Mycobacterial 3-hydroxyacyl-l-thioester dehydratase Y derived from Mycobacterium tuberculosis induces COX-2 expression in mouse macrophages through MAPK-NF-κB pathway.

Abstract:

:Tuberculosis (TB) is a leading cause of global mortality due to infectious diseases. Expression of cyclooxygenase-2 (COX-2) acts as an important influencing factor favoring bacillary survival during TB infection. In this study, we investigated the Mycobacterium tuberculosis proteins recognized by sera from TB patient collected before and after anti-TB therapy by dynamic immunoproteomics and identified a novel immune-regulating protein 3-hydroxyacyl-l-thioester dehydratase Y (HtdY), which could induce COX-2 expression in mouse macrophages. Signaling perturbation data showed that the activation of p38, ERK 1/2 and JNK 1/2 MAPK as well as NF-κB played critical role in this immune response. Taken together, our findings indicated that mycobacterial HtdY might contribute to the persistence of the TB infection by inducing COX-2 expression through MAPK-NF-κB signaling pathway.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Zhao JW,Sun ZQ,Zhang XY,Zhang Y,Liu J,Ye J,Chen CC,Samten B,Wang HH,Guo XK,Zhang SL

doi

10.1016/j.imlet.2014.05.013

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

125-32

issue

1

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(14)00112-6

journal_volume

161

pub_type

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