Interleukin 10 Produced by Macrophages Inoculated with<i>Mycobacterium avium</i>Attenuates Mycobacteria‐Induced Apoptosis by Reduction of TNF‐α Activity

Balcewicz-Sablinska, M K; Gan, Huixian; Remold, Heinz G.

doi:10.1086/315011

Cited by 81 publications

(73 citation statements)

References 41 publications

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“…Bcl-2 is known to downregulate the apoptosis in human mononuclear phagocytes after infection with M. tuberculosis (16)(17)(18), and further, the downregulation of Bcl-2 is accompanied by upregulation of Bax, which has recognized apoptotic effects (16). Balcewicz-Sablinska et al (2) reported that IL-10 downregulates apoptosis by inhibiting the TNF-α production of the inoculated macrophages and by inducing the release of soluble TNF receptor type 2 from the macrophages, which leads to inactivation of TNF-α. It is considered from these reports and our data that in the early phase of infection with both M. tuberculosis H37Ra and H37Rv, the release of a relatively higher amount of TNF-α compared with that of IL-10 might be enhanced in the infected cells, which induces negative modulation of cysteine protease and Bcl-2 expression, leading the cells to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Survival of Virulent Mycobacterium tuberculosis Involves Preventing Apoptosis Induced by Bcl‐2 Upregulation and Release Resulting from Necrosis in J774 Macrophages

Zhang

Jiang

Takayama

et al. 2005

Microbiology and Immunology

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Macrophage apoptosis plays a role in mycobacterial infection. To define the mechanism by which virulent Mycobacterium tuberculosis escapes apoptosis and killing in macrophages, J774 macrophages were infected with virulent M. tuberculosis H37Rv and attenuated H37Ra strains. H37Rv induced less apoptosis than H37Ra, and caspase 3 was activated in H37Ra‐ and H37Rv‐infected macrophages. Intracellular H37Rv bacilli were released at a higher rate into the supernatant than were H37Ra by the sixth day of infection, and this was simultaneously accompanied by the increased necrosis of infected cells showing lactate dehydrogenase (LDH) release. Fas mRNA expression was downregulated and FasL was upregulated in H37Ra‐ and H37Rv‐infected macrophages, while Bcl‐2 was upregulated in H37Rv‐infected macrophages but downregulated in H37Ra‐infected macrophages as seen by real‐time PCR. These results indicate that M. tuberculosis H37Ra and H37Rv proliferate in macrophages by preventing them from inducing apoptosis during the early phase of infection, and that M. tuberculosis H37Rv‐infected macrophages are found to express Bcl‐2 mRNA, which leads to anti‐apoptotic activity, and that relatively distinct necrosis might occur during the later phase of infection.

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Section: Discussionmentioning

confidence: 99%

Survival of Virulent Mycobacterium tuberculosis Involves Preventing Apoptosis Induced by Bcl‐2 Upregulation and Release Resulting from Necrosis in J774 Macrophages

Zhang

Jiang

Takayama

et al. 2005

Microbiology and Immunology

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“…ATP-induced apoptosis in macrophages resulted in killing of M. bovis BCG (53,54). In addition, mycobacterial infection itself can induce apoptosis in infected macrophages (55). Ingestion of infected apoptotic macrophages by uninfected macrophages results in increased control of mycobacterial growth (56).…”

Section: Discussionmentioning

confidence: 99%

CD4+ and CD8+ T Cells Kill IntracellularMycobacterium tuberculosisby a Perforin and Fas/Fas Ligand-Independent Mechanism

