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Constitutive and Antigen‐Induced Secretion of Cytokines by Peripheral Blood Mononuclear Cells of Tuberculosis Patients
Author(s) -
Mustafa AbuSalim
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.507.10
Subject(s) - peripheral blood mononuclear cell , immunology , tuberculosis , proinflammatory cytokine , antigen , pathogenesis , secretion , medicine , cytokine , in vitro , inflammation , biology , pathology , biochemistry
Cytokines play a major role in protection against and pathogenesis of tuberculosis. Generally, T‐helper (Th)1 and pro‐inflammatory cytokines are considered protective, and anti‐inflammatory and Th2 cytokines are responsible for pathogenesis of tuberculosis. In order to study the release of various cytokines in response to a variety of antigenic stimuli, the in vitro secretion of cytokines was assessed using peripheral blood mononuclear cells from tuberculosis patients (diabetic and non‐diabetic) and healthy subjects in response to various mycobacterial antigens, including whole cells, culture filtrate, cell walls and pools of synthetic peptides corresponding to M. tuberculosis ‐specific genomic regions, i.e. the regions of differences (RDs). The results showed that the concentrations of antigen‐induced Th2 cytokines were low/undetected and the pro‐inflammatory cytokines were non‐discriminatory. However, with regard to the Th1 and anti‐inflammatory cytokines, the antigens could be divided into two groups; the first group showed Th1‐bias (culture filtrate, RD1, RD5, RD7, RD9, RD10 and RD15), and the second group had anti‐inflammatory‐bias (whole bacilli and cell walls of M. tuberculosis , RD12 and RD13). Interestingly, the RD1 peptide pool induced the strongest Th1‐bias, and the addition of RD12 and RD13 peptides to the cultures suppressed the secretion of RD1‐induced Th1‐cytokines. Furthermore, when data were compared between diabetic and non‐diabetic TB patients, there was a shift towards pathologic (Th2/anti‐inflammatory) cytokines in diabetic TB patients, which may explain, at least in part, a faster deterioration in clinical condition of diabetic TB patients. Supported by Kuwait University Research Sector grants MI01/10 and SRUL02/13.