An important role of prostanoid receptor EP2 in host resistance to Mycobacterium tuberculosis infection in mice.

Kaul V, Bhattacharya D, Singh Y, Van Kaer L, Peters-Golden M, Bishai WR, Das G
J Infect Dis. 2012 206 (12): 1816-25

PMID: 23033144 · PMCID: PMC3502376 · DOI:10.1093/infdis/jis609

Mycobacterium tuberculosis, the causative agent of tuberculosis, resides and replicates within susceptible hosts by inhibiting host antimicrobial mechanisms. Prostaglandin E(2) (PGE(2)), produced by M. tuberculosis-infected macrophages, exerts a variety of immunomodulatory functions via 4 receptors (EP1-EP4), each mediating distinct PGE(2) functions. Here, we show that M. tuberculosis infection selectively upregulates EP2 messenger RNA expression in CD4(+) T cells. We found that EP2 deficiency in mice increases susceptibility to M. tuberculosis infection, which correlated with reduced antigen-specific T-cell responses and increased levels of CD4(+)CD25(+)Foxp3(+) T-regulatory cells. These findings have revealed an important role for EP2 in host immune defense against tuberculosis. As a G protein-coupled receptor, EP2 could serve as a target for immunotherapy of tuberculosis.

MeSH Terms (14)

Animals CD4-Positive T-Lymphocytes Disease Models, Animal Forkhead Transcription Factors Gene Expression Gene Expression Profiling Immunophenotyping Interleukin-2 Receptor alpha Subunit Mice Mice, Inbred C57BL Mycobacterium tuberculosis Receptors, Prostaglandin E, EP2 Subtype T-Lymphocytes, Regulatory Tuberculosis

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