Canaday

Wilkinson

Silver

et al. 2001

The Journal of Immunology

180

136

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Cytotoxic effector phenotype and function of MHC-restricted Mycobacterium tuberculosis (MTB)-reactive CD4+ and CD8+ T lymphocytes were analyzed from healthy tuberculin skin test-positive persons. After stimulation in vitro with MTB, both CD4+ and CD8+ T cells up-regulated mRNA expression for granzyme A and B, granulysin, perforin, and CD95L (Fas ligand). mRNA levels for these molecules were greater for resting CD8+ than CD4+ T cells. After MTB stimulation, mRNA levels were similar for both T cell subsets. Increased perforin and granulysin protein expression was confirmed in both in CD4+ and CD8+ T cells by flow cytometry. Both T cell subsets lysed MTB-infected monocytes. Biochemical inhibition of the granule exocytosis pathway in CD4+ and CD8+ T cells decreased cytolytic function by >90% in both T cell subsets. Ab blockade of the CD95-CD95L interaction decreased cytolytic function for both T cell populations by 25%. CD4+ and CD8+ T cells inhibited growth of intracellular MTB in autologous monocytes by 74% and 84%, respectively. However, inhibition of perforin activity, the CD95-CD95L interaction, or both CTL mechanisms did not affect CD4+ and CD8+ T cell mediated restriction of MTB growth. Thus, perforin and CD95-CD95L were not involved in CD4+ and CD8+ T cell mediated restriction of MTB growth.

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“…Patients and controls were selected from the California Collaborative Treatment Group 552 trial, which compared the efficacy of azithromycin to that of rifabutin with the combination of both drugs for the prevention of MAC infection (11). At entry, HIV-1-infected persons had CD4 counts of Ͻ100 cells/mm 3 and no history of MAC bacteremia. Disseminated MAC was determined on the basis of a positive culture of blood or another normally sterile site.…”

Section: Methodsmentioning

confidence: 99%

Serum Interleukin-6 (IL-6), IL-10, Tumor Necrosis Factor (TNF) Alpha, Soluble Type II TNF Receptor, and Transforming Growth Factor Beta Levels in Human Immunodeficiency Virus Type 1-Infected Individuals withMycobacterium aviumComplex Disease

et al. 2001

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To characterize changes in serum cytokine levels in human immunodeficiency virus type 1 (HIV-1)-infected persons with Mycobacterium avium complex (MAC) bacteremia, the levels of IL-1␣ (interleukin-1␣), IL-6, IL-10, tumor necrosis factor alpha (TNF-␣), soluble type II TNF receptor (sTNF-RII), and transforming growth factor ␤ (TGF-␤) in serum were measured in two cohorts of HIV-1-infected persons with MAC bacteremia. The first cohort was part of a MAC prophylaxis study. Patients with bacteremia were matched with controls without bacteremia. Elevated IL-6, IL-10, TNF-␣, sTNF-RII, and TGF-␤ levels were noted at baseline for all subjects, a result consistent with advanced HIV-1 disease. IL-1␣ was not detected. No differences in cytokine levels in serum were noted at baseline and at the time of bacteremia between patients with MAC and controls. In the second cohort, subjects had serum samples collected at the time of MAC bacteremia and thereafter while on macrolide therapy. Serum samples at time of bacteremia were collected from HIV-1-infected persons at a time when neither highly active antiretroviral therapy (HAART) nor MAC prophylaxis was used routinely. MAC treatment resulted in decreased levels of IL-6 and TNF-␣ in serum, which were evident for IL-6 by 4 to 6 weeks and for TNF-␣ by 8 to 16 weeks. Thus, antibiotic treatment for MAC results in decreased levels of IL-6 and TNF-␣ in serum in HIV-1-infected persons who are not on HAART.

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Interleukin 10 Produced by Macrophages Inoculated withMycobacterium aviumAttenuates Mycobacteria‐Induced Apoptosis by Reduction of TNF‐α Activity

Cited by 81 publications

References 41 publications

Survival of Virulent Mycobacterium tuberculosis Involves Preventing Apoptosis Induced by Bcl‐2 Upregulation and Release Resulting from Necrosis in J774 Macrophages

Survival of Virulent Mycobacterium tuberculosis Involves Preventing Apoptosis Induced by Bcl‐2 Upregulation and Release Resulting from Necrosis in J774 Macrophages

CD4+ and CD8+ T Cells Kill IntracellularMycobacterium tuberculosisby a Perforin and Fas/Fas Ligand-Independent Mechanism

Serum Interleukin-6 (IL-6), IL-10, Tumor Necrosis Factor (TNF) Alpha, Soluble Type II TNF Receptor, and Transforming Growth Factor Beta Levels in Human Immunodeficiency Virus Type 1-Infected Individuals withMycobacterium aviumComplex Disease

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