Tumour necrosis factor-alpha (TNF-α) in the host resistance to mycobacteria of distinct virulence

Appelberg, Rui; Sarmento, Amélia; Castro, Albert

doi:10.1111/j.1365-2249.1995.tb08356.x

Cited by 34 publications

(32 citation statements)

References 18 publications

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“…Although morphotypes of the same strain are very closely related, previous studies have demonstrated that the smooth-transparent variant is usually better able to survive and grow intracellularly than the opaque morphotype (21,22). With regard to the M. avium morphotypes used in this study (2151 SmT and SmO), this pattern has been confirmed both in murine macrophages and in a mouse model of infection (23,24).…”

supporting

confidence: 67%

Capsular Arabinomannans from Mycobacterium avium with Morphotype-specific Structural Differences but Identical Biological Activity

Wittkowski

Mittelstädt

Brandau

et al. 2007

Journal of Biological Chemistry

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The capsules of two colony morphotypes of Mycobacterium avium strain 2151 were investigated, i.e. the virulent smoothtransparent (SmT1) and the nonvirulent smooth-opaque (SmO) types. From both morphotypes we separated a nonacylated arabinomannan (AM) from an acylated polysaccharide fraction by affinity chromatography, of which the AMs were structurally characterized. The AMs from the virulent morphotype, in contrast to that from the nonvirulent form, possessed a larger mannan chain and a shorter arabinan chain. Incubation of murine bone marrow-derived macrophages and human dendritic cells showed that the acylated polysaccharide fractions were potent inducers of tumor necrosis factor-␣, interleukin-12, and interleukin-10 compared with nonacylated AMs, which led to only a marginal cytokine release. Further in vitro experiments showed that both the acylated polysaccharide fractions and the nonacylated AMs were able to induce in vitro anti-tumor cytotoxicity of human peripheral blood mononuclear cells. Thus, morphotype-specific structural differences in the capsular AMs of M. avium do not correlate with biological activity; however, their acylation is a prerequisite for effective stimulation of murine macrophages and human dendritic cells.

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supporting

confidence: 67%

Capsular Arabinomannans from Mycobacterium avium with Morphotype-specific Structural Differences but Identical Biological Activity

Wittkowski

Mittelstädt

Brandau

et al. 2007

Journal of Biological Chemistry

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“…Moreover, we observed significantly higher levels of TNF-␣ secreted by M tuberculosis H37Ra-infected BMMs compared with H37Rv-infected BMMs, as observed previously. 37 The TNF-␣ produced by H37Ra-but not H37Rv-infected BMMs was also significantly decreased in cells treated with the 2A11 blocking antibody compared with untreated or isotype control ( Figure 6B). …”

Section: Dectin-1 Facilitates Tnf-␣ Production In Macrophages Infectementioning

confidence: 89%

The β-glucan receptor dectin-1 functions together with TLR2 to mediate macrophage activation by mycobacteria

Yadav

Schorey

2006

Blood

364

294

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Pattern recognition receptors (PRRs) play an essential role in a macrophage's response to mycobacterial infections. However, how these receptors work in concert to promote this macrophage response remains unclear. In this study, we used bone marrow-derived macrophages isolated from mannose receptor (MR), complement receptor 3 (CR3), MyD88, Toll-like receptor 4 (TLR4), and TLR2 knockout mice to examine the significance of these receptors in mediating a macrophage's response to a mycobacterial infection. We determined that mitogenactivated protein kinase (MAPK) activation and tumor necrosis factor-␣ (TNF-␣) production in macrophage infected with Mycobacterium avium or M smegmatis is dependent on myeloid differentiation factor 88 (MyD88) and TLR2 but not TLR4, MR, or CR3. Interestingly, the TLR2-mediated production of TNF-␣ by macrophages infected with M smegmatis required the ␤-glucan receptor dectin-1. A similar requirement for dectin-1 in TNF-␣ production was observed for macrophages infected with M bovis Bacillus Calmette-Guerin (BCG), M phlei, M avium 2151-rough, and M tuberculosis H37Ra. The limited production of TNF-␣ by virulent M avium 724 and M tuberculosis H37Rv was not dependent on dectin-1. Furthermore, dectin-1 facilitated interleukin-6 (IL-6), RANTES (regulated on activation, normal T expressed and secreted), and granulocyte colony-stimulating factor (G-CSF) production by mycobacteriainfected macrophages. These are the first results to establish a significant role for dectin-1, in cooperation with TLR2, to activate a macrophage's proinflammatory response to a mycobacterial infection. IntroductionThe immune system has the complex task of separating friend from foe. To accomplish this mission, the immune system has evolved receptors that recognize molecules present on pathogenic organisms but which show limited interaction with host components. These receptors, referred to as pattern recognition receptors (PRRs), function to promote an innate immune response and include such members as the mannose receptor (MR), scavenger receptors, and Toll-like receptors (TLRs), among others. PRRs bind to conserved microbial structures called pathogen-associated molecular patterns (PAMPs). The expression of these receptors allows the immune system to recognize a wide variety of pathogens that express one or more of these PAMPs, and their engagement initiates the subsequent immune response. Not surprisingly, the PRRs are expressed on cells of the innate immune system, including macrophages, neutrophils, dendritic cells, and natural killer (NK) cells. 1 Binding of microbial products by PRRs elicits a signaling response within the leukocyte, resulting in the production of specific immune modulators. Which PRRs are engaged and in what combination, along with the specific ligands involved, will dictate the overall response by the immune cell. This complexity allows the immune system to tailor its response to a specific pathogen, yet remain flexible enough to recognize a large number of potential pathogens.One of the most...

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“…Unlike M. tuberculosis, however, M. avium proliferation in vivo in mice is under the control of the Nramp1 gene (Appelberg & Sarmento, 1990 ;Medina et al, 1996). NRAMP1 is a transmembrane protein expressed in endosomal and phagosomal membranes of macrophages, that contributes to inhibition of growth of several intracellular pathogens, including Mycobacterium bovis, M. avium, Leishmania donovani and Salmonella typhimurium (Gruenheid & Gros, 2000).…”

Section: Discussionmentioning

confidence: 99%

NRAMP1- or cytokine-induced bacteriostasis of Mycobacterium avium by mouse macrophages is independent of the respiratory burst

Gomes

Appelberg

2002

Microbiology

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Restriction of the growth of Mycobacterium avium was studied in wild-type and p47phox -deficient macrophages. The ability of gamma interferon and tumour necrosis factor alpha to induce antimycobacterial activity in bonemarrow-derived macrophages or the expression of the NRAMP1-mediated resistance to M. avium were not affected by the deficiency in p47phox . The addition of exogenous iron increased mycobacterial growth in macrophages expressing a functional NRAMP1 protein or a mutant NRAMP1 protein. Reactive oxygen species are therefore not involved in the constitutive or induced anti-M. avium activities of the mouse macrophage.

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Tumour necrosis factor-alpha (TNF-α) in the host resistance to mycobacteria of distinct virulence

Cited by 34 publications

References 18 publications

Capsular Arabinomannans from Mycobacterium avium with Morphotype-specific Structural Differences but Identical Biological Activity

Capsular Arabinomannans from Mycobacterium avium with Morphotype-specific Structural Differences but Identical Biological Activity

The β-glucan receptor dectin-1 functions together with TLR2 to mediate macrophage activation by mycobacteria

NRAMP1- or cytokine-induced bacteriostasis of Mycobacterium avium by mouse macrophages is independent of the respiratory burst

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