TRIM22 regulates macrophage autophagy and enhances Mycobacterium tuberculosis clearance by targeting the nuclear factor-multiplicity κB/beclin 1 pathway
Abstract
Autophagy is a crucial host-defense mechanism against Mycobacterium tuberculosis (Mtb) infection by spanning innate and adaptive immune functions. TRIM22 is a member of tripartite motif family protein which involved in innate immunity and autophagy process. However, its role in the modulation of bacterial infection has not been investigated. Here, we demonstrated that TRIM22 is upregulated in a dose-dependent and time-dependent manner during Mtb infection of THP-1 cells. Downregulation of TRIM22 significantly decreased light chain 3 (LC3)-II protein level and the formation of LC3 puncta, while it markedly increased SQSTM1, a marker of autophagic degradation, in Mtb-infected THP-1 cells. What is more, enhanced bacterial survival was observed in TRIM22 knockdown THP-1 cells, while rapamycin abrogated this effect. In the presence of vector containing TRIM22 in THP-1 cells prior to infection, the survival of Mtb was decreased, while BafA restored this effect. Further study demonstrated that TRIM22 expression was regulated by MicroRNA-20b, and that TRIM22 regulates Mtb-infected THP-1 autophagy via the nuclear factor-κB/beclin 1 pathway. Using a nuclear factor-κB inhibitor BAY 11-7082, we found that TRIM22-induced high expression of ...Continue Reading
References
Citations
Related Concepts
Related Feeds
Autophagy & Model Organisms
Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms