Induction of interferon‐γ production and Ia expression by interleukin 1 in bone marrow culture cells

Puri, Joseph; Eglash, Barbara; Lonai, Peter

doi:10.1002/eji.1830170212

Cited by 5 publications

(3 citation statements)

References 37 publications

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“…Another way that macrophages may be stimulated indirectly by IL-1 is through gamma interferon induction. IL-1 is reported to enhance the release of gamma interferon [6,7], a known macrophage activator [19]. Therefore, it may be possible that IL-1 stimulated the release of gamma interferon or primed responding cells to enhance the release/effect of this lymphokine following a bacterial stimulus.…”

Section: Discussionmentioning

confidence: 96%

“…In addition to its ability to induce fever [2], IL-1 has a wide range of biological activities which include stimulating the release of various mediators such as colony stimulating factor [3][4][5], gamma interferon [6], and hepatic acute phase proteins [8,9]. The ability of these factors to increase cell numbers and function suggest a potential for IL-I to enhance host resistance to infection.…”

Section: Introductionmentioning

confidence: 99%

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Enhanced antibacterial resistance in neutropenic mice treated with human recombinant interleukin-1 beta

1988

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Human Recombinant IL-1 was investigated for its ability to increase non-specific resistance to Staphylococcus aureus in neutropenic mice. Mice, rendered neutropenic with cyclophosphamide and then administered IL-1 intraperitoneally, demonstrated enhanced resistance to subsequent challenge with S. aureus as measured by increased survival and bacterial clearance. No protective effects were observed with heat inactivated IL-1. Efficacy was observed only when both IL-1 and the subsequent bacterial challenge were administered into the same site. Despite the observed protective effects, animals treated with IL-1 did not have increased numbers of blood leukocytes or peritoneal phagocytes prior to infection or at the times coincident with bacterial clearance. Based upon these observations, enhanced activity of resident macrophages may be responsible for the protective effects observed in IL-1 treated mice.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Enhanced antibacterial resistance in neutropenic mice treated with human recombinant interleukin-1 beta

1988

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“…In T lymphocytes, macrophages, peripheral blood mononuclear cells, and leukemic cell lines, IL-1␤ influences cell proliferation by inducing IFN-␥ production. [20][21][22][23][24][25] Within the liver, investigators have documented IFN-␥ production in infectious settings resulting from hepatitis C and Listeria monocytogenes and inflammatory states such as that found during acute rejection in orthotopic liver transplantation. [26][27][28] However, no one has previously addressed the capability of hepatocytes to produce IFN in response to IL-1␤ stimulation.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 1β-stimulated production of nitric oxide in rat hepatocytes is mediated through endogenous synthesis of interferon gamma

