Expression of toll-like receptor 2 and plasma level of interleukin-10 are associated with outcome in tuberculosis

J. Y. Wang, J. T. Wang, H. C. Chang, J. L. Liu, L. N. Lee, C. C. Shu, C. H. Lee

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

Abstract

Toll-like receptor (TLR) 2-mediated innate immunity is an important defense system against Mycobacterium tuberculosis infection. Studies on TLR2 protein expression and downstreamcytokines in tuberculosis patients are lacking. TLR2 expression in the peripheral blood monocytes of 87 tuberculosis patients and 94 healthy subjects was evaluated using flow cytometry. TLR2 expression and its downstream cytokines, including interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and interferon-gamma, were correlated with the clinical manifestations and outcomes of tuberculosis. The TLR2 expression in peripheral blood monocytes was higher in tuberculosis patients than in healthy subjects. Among the tuberculosis patients, those aged ≥70 years with disseminated tuberculosis or aged <70 years with symptom duration ≥14 days had lower initial TLR2 expression. After two months of treatment, TLR2 expression decreased in most patients, except in those whose sputum samples remained culture-positive for M. tuberculosis. Proportional hazards regression analyses revealed that high initial TLR2 expression and IL-10 plasma level were associated with shorter survival. TLR2 may play an important role in the course of tuberculosis. Its expression on peripheral blood monocytes and the plasma level of the downstream anti-inflammatory cytokine IL-10 may be important outcome predictors and have potential use in the management of tuberculosis patients.

Original languageEnglish
Pages (from-to)2327-2333
Number of pages7
JournalEuropean Journal of Clinical Microbiology and Infectious Diseases
Volume31
Issue number9
DOIs
Publication statusPublished - Sept 2012
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases

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