Mycobacterium tuberculosis Rv2387 Facilitates Mycobacterial Survival by Silencing TLR2/p38/JNK Signaling.
Pathogens
; 11(9)2022 Aug 27.
Article
em En
| MEDLINE
| ID: mdl-36145413
ABSTRACT
Mycobacterium tuberculosis (Mtb) can evade antimicrobial immunity and persist within macrophages by interfering with multiple host cellular functions through its virulence factors, causing latent tuberculosis. The Rv2387 protein has been identified as a putative effector that potentially participates in Mtb pathogenicity. To explore the role of the Rv2387 protein in host-mycobacteria interactions, we established recombinant M. smegmatis strains and RAW264.7 cell lines that stably express the Rv2387 protein. We found that this protein suppresses mycobacteria infection-induced macrophage apoptosis by inactivating caspase-3/-8, thus facilitating the intracellular survival of mycobacteria. In addition, Rv2387 inhibits the production of inflammatory cytokines in macrophages by specifically suppressing TLR2-dependent stimulation of p38 and JNK MAPK pathways. Moreover, we further determined that the Rv2387 protein conferred a growth advantage over recombinant M. smegmatis and suppressed the inflammatory response in a mouse infection model. Overall, these data suggested that Rv2387 facilitates mycobacteria to escape host immunity and might be an essential virulence factor in Mtb.
Texto completo:
1
Base de dados:
MEDLINE
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
Pathogens
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China