Schroeder

Kuo

1998

Hepatology

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Hepatocyte expression of inducible nitric oxide synthase (iNOS) and subsequent elaboration of NO is associated with multiple cellular and biochemical functions, such as inhibition of mitochondrial electron transport, activation of soluble guanylyl cyclase, regulation of glutathione synthesis, and protection against oxidative injury. 1-3 Although tumor necrosis factor ␣ (TNF-␣), interleukin 1␤ (IL-1␤), interferon gamma (IFN-␥), and endotoxin are known to synergistically induce maximal iNOS expression, investigators have recently shown that IL-1␤ alone is sufficient to induce expression of iNOS in hepatocyte cultures. [4][5][6] However, studies using other cell systems, such as the macrophage, have indicated a central role for IFN-␥ rather than IL-1␤ in the expression of iNOS. [7][8][9] Murine macrophages express iNOS in response to synergistic combinations of IFN-␥, IFN-␣, and IFN-␤ with or without endotoxin. 8,10 The murine and rat iNOS promoter sequences both have 10 copies of the IFN-␥ response element and two copies of the IFN-␣-stimulated response element. 8,11 Last, IL-1␤ is a multifunctional cytokine, affecting all cell types, and often acts in concert with other cytokines or small mediator molecules. Specifically, IL-1␤ is known to initiate expression of a variety of genes, including IFN-␣, ␤, and ␥, TNF, and IL-1 and to increase cell surface expression of IFN and TNF receptors. 12,13 On the basis of these considerations, we hypothesized that IL-1␤-induced iNOS expression in rat hepatocytes is dependent on endogenous production of IFN-␥. In a model of rat hepatocytes in primary culture, we have characterized the expression of IFN-␥ and NO synthesis in the setting of IL-1␤ stimulation. Using antisense IFN-␥ to inhibit translation of IFN-␥ messenger RNA (mRNA), we defined the role of IFN-␥ in IL-1␤-mediated NO synthesis. Finally, rat hepatocytes were transiently transfected with a plasmid reporter gene construct containing the rat hepatocyte iNOS promoter to define the action of IFN-␥ in IL-1␤ activation of the iNOS promoter. Our results suggest that IFN-␥ is a necessary but not sufficient component of the cascade required for maximal IL-1␤-associated hepatocyte expression of iNOS. MATERIALS AND METHODSRat Hepatocyte Isolation. Male Lewis rats (range, 200-300 g; Harlan Inc., Indianapolis, IN) fed water and chow ad libitum were used for hepatocyte isolation as described by Schuetz et al. 14 After anesthetization with pentobarbital sodium, the portal vein was cannulated. The liver was perfused with calcium-free Krebs' bicarbonate buffer followed by 150 mg collagenase D in 200 mL of Krebs' bicarbonate buffer containing 1.2 mmol/L CaCl 2 and 1.8% bovine serum albumin. All solutions were maintained at 37°C and aerated with 95% O 2 /5% CO 2 . The partially digested liver was excised, passed Abbreviations: iNOS, inducible nitric oxide synthase; TNF-␣, tumor necrosis factor ␣; IL-1␤, interleukin 1␤; IFN-␥, interferon gamma; mRNA, messenger RNA; DPBS, Dulbecco' s phosphate-buffered saline; PBS, phosphate-buffered s...

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Granulocyte‐macrophage colony‐stimulating factor‐cultured bone marrow‐derived macrophages reveal accessory cell function and synthesis of MHC class II determinants in the absence of external stimuli

et al. 1988

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The antigen-mediated activation of a number of T cell clones by bone marrow (BM) cells cultivated in the presence of various colony-stimulating factor (CSF) preparations was investigated. BM macrophages (BMM phi) grown in L929 cell supernatant as a crude source of macrophage colony-stimulating factor (M-CSF) as well as BM cells propagated in the presence of recombinant M-CSF exhibited transient antigen presentation potential to some T cell clones, being maximal on day 7 and having declined to a low level by day 19 of in vitro culture. Treatment of these long-term-cultivated BMM phi populations with recombinant interferon-gamma (IFN-gamma) resulted in predominant antigen presentation capacity. In contrast, BM cells differentiated in the presence of recombinant granulocyte (G)M-CSF developed highly efficient accessory cell function to all T cell clones examined. This function became apparent earlier, was retained during the time period tested (up to day 19 of continuous culture) and did not require prior stimulation by IFN-gamma. The functionally competent cells were shown to belong to the monocyte/macrophage lineage. These findings are consistent with the demonstration of substantial levels of major histocompatibility complex (MHC) class II molecules synthesized by GM-CSF-cultured BM cells in the absence of exogenous IFN-gamma. In contrast, M-CSF grown BM cells synthesized only minute amounts of Ia antigens unless they were stimulated by IFN-gamma. Because GM-CSF-cultivated BM cells proved clearly superior to M-CSF-grown and IFN-gamma-activated BM cells with respect to antigen-presenting capacity but exhibited lower levels of MHC class II molecules, other properties acting in addition to surface Ia antigens might be responsible for their pronounced T cell accessory function.

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Induction of interferon‐γ production and Ia expression by interleukin 1 in bone marrow culture cells

Cited by 5 publications

References 37 publications

Enhanced antibacterial resistance in neutropenic mice treated with human recombinant interleukin-1 beta

Enhanced antibacterial resistance in neutropenic mice treated with human recombinant interleukin-1 beta

Interleukin 1β-stimulated production of nitric oxide in rat hepatocytes is mediated through endogenous synthesis of interferon gamma

Granulocyte‐macrophage colony‐stimulating factor‐cultured bone marrow‐derived macrophages reveal accessory cell function and synthesis of MHC class II determinants in the absence of external stimuli

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