Mycobacterial cell wall components induce the production of TNF-α, IL-1, and IL-6 by bovine monocytes and the murine macrophage cell line RAW 264.7

Adams, Jacquelyn H.; Czuprynski, Charles J.

doi:10.1006/mpat.1994.1040

Cited by 51 publications

(33 citation statements)

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“…TNF-␣ bioactivity was analyzed by the WEHI-164 cytotoxicity assay as previously described (2,26). WEHI-164 cells were grown to confluence in Dulbecco's modified Eagle's medium supplemented with 5% fetal bovine serum and 100 U of penicillin G at 37°C and 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

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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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Section: Methodsmentioning

confidence: 99%

“…paratuberculosis organisms with monocyte-derived macrophages (2,7,30,31,34,35). The results of these studies indicate that, although they are readily phagocytized, M. avium subsp.…”

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confidence: 99%

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

et al. 2002

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“…However, questions remain regarding which pathways are initiated and/or modulated by a mycobacterial infection. Previous studies have shown that mycobacterial components such as lipoarabinomannan (LAM) can stimulate a macrophage response, resulting in the production and secretion of TNF-␣ and IL-1␤ (1). Studies have also indicated that arabinofuranosyl-terminated LAM isolated from nonpathogenic mycobacteria stimulates a stronger cytokine response in treated macrophages than does mannose-capped LAM (ManLAM) from pathogenic mycobacteria (50,52).…”

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confidence: 99%

Differential Regulation of the Mitogen-Activated Protein Kinases by Pathogenic and Nonpathogenic Mycobacteria

2002

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Mycobacteria are the etiologic agents of numerous diseases which account for significant morbidity and mortality in humans and other animal species. Many mycobacteria are intramacrophage pathogens and therefore the macrophage response to infection, which includes synthesis of cytokines such as tumor necrosis factor alpha (TNF-␣) and production of nitric oxide, has important consequences for host immunity. However, very little is known about the macrophage cell signaling pathways initiated upon infection or how pathogenic mycobacteria may modulate the macrophage responses. Using primary murine bone marrow macrophages, we established that p38 and extracellular signal-regulated kinases 1 and 2 of the mitogen-activated protein kinase (MAPK) pathways are activated upon infection with different species of mycobacteria. However, we observed decreased MAPK activity over time in macrophages infected with pathogenic Mycobacterium avium strains relative to infections with nonpathogenic mycobacteria. Furthermore, macrophages infected with M. avium produced lower levels of TNF-␣, interleukin 1␤, and inducible nitric oxide synthase 2 than macrophages infected with nonpathogenic species. Inhibitor studies indicate that the MAPKs are required for the Mycobacterium-mediated induction of these effector proteins. Our data indicate that MAPKs are activated in macrophages upon invasion by mycobacteria and that this activation is diminished in macrophages infected with pathogenic strains of M. avium, resulting in decreased production of important immune effector proteins. The decreased MAPK activation associated with M. avium infections suggests a novel point of immune intervention by this mycobacterial species.Mycobacterium spp. are intramacrophage pathogens and therefore the engagement of macrophage receptors by mycobacteria is one of the initial steps in the infection process. A macrophage may respond to a mycobacterial infection by secreting cytokines such as tumor necrosis factor alpha (TNF-␣) or interleukin 1␤ (IL-1␤) and by producing reactive oxygen and nitrogen intermediates. These effects, among others, are the end result of activating various macrophage-signaling pathways. However, questions remain regarding which pathways are initiated and/or modulated by a mycobacterial infection. Previous studies have shown that mycobacterial components such as lipoarabinomannan (LAM) can stimulate a macrophage response, resulting in the production and secretion of TNF-␣ and IL-1␤ (1). Studies have also indicated that arabinofuranosyl-terminated LAM isolated from nonpathogenic mycobacteria stimulates a stronger cytokine response in treated macrophages than does mannose-capped LAM (ManLAM) from pathogenic mycobacteria (50, 52). Furthermore, recent work by Ting et al. indicates that human macrophages infected with Mycobacterium tuberculosis are less responsive to gamma interferon, due to a disruption in STAT1 binding to the transcription factor CREB (55). These experiments suggest that mycobacteria and mycobacterial components can modulate...

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“…paratuberculosis infection (1,2). During the long subclinical stage of infection, the initial cytotoxic or Th1-like response is often replaced by an antibody or Th2-like response characterized by production of immunoglobulin G1 antibodies (for a review see reference 14).…”

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confidence: 99%

Evidence for a Novel Gene Expression Program in Peripheral Blood Mononuclear Cells from Mycobacterium avium subsp. paratuberculosis -Infected Cattle

et al. 2003

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Mycobacterial cell wall components induce the production of TNF-α, IL-1, and IL-6 by bovine monocytes and the murine macrophage cell line RAW 264.7

Cited by 51 publications

References 0 publications

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

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

Differential Regulation of the Mitogen-Activated Protein Kinases by Pathogenic and Nonpathogenic Mycobacteria

Evidence for a Novel Gene Expression Program in Peripheral Blood Mononuclear Cells from Mycobacterium avium subsp. paratuberculosis -Infected Cattle

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