Human tumor necrosis factor increases the resistance against Listeria infection in mice

Kato, K; Nakane, Akio; Minagawa, Tomonori; Kasai, Noriyuki; Satô, Noboru; Tsuruoka, Nobuo

doi:10.1007/bf00197452

Cited by 42 publications

(28 citation statements)

References 38 publications

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“…Through the activation of nuclear factor kappa B (NF-rB), a key transcriptional factor for immunological system, TNF-a facilitates the protection from invading pathogens [2]. By utilizing neutralizing anti-TNF-a antibodies, studies have demonstrated that host defense against exogenous pathogens is severely compromised in the absence of TNFa [3][4][5]. However, dys-regulated TNF-a has been implicated as a host-attacking mediator in a variety of human diseases, including autoimmune diseases, inflammatory bowel disease (IBD) and osteoporosis [6,7].…”

Section: Introductionmentioning

confidence: 99%

Naringin rescued the TNF-α-induced inhibition of osteogenesis of bone marrow-derived mesenchymal stem cells by depressing the activation of NF-кB signaling pathway

et al. 2015

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Naringin exhibits antiinflammatory activity and is shown to induce bone formation. Yet the impact of naringin on inflammation-affected bone marrow-derived mesenchymal stem cell (BM-MSC), a promising tool for the regenerative treatment of bone injury, remained to be investigated. We first cultured and characterized the BM-MSCs in vitro and observe the effects of treatments of TNF-α, naringin, or the combination of both on osteogenic differentiation. TNF-α administered at the concentration of 20 ng/ml results in significant reductions in MSC's cell survival, alkaline phosphatase activity and expressions of two osteogenic genes, Runx2 and Osx. Simultaneous treatment of both TNF-α and naringin is able to rescue such reductions. Further mechanistic studies indicate that TNF-α treatment activates the NF-кB signaling pathway, evidenced by elevated p-IкBα level as well as the increased nuclear fraction of NF-кB subunit, p65. Finally, treatment with both TNF-α and naringin decreases expressions of p-IкBα and nuclear p65, and thus represses NF-кB pathway activated by sole TNF-α treatment. Our findings provide a molecular basis by which naringin restores the TNF-α-induced damage in MSCs and provide novel insights into the application of naringin in the MSC-based treatments for inflammation-induced bone injury.

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Section: Introductionmentioning

confidence: 99%

Naringin rescued the TNF-α-induced inhibition of osteogenesis of bone marrow-derived mesenchymal stem cells by depressing the activation of NF-кB signaling pathway

et al. 2015

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“…TNF is produced shortly following infection with L. monocytogenes, and neutralization of TNF with specific antibodies exacerbates listeriosis in mice (16,17,27). Administration of recombinant human TNF can also reduce the severity of primary infection with L. monocytogenes in mice (20,33). The importance of this cytokine-receptor pair during the primary immune response to L. monocytogenes was confirmed when TNF Ϫ/Ϫ (28) and TNFRI Ϫ/Ϫ (9, 30, 34) mice were found to be highly susceptible to primary listeriosis.…”

mentioning

confidence: 99%

Adaptive Immunity againstListeria monocytogenesin the Absence of Type I Tumor Necrosis Factor Receptor p55

White¹,

Badovinac

Fan

et al. 2000

Infect Immun

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Tumor necrosis factor (TNF) and the type I TNF receptor (TNFRI), p55, are critical for resistance against primary infections with the intracellular bacterial pathogen Listeria monocytogenes. Importantly, however, susceptibility to primary listeriosis in cytokine-deficient mice does not preclude the development or expression of effective adaptive immunity against virulent L. monocytogenes. We used TNFRI ؊/؊ mice to study adaptive antilisterial immunity in the absence of interactions between TNF and TNFRI. Our experiments indicate that TNFRI ؊/؊ mice survive and clear high-dose challenges with an attenuated strain of L. monocytogenes that is incapable of cell-to-cell spread. Furthermore, TNFRI ؊/؊ mice immunized with attenuated L. monocytogenes go on to develop potent adaptive immunity to subsequent high-dose challenges with virulent L. monocytogenes. Interestingly, CD8؉ T-cell depletion in vivo inhibits immunity to L. monocytogenes in the spleen but not in the liver of TNFRI ؊/؊ mice. The adaptive immune response in these animals is characterized by activation of listeriolysin O-specific CD8 ؉ T cells, which are capable of transferring antilisterial immunity to naive wild-type C57BL/6 host mice. These experiments demonstrate the development and expression of potent CD8 ؉ T-cellmediated antilisterial immunity in the absence of TNFRI.

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“…Since IL-12 [33,34] or TNF-α [35] have been shown to reduce bacilli burdens during bacterial infection, We evaluated if statin treatment also enhanced IL-12p40 and TNF- α production in BMDMs. Macrophages were treated with simvastatin and stimulated with IFN-γ for 18 hours and subsequently infected with L.…”

Section: Resultsmentioning

confidence: 99%

Simvastatin Enhances Protection against Listeria monocytogenes Infection in Mice by Counteracting Listeria-Induced Phagosomal Escape

et al. 2013

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Statins are well-known cholesterol lowering drugs targeting HMG-CoA-reductase, reducing the risk of coronary disorders and hypercholesterolemia. Statins are also involved in immunomodulation, which might influence the outcome of bacterial infection. Hence, a possible effect of statin treatment on Listeriosis was explored in mice. Statin treatment prior to subsequent L. monocytogenes infection strikingly reduced bacterial burden in liver and spleen (up to 100-fold) and reduced histopathological lesions. Statin-treatment in infected macrophages resulted in increased IL-12p40 and TNF-α and up to 4-fold reduced bacterial burden within 6 hours post infection, demonstrating a direct effect of statins on limiting bacterial growth in macrophages. Bacterial uptake was normal investigated in microbeads and GFP-expressing Listeria experiments by confocal microscopy. However, intracellular membrane-bound cholesterol level was decreased, as analyzed by cholesterol-dependent filipin staining and cellular lipid extraction. Mevalonate supplementation restored statin-inhibited cholesterol biosynthesis and reverted bacterial growth in Listeria monocytogenes but not in listeriolysin O (LLO)-deficient Listeria. Together, these results suggest that statin pretreatment increases protection against L. monocytogenes infection by reducing membrane cholesterol in macrophages and thereby preventing effectivity of the cholesterol-dependent LLO-mediated phagosomal escape of bacteria.

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Human tumor necrosis factor increases the resistance against Listeria infection in mice

Cited by 42 publications

References 38 publications

Naringin rescued the TNF-α-induced inhibition of osteogenesis of bone marrow-derived mesenchymal stem cells by depressing the activation of NF-кB signaling pathway

Naringin rescued the TNF-α-induced inhibition of osteogenesis of bone marrow-derived mesenchymal stem cells by depressing the activation of NF-кB signaling pathway

Adaptive Immunity againstListeria monocytogenesin the Absence of Type I Tumor Necrosis Factor Receptor p55

Simvastatin Enhances Protection against Listeria monocytogenes Infection in Mice by Counteracting Listeria-Induced Phagosomal Escape

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