Abstract

It has been reported that IFN-γ, TNF-α, and IL-12 stimulate, and that IL-10, TGF-β, and IL-4 suppress the protective immune response against tuberculosis. We aim to evaluate changes in the serum levels of pro and antiinflammatory cytokines in active pulmonary tuberculosis (APTB) and the possible effects of treatment on these changes. Serum IL-12p40, IL-4, IL-10, TNF-α, IFN-γ, and TGF-β1 levels were determined in 20 APTB cases (group 1) before and 2, 4, and 6 months after therapy. The same parameters were also determined in 9 inactive pulmonary tuberculosis (IPTB) cases (group 2) and 9 healthy controls (HC, group 3). Before treatment, the mean serum IFN-γ, TNF-α, and IL-10 levels in group 1 were statistically higher than those in group 2 (P = .001, P = .024, P = .016, resp) or group 3 (P = .003, P = .002, P = .011, resp). The levels in group 1 decreased significantly after treatment (P = .001 for IFN-γ, P = .004 for TNF-α, P = .000 for IL-10). The serum levels of IL-12p40 were significantly higher in group 1 than in group 3 (P = .012) and decreased insignificantly after treatment. There was no difference in serum IL-4 and TGF-β1 levels among the groups (P > .05). Because the serum IL-12p40, IL-10, TNF-α, and IFN-γ levels were high in APTB, we believe that these cytokines have important roles in the immune response to Mycobacterium tuberculosis (M tuberculosis). These parameters could be used in follow-up as indicators of the success of APTB therapy.

Highlights

  • Mycobacterium tuberculosis (M tuberculosis) is one of the most widespread pathogens; it is estimated that roughly one third of the world’s population is infected with the bacillus and approximately 8–10 million people become infected every year

  • Because the serum IL-12p40, IL-10, TNF-α, and IFN-γ levels were high in active pulmonary tuberculosis (APTB), we believe that these cytokines have important roles in the immune response to Mycobacterium tuberculosis (M tuberculosis)

  • The mean PPD response was statistically higher in the APTB (14.9 ± 2.3 mm) and inactive pulmonary tuberculosis (IPTB) (14.7 ± 1.7 mm) cases than the HC (12.2 ± 2.2 mm) (P = .011 for APTB and P = .025 for IPTB compared with HC)

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Summary

Introduction

Mycobacterium tuberculosis (M tuberculosis) is one of the most widespread pathogens; it is estimated that roughly one third of the world’s population is infected with the bacillus and approximately 8–10 million people become infected every year It is responsible for 8–12 million cases of active tuberculosis each year, and 3 million deaths [1, 2, 3]. The interaction of T cells with infected macrophages is central to protective immunity against M tuberculosis and depends on the interplay of cytokines produced by each cell [5]. TNF-α, IL-12, and IFN-γ are central cytokines in the regulatory and effector phases of the immune response to M tuberculosis [6]. The production of antiinflammatory cytokines such as IL-4, IL-10 and TGF-β in response to M tuberculosis may down-regulate the immune response and limit tissue injury, but excessive production of these cytokines may result in failure to control the infection [9]

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