved in pathogenic mycobacterium, but not conserved in non-pathogenic mycobacterium, which may be a potential virulence gene, and inhibit the secretion of inflammatory factors in RAW264.7 cells and inhibit cell apoptosis. Based on previous studies, the function of Rv3435c gene in mice was studied by infecting mice with recombinant strains. In vivo infection experiments showed that overexpression of Rv3435c significantly promoted the survival of Ms in the lung. Ms-pMV361-Rv3435c specifically inhibits the secretion of inflammatory cytokines, including TNF-α, IL-6, IL-1β, IL-12, and IFN-γ. Rv3435c can inhibit lung cell apoptosis and cause pathological damage to lung. Therefore, Rv3435c enhances the survival of mycobacterium in mice and promotes the pathogenicity and spread of Mycobacterium tuberculosis by inhibiting the production of cytokines.
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