Role of IFN-γ on dissociation between nitric oxide and TNF/IL-6 production by murine peritoneal cells after restimulation with bacterial lipopolysaccharide

Tominaga, Kaoru; Saito, Shinji; Matsuura, Motohiro; Funatogawa, Keiji; Matsumura, Haruo; Nakano, Masayasu

doi:10.1002/jlb.66.6.974

Cited by 8 publications

(5 citation statements)

References 39 publications

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“…These findings have been confirmed in mouse thioglycollate-elicited peritoneal macrophage and murine peritoneal exudate cells. 124,125 However, some studies have demonstrated decrease NO production in LPS-tolerant cells. 126 These studies may reflect differences in the tolerance-inducing regimen.…”

Section: Autocrine Mediators Of Endotoxin Tolerancementioning

confidence: 99%

Molecular mechanisms of endotoxin tolerance

Fan¹,

Cook²

2004

J. Endotoxin Res.

376

344

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The phenomenon of endotoxin tolerance has been widely investigated, but to date, the molecular mechanisms of endotoxin tolerance remain to be resolved clearly. The discovery of the Toll-like receptor (TLR) family as the major receptors for lipopolysaccharide (LPS) and other bacterial products has prompted a resurgence of interest in endotoxin tolerance mechanisms. Changes of cell surface molecules, signaling proteins, pro-inflammatory and anti-inflammatory cytokines and other mediators have been examined. During tolerance expression of LPS-binding protein (LBP), CD14, myeloid differentiation protein-2 (MD-2) and TLR2 are unchanged or up-regulated, whereas TLR4 is transiently suppressed or unchanged. Proximal post-receptor signaling proteins that are altered in tolerance include augmented degradation of interleukin-1 receptor-associated kinase (IRAK), and decreased TLR4-myeloid differentiation factor 88 (MyD88) and IRAK-MyD88 association. Tolerance has also been shown to be associated with decreased Gi protein content and activity, decreased protein kinase C (PKC) activity, reduction in mitogen-activated protein kinase (MAP kinase) activity, and reduced activator protein-1 (AP-1) and nuclear factor kappa B (NF-kappaB) induced gene transactivation. However, not all signaling proteins and pathways are suppressed in tolerance and induction of specific anti-inflammatory proteins and signaling pathways may serve important counter inflammatory functions. The latter include induction of IRAK-M and suppressor of cytokine-signaling-1 (SOCS-1), phosphoinositide-3-kinase (PI3K) signaling, and increased or maintained expression of inhibitor-kappaB (IkappaB) isoforms. Also at the nuclear level, increase in the NF-kappaB subunit p50 homodimer expression and increased activation of peroxisome-proliferator-activated receptors-gamma (PPARgamma) have been linked to tolerance phenotype. Although there are species and cellular variations in manifestation of the LPS tolerant phenotype, it is clear that the tolerance phenomena have evolved as a complex orchestrated counter regulatory response to inflammation.

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Section: Autocrine Mediators Of Endotoxin Tolerancementioning

confidence: 99%

Molecular mechanisms of endotoxin tolerance

Fan¹,

Cook²

2004

J. Endotoxin Res.

376

344

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show abstract

“…This mechanism is, however, hard to consider as the main underlying mechanism of LPS‐induced IFN‐γ production in vivo , in view of the large amount of IFN‐γ (detectable as protein level) secreted in the serum of mice after LPS challenge. Recently, LPS‐induced production of IFN‐γ in large amounts in in vitro systems was reported by our group using murine peritoneal cells [23] and by other groups using murine spleen cells [24,25]. These results indicate that additional cellular populations, besides the macrophage population, are required for effective production of IFN‐γ in response to LPS, unlike the production of the usual LPS mediators such as IL‐1, IL‐6 and tumor necrosis factor‐α (TNF‐α), for which the macrophage population alone is sufficient.…”

mentioning

confidence: 99%

“…In the course of our study concerning the mechanism of LPS‐induced NO production, participation of IFN‐γ was not suggested when murine macrophage cell lines such as RAW264.7 [26] and J774.1 [27] were used. However, in a study using murine peritoneal cells [23], participation of endogenously produced IFN‐γ in LPS‐induced NO production was thought to occur. In the present study, we aimed to clarify the role of IFN‐γ in LPS‐induced NO production and revealed the important role of IFN‐γ as a key mediator in the main pathway for LPS‐induced NO production in murine peritoneal cell culture.…”

mentioning

confidence: 99%

A pathway through interferon‐γ is the main pathway for induction of nitric oxide upon stimulation with bacterial lipopolysaccharide in mouse peritoneal cells

