Human in vitro immune responses to Mycobacterium tuberculosis

Wilsher, Margaret; Hagan, Cassidy; Prestidge, Ross L.; Wells, Athol U.; Murison, G.L.

doi:10.1054/tuld.1999.0223

Cited by 47 publications

(39 citation statements)

References 21 publications

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“…In this study, although the average concentration of IL-5 was low in all the groups analyzed, it was observed that there was a slight increase in the average level of this cytokine after the treatment, though it was not statistically significant. Other authors, in similar studies, also obtained low levels of IL-5 and IL-4 in patients with tuberculosis (Lin et al 1996, Torres et al 1998, Wilsher et al 1999.…”

Section: Discussionmentioning

confidence: 75%

“…Nevertheless, to date, it is still unclear if the increase in the production of IFN-γ after treatment is related to cell stimulation by antigens released after the death of mycobacteria caused by chemotherapy, by reverting the antigenic status or by the reduction of the transit of T lymphocytes antigen specific to the lungs. Some authors have shown that there is a relationship between the production of some cytokines by PBMC and the severity of the disease (Wilsher et al 1999). Dlugovitzky et al (2000) observed that patients with the disease in a moderate stage presented significantly higher levels of IFN-γ compared to the levels presented by patients with the disease in an advanced stage.…”

Section: Dosage Of Ifn-γ and Other Cytokines -mentioning

confidence: 98%

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Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Moura¹,

Toledo²,

Oliveira

et al. 2004

Mem. Inst. Oswaldo Cruz

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Tuberculosis (TB) is a disease caused by Mycobacterium tuberculosis whose interaction with the host may lead to a cell-mediated protective immune response. The presence of interferon-γ (IFN-γ) is related to this response. With the purpose of understanding the immunological mechanisms involved in this protection, the lymphoproliferative response, IFN-γ and other cytokines like interleukin , and tumor necrosis factor alpha (TNF-α) Key words: tuberculosis -interleukin-5 -interleukin-10 -tumor necrosis factor alpha -interferon-γ -peripheral blood mononuclear cells Tuberculosis (TB), a chronic infective-contagious disease, is caused by Mycobacterium tuberculosis and remains an important public health problem whose mechanisms related to a protective immunity in humans are not clear. The resurgence of TB has stimulated studies for the development of vaccines, new diagnostic methods and less toxic and more effective drugs for treatment (Laal et al. 1997). The cellular immunity plays an important role in TB healing (Ladel et al. 1997, Torres et al. 1998, Turner et al. 2000, Chackerian et al. 2001). Resistance to mycobacterial infections is conferred by immunological mechanisms mediated by T CD4 + lymphocytes, involving cytokines that increase the microbicide activity of macrophages (Dlugovitzky et al. 2000, Oberholzer et al. 2000. Studies in murine and human models allow differentiating two subpopulations of T CD4 + lymphocytes termed Th1 and Th2, that mediate the protection or the aggravation of the disease (Ladel et al. 1997, Kori et al. 2000. This existing dichotomy between the protective or non-protective immune responses is likely to be correlated with cytokine patterns produced by different subpopulations of lymphocytes during initial surviving stages of the pathogens inside macrophages. Interferon-γ (IFN- γ) acts as a powerful macrophage activator, increasing the molecule expression of the main class II histocompatibility complex and the potentialization of the cell response, including the production of cytokines, nitric oxide, and the increase of the cytolitic activity, with a main role in the Th1 type (Flesh et al. 1995). Studies carried out by Cooper et al. (1993) and Flynn et al. (1993) demonstrated that mice without the IFN-γ gene were not able to fight off the infection caused by M. tuberculosis. In humans, individuals who presented genetic mutations in the receptors for IFN-γ were observed to have had a high susceptibility to acquire infections caused by atypical mycobacteria (Jouanguy et al. 1996), suggesting an important role of IFN-γ in the protective response against TB.Besides the importance of better understanding the immunological mechanisms that may contribute to the healing, it becomes essential to determine markers of healing lesions, once this is currently carried out based on the clinical, radiological, and negative bacterioscopy.In this work, we proposed the in vitro evaluation of IFN-γ levels produced by peripheral blood mononuclear cells (PBMC) after Bacillus Calmette-Guerin (BCG) stimulati...

