The Inflammatory Response in Mycobacterium Tuberculosis Infection

Toossi, Zahra

doi:10.1007/978-94-015-9702-9_11

Cited by 29 publications

(27 citation statements)

References 71 publications

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“…IFN-gamma produced by all classes of lymphocytes and potentially by alveolar macrophages, up-regulates production of TNF-alpha [1,5,8]. In our study, we observed gradual decline of IFN-gamma serum levels during the first four weeks of treatment, especially in prednisone recipients.…”

Section: Discussionsupporting

confidence: 51%

“…The interaction between T cells and macrophages is essential immune defense mechanisms in Mycobacterium tuberculosis (MTB) infection, resulting in the release production and release of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) interferon gamma (IFN-gamma) and interleukin 1-beta (IL-1 beta) by these cells [1][2][3]. Cellular immune responses triggered by these inflammatory cytokines activate typical immune defense mechanisms against MTB inflammation [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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Influence of prednisone on serum level of tumor necrosis factor alpha, interferon gamma and interleukin-1 beta, in active pulmonary tuberculosis

Rybacka-Chabros

Pietrzak

Milanowski

et al. 2014

Polish Journal of Public Health

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Aim. The aim of the study was a potential impact of prednisone on the early immune response in HIV-negative young adults with active pulmonary tuberculosis, during the first four weeks of treatment.Material and methods. The study included 38 adults, aged 18-39 years, with active pulmonary tuberculosis. The first group of patients received only anti-tuberculosis chemotherapy whereas the second group of patients was administered antituberculosis chemotherapy and 20 mg prednisone, once daily. Serum levels of tumor necrosis factor-alpha, interferon-gamma and interleukin 1-beta were measured using ELISA kits before treatment initiation as well after two and four weeks of treatment, in both study groups.Results. The highest serum levels of evaluated cytokines were observed before treatment initiation. Serum levels of cytokines were significantly decreased in patients who received anti-tuberculosis drugs and prednisone, compare to those not treated with prednisone (p<0.001), in all study periods.Conclusions. Adjunctive therapy, like 20 mg prednisone daily, remarkably inhibited the secretion of inflammatory cytokines during the early stage of active pulmonary tuberculosis in HIV-negative young adults, which is likely to be beneficial for this group of patients.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Influence of prednisone on serum level of tumor necrosis factor alpha, interferon gamma and interleukin-1 beta, in active pulmonary tuberculosis

Rybacka-Chabros

Pietrzak

Milanowski

et al. 2014

Polish Journal of Public Health

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“…Upregulated Smad3 mediates pro-fibrotic activities of TGF-b [71]. Therefore, TGF-b is involved as both a critical cytokine of immunosuppression and contributes to structural and cellular composition of lung granulomas [72]. Transcription of IDO in H37Rv-infected WT lungs was only modestly enhanced at d30 p.i., whereas gene transcription of tryptophanyl-tRNA synthetase (WARS) was strongly induced in iNOS -/-mice and modestly in WT mice.…”

Section: Immunosuppressionmentioning

confidence: 99%

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Beisiegel¹,

Mollenkopf²,

Hahnke³

et al. 2009

Eur J Immunol

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Progression and outcome of tuberculosis is governed by extensive crosstalk between pathogen and host. Analyses of global changes in gene expression during immune response to infection with Mycobacterium tuberculosis (M.tb) can help identify molecular markers of disease state and progression. Global distribution of M.tb strains with different degrees of virulence and drug resistance, especially for the immunocompromised host, make closer analyses of host responses more pressing than ever. Here, we describe global transcriptional responses of inducible nitric oxide synthase-deficient (iNOS -/-) and WT mice infected with two related M.tb strains of markedly different virulence, namely the M.tb laboratory strains H37Rv and H37Ra. Both hosts exhibited highly similar resistance to infection with H37Ra. In contrast, iNOS -/-mice rapidly succumbed to H37Rv, whereas WT mice developed chronic course of disease. By differential analyses, virulence-specific changes in global host gene expression were analyzed to identify molecular markers characteristic for chronic versus acute infection. We identified several markers unique for different stages of disease progression and not previously associated with virulencespecific host responses in tuberculosis.

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“…The immune system sequesters persistent sources of antigen by establishment of a granulomatous barrier (36,47,53). Infections with Schistosoma mansoni or Mycobacterium spp.…”

mentioning

confidence: 99%

Interleukin-10 Limits Local and Body Cavity Inflammation during Infection with Muscle-StageTrichinella spiralis

et al. 2004

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The aim of this study was to characterize cellular responses to muscle-stage Trichinella spiralis. From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elicit a strong systemic host immune response. Despite the magnitude and prolonged nature of this response, nurse cells are rarely destroyed by infiltrating cells. We tested the hypothesis that the anti-inflammatory cytokine interleukin-10 (IL-10) moderates cellular responses to muscle-stage parasites. Trichinella larvae colonize the diaphragm in large numbers, prompting us to evaluate regional responses in body cavities in addition to local responses in muscle. Mice deficient in IL-10 demonstrated an exaggerated inflammatory response around nurse cells and in the pleural cavity. The effect of IL-10 was most evident 20 days following muscle infection. The increased intensity of the response in IL-10-deficient mice did not affect parasite establishment or survival. Between 20 and 50 days postinfection, the inflammatory response was diminished in both wild-type and IL-10-deficient mice. Muscle infection also elicited an antibody response, characterized initially by mixed isotypes directed at somatic larval antigens and changing to an immunoglobulin G1-dominated response directed at tyvelosebearing excreted or secreted antigens. We conclude that IL-10 limits local and regional inflammation during the early stages of muscle infection but that chronic inflammation is controlled by an IL-10-independent mechanism that is coincident with a Th2 response.

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The Inflammatory Response in Mycobacterium Tuberculosis Infection

Cited by 29 publications

References 71 publications

Influence of prednisone on serum level of tumor necrosis factor alpha, interferon gamma and interleukin-1 beta, in active pulmonary tuberculosis

Influence of prednisone on serum level of tumor necrosis factor alpha, interferon gamma and interleukin-1 beta, in active pulmonary tuberculosis

Combination of host susceptibility and Mycobacterium tuberculosis virulence define gene expression profile in the host

Interleukin-10 Limits Local and Body Cavity Inflammation during Infection with Muscle-StageTrichinella spiralis

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