Matsuura

Saito

Hirai

et al. 2003

European Journal of Biochemistry

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Production of nitric oxide (NO) in response to bacterial lipopolysaccharide (LPS) was investigated using cultures of mouse peritoneal exudate cells (PEC) and the macrophage cell line RAW264.7. In the presence of anti-(interferon-c) (IFN-c), NO production was markedly suppressed in the PEC culture but not in the RAW264.7 culture. In the PEC culture, LPS induced both IFN-c production and activation of IFN response factor-1, which leads to the gene expression of inducible NO synthase, but neither was induced in the culture of RAW264.7 cells. In addition to anti-(IFN-c), antibodies against interleukin (IL)-12 and IL-18 showed a suppressive effect on LPS-induced NO production in the PEC culture, and these antibodies in synergy showed strong suppression. Stimulation of the PEC culture with IL-12 or IL-18 induced production of IFN-c and NO, and these cytokines, in combination, exhibited marked synergism. Stimulation of the culture with IFN-c induced production of NO, but not IL-12. The macrophage population in the PEC, prepared as adherent cells, responded well to LPS for IL-12 production, but weakly for production of IFN-c and NO. The macrophages also responded well to IFN-c for NO production. For production of IFN-c by stimulation with LPS or IL-12 + IL-18, nonadherent cells were required in the PEC culture. Considering these results overall, the indirect pathway, through the production of intermediates (such as IFN-c-inducing cytokines and IFN-c) by the cooperation of macrophages with nonadherent cells, was revealed to play the main role in the LPS-induced NO production pathway, as opposed to the direct pathway requiring only a macrophage population.

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“…The culture medium was removed gently by aspiration and changed to fresh culture medium. The PECs used for experiments routinely contained 87% to 92% macrophages (34). Then, cell lines were implanted into these wells at a ratio of 1:1.…”

Section: Methodsmentioning

confidence: 99%

A Special Linker between Macrophage and Hematopoietic Malignant Cells: Membrane Form of Macrophage Colony-Stimulating Factor

Wang

Zheng

et al. 2008

Cancer Research

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The membrane form of macrophage colony-stimulating factor (mM-CSF) is an alternative splicing variant of this cytokine. Although its high expression was detected in hematopoietic malignancies, its physiologic and pathologic roles in hematopoietic system have not been established. In this report, stable transfectant clones expressing mM-CSF (Namalwa-M and Ramos-M) were obtained, which showed reduced proliferation potential in vitro. Moreover, the in vivo study showed that Namalwa-M and Ramos-M exhibited enhanced oncogenicity in tumor size in nude mice model, which could be inhibited by M-CSF monoclonal antibody. A remarkable increase in infiltrating macrophage and the vessel densities was found in tumor tissues formed by lymphoma cell lines that stably expressed mM-

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Role of IFN-γ on dissociation between nitric oxide and TNF/IL-6 production by murine peritoneal cells after restimulation with bacterial lipopolysaccharide

Abstract: Murine peritoneal exudate cells (PEC) pre-exposed to bacterial lipopolysaccharide (LPS) show augmented

Cited by 8 publications

References 39 publications

Molecular mechanisms of endotoxin tolerance

Molecular mechanisms of endotoxin tolerance

A pathway through interferon‐γ is the main pathway for induction of nitric oxide upon stimulation with bacterial lipopolysaccharide in mouse peritoneal cells

A Special Linker between Macrophage and Hematopoietic Malignant Cells: Membrane Form of Macrophage Colony-Stimulating Factor

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