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Section: Discussionmentioning

confidence: 75%

Section: Dosage Of Ifn-γ and Other Cytokines -mentioning

confidence: 98%

Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Moura¹,

Toledo²,

Oliveira

et al. 2004

Mem. Inst. Oswaldo Cruz

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“…Testing for tuberculosis sensitivity often uses an extract of whole Mtb called purified protein derivative (PPD). This response is known to be suppressed in individuals infected with Mtb (Wilsher et al 1999). It has Table 3 Eukaryotic molecular chaperones that modulate macrophage activity Hsp10 (Johnson et al 2005) Inhibits LPS-induced caMØ activation Thioredoxin (Trx)80 (Pekkari et al 2005) Induce novel macrophage activation state Trx (Billiet et al 2005) Inhibits LPS-induced caMØ activation Cyclophilin A (Sherry et al 1992) Induces a caMØ state Peroxiredoxin (Donnelly et al 2005) Induces an aaMØ state Hsp27 (De et al 2000) Induces IL-10 synthesis but not TNF-α presumably an aaMØ state Hsp60 (Maguire et al 2002) a Induces caMØ state Hsp70 (Vabulas et al 2002) Induces caMØ state BiP (Panayi and Corrigall 2008) Inhibits monocyte activation and similar to Hsp27, presumably and aaMØ state Gp96 (Vabulas et al 2002a) Induces caMØ state Clusterin (Xie et al 2005) Induces what appears to be caMØ Haptoglobin (Moestrup and Møller 2004) Induces an aaMØ state caMØ classically activated macrophage, aaMØ alternatively activated macrophage a Mycobacterium tuberculosis Hsp60 induces alternative activation state recently been reported that Mtb Hsp60.1 inhibits the PPDinduced formation of the key cytokine IL-12 p40 subunit.…”

Section: Hsp60mentioning

confidence: 99%

Unfolding the relationship between secreted molecular chaperones and macrophage activation states

Henderson

2009

Cell Stress and Chaperones

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Over the last 20 years, it has emerged that many molecular chaperones and protein-folding catalysts are secreted from cells and function, somewhat in the manner of cytokines, as pleiotropic signals for a variety of cells, with much attention being focused on the macrophage. During the last decade, it has become clear that macrophages respond to bacterial, protozoal, parasitic and host signals to generate phenotypically distinct states of activation. These activation states have been termed 'classical' and 'alternative' and represent not a simple bifurcation in response to external signals but a range of cellular phenotypes. From an examination of the literature, the hypothesis is propounded that mammalian molecular chaperones are able to induce a wide variety of alternative macrophage activation states, and this may be a system for relating cellular or tissue stress to appropriate macrophage responses to restore homeostatic equilibrium.

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“…The purified protein derivative (PPD) used in intradermal tuberculin tests to detect delayed-type hypersensitivity (the Mantoux test) has limited diagnostic value, as clinically healthy individuals can have a positive tuberculin test (PPD) (> 10mm), without this reactivity being reflected in tests for specific antibodies [8][9][10]. Furthermore, people who have been vaccinated with bacillus Calmette-Guérin (BCG) and/or have been in contact with other species of mycobacteria can have positive results as well [11].…”

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confidence: 99%

A study of iga antibody response to different mycobacterium tuberculosis antigens in the diagnosis and monitoring of pulmonary tuberculosis

Bezerra¹,

Beck²,

Kanunfre³

et al. 2009

Braz J Infect Dis

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We evaluated the performance of the ELISA technique in the detection of IgA antibodies against different Mycobacterium tuberculosis antigenic preparations in serum samples from 49 patients with pulmonary tuberculosis collected before and after the start of specific treatment. The controls consisted of serum samples from healthy patients without any prior contact with the bacteria and serum samples from patients with other pneumopathies. Glycolipid antigen gave the best diagnostic performance, with a sensitivity of 88% and specificities varying from 88 to 100% in the control groups. These antigens constitute a powerful tool for the diagnosis and monitoring of patients with pulmonary tuberculosis.

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Human in vitro immune responses to Mycobacterium tuberculosis

Cited by 47 publications

References 21 publications

Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Unfolding the relationship between secreted molecular chaperones and macrophage activation states

A study of iga antibody response to different mycobacterium tuberculosis antigens in the diagnosis and monitoring of pulmonary tuberculosis

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