The modulating effects of proinflammatory cytokines interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α), and immunoregulating cytokines IL-10 and transforming growth factor-beta (TGF-β), on anti-microbial activity of murine peritoneal macrophages against<i>Mycobacterium avium</i>-<i>intracellulare</i>complex

Sano, Chiaki; Sato, Katsumasa; Shimizu, Toshiaki; Kajitani, Hiroko; Kawauchi, Hideyuki; Tomioka, Haruaki

doi:10.1046/j.1365-2249.1999.00838.x

Cited by 27 publications

(19 citation statements)

References 40 publications

(45 reference statements)

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“…It is possible that this reduction in TNF is linked to the balance of cytokines produced by the infected macrophage, i.e., an increase in levels of cytokines that would inhibit release of TNF. This is supported by our finding of enhanced IL-10 production by SP-A complex-MAC (data not shown) and by the recent report that MAC-induced production of IL-10 by human macrophages reduces levels of released TNF [42,43].…”

Section: Discussionsupporting

confidence: 89%

Surfactant protein A enhances Mycobacterium avium ingestion but not killing by rat macrophages

Lopez

Clark

Shepherd

2003

Journal of Leukocyte Biology

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Mycobacterium avium complex (MAC) is a significant cause of opportunistic infection in patients with acquired immunodeficiency syndrome. Although the major route of entry of MAC is via the gastrointestinal tract, MAC can infect humans through the respiratory tract and eventually encounter alveolar macrophages within the lung. Once in the lung, MAC can potentially interact with surfactant protein A (SP-A), an important component of the pulmonary innate-immune response. Previous work on other pulmonary pathogens including Mycobacterium bovis Bacillus Calmette-Guerin (BCG) suggests that SP-A participates in promoting efficient clearance of these organisms by alveolar macrophages. In the present study, we investigated the role of SP-A in clearance of MAC by cultured rat macrophages. SP-A bound to MAC organisms and enhanced the ingestion of the mycobacteria by macrophages. Infection of macrophages with SP-A-MAC complexes induced the production of nitric oxide (NO) and tumor necrosis factor-alpha. However, intracellular survival of MAC was not altered by preopsonization with SP-A. In addition, inhibitors of inducible NO synthase did not alter MAC clearance. These results suggest that SP-A can bind to and enhance the uptake of MAC by alveolar macrophages, similar to previous findings with BCG and Mycobacterium tuberculosis.However, unlike BCG and other pulmonary pathogens that are cleared effectively in the presence of SP-A via a NO-dependent pathway, macrophage-mediated clearance of MAC is not enhanced by SP-A.

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Section: Discussionsupporting

confidence: 89%

Surfactant protein A enhances Mycobacterium avium ingestion but not killing by rat macrophages

Lopez

Clark

Shepherd

2003

Journal of Leukocyte Biology

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“…In addition, TGF-b seems to enhance the survival of mycobacteria within the host cell, since this factor downregulates the production of pro-inflammatory cytokines such as TNF-a and IFN-g, which are important to facilitate mycobacteria growth [49,50]. Another report has shown that TGF-b has no effect in the evolution of M. avium infection [51]. Here, we showed that ECs surrogates produced higher amounts of TGF-b, even when these cells were not infected with M. avium.…”

Section: Discussionmentioning

confidence: 99%

Recombinant interleukin-4-treated macrophages, epithelioid cell surrogates, harbor and arrest Mycobacterium avium multiplication in vitro

Chinen

Cipriano²,

Oliveira

et al. 2006

Microbes and Infection

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“…Previous studies have documented that the TNF-␣/IL-10 balance is a major determinant of macrophage activation status (4,5,22,15,29). TNF-␣ is a major activator of both inflammatory and immune responses and is important in granuloma formation and initiation of a protective immune response in mycobacterial infections (14,19,15,16,28). Alternatively, IL-10 is a major anti-inflammatory and anti-immune cytokine.…”

Section: Discussionmentioning

confidence: 99%

Differential Responses of Bovine Macrophages toMycobacterium aviumsubsp.paratuberculosisandMycobacterium aviumsubsp.avium

et al. 2002

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Mycobacterium avium subsp. paratuberculosis and Mycobacterium avium subsp. avium are antigenically and genetically similar organisms; however, they differ in their virulence for cattle. M. avium subsp. paratuberculosis causes a chronic intestinal infection leading to a chronic wasting disease termed paratuberculosis or Johne's disease, whereas M. avium subsp. avium causes only a transient infection. We compared the response of bovine monocyte-derived macrophages to ingestion of M. avium subsp. paratuberculosis and M. avium subsp. avium organisms by determining organism survival, superoxide and nitric oxide production, and expression of the cytokines tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), interleukin-8 (IL-8), IL-10, IL-12, and granulocyte-monocyte colony-stimulating factor (GM-CSF). Unlike M. avium subsp. paratuberculosis, macrophages were able to kill approximately half of the M. avium subsp. avium organisms after 96 h of incubation. This difference in killing efficiency was not related to differences in nitric oxide or superoxide production. Compared to macrophages activated with IFN-γ and lipopolysaccharide, macrophages incubated with M. avium subsp. paratuberculosis showed greater expression of IL-10 and GM-CSF (all time points) and IL-8 (72 h) and less expression of IL-12 (72 h), IFN-γ (6 h), and TNF-α (6 h). When cytokine expression by macrophages incubated with M. avium subsp. paratuberculosis was compared to those of macrophages incubated with M. avium subsp. avium, M. avium subsp. paratuberculosis-infected cells showed greater expression of IL-10 (6 and 24 h) and less expression of TNF-α (6 h). Therefore, the combination of inherent resistance to intracellular degradation and suppression of macrophage activation through oversecretion of IL-10 may contribute to the virulence of M. avium subsp. paratuberculosis in cattle

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Cited by 27 publications

References 40 publications

Surfactant protein A enhances Mycobacterium avium ingestion but not killing by rat macrophages

Surfactant protein A enhances Mycobacterium avium ingestion but not killing by rat macrophages

Recombinant interleukin-4-treated macrophages, epithelioid cell surrogates, harbor and arrest Mycobacterium avium multiplication in vitro

Differential Responses of Bovine Macrophages toMycobacterium aviumsubsp.paratuberculosisandMycobacterium aviumsubsp.avium

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