Endogenous tumor necrosis factor (cachectin) is essential to host resistance against Listeria monocytogenes infection

Nakane, Akio; Minagawa, Tomonori; Kato, K

doi:10.1128/iai.56.10.2563-2569.1988

Cited by 316 publications

(151 citation statements)

References 39 publications

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“…The in vitro incubation of BRM-induced effectors with cytokines such as IFNy, TNFa and IL-2, known to activate microbicidal activity of macrophages and PMN in other experimental systems [16,48,49], did not induce anti-GBS-090 activity.…”

Section: Discussionmentioning

confidence: 90%

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Scaringi

1994

FEMS Immunology and Medical Microbiology

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There is ample evidence that protection against group B streptococcal (GBS) disease, both in experimental animals and in humans, is related to the presence of specific antibodies and complement. However, until now the possibility of increasing resistance to GBS infection by potentiating natural cell-mediated immunity in the host, has not been explored. In this study we examine the effect of administering in vivo MVE-2 (a polymer fraction of 1,2-co-polymer of divinyl ether and maleic anhydride) and inactivated Candida albicans (CA) cells on mouse resistance to the reference strain type Ia 090 GBS (GBS-090) lethal infection. MVE-2 and CA, respectively a synthetic and a microbial biological response modifier (BRM), are strong inducers and activators of natural resistance effectors, such as natural killer (NK) cells, macrophages and polymorphonuclear cells (PMN). The results showed that MVE-2 protected 100% CD-1 mice from a systemic lethal challenge with GBS-090 (5 x 10(3) microorganisms/mouse) when administered 3 days before infection at dose of 50 mg kg-1. CA treatment, in five doses (CA-5d) over 14 days protected 100% mice when administered at 2 x 10(7) cells/mouse and when the last CA injection was given 1 day before the GBS-090 challenge. Instead, when the GBS-090 challenge was performed by intraperitoneal route, protection was obtained with CA-5d treatment but not with MVE-2. The possibility that MVE-2 or CA stimulated a rapid production of specific antibodies against GBS-090 infection was excluded by the ELISA assay. Evidence exists that NK cells do not play a primary role as effectors in the MVE-2 and CA conferred protection since the strong reduction in NK activity, due to in vivo administration of anti-asialo GM1 antibodies before GBS-090 infection, did not influence the BRM-induced protection. Besides, high NK activity levels, induced by in vivo rhIL-2 administration, did not protect the mice against GBS-090 infection. Both studies on in vivo clearance and in vitro microbicidal activity, showed that, after 1 h, immunopotentiated effectors were unable to kill GBS-090, but were highly effective against GBS type VI. These results seem to indicate that intracellular GBS-090 killing is a slow process requiring more than 1 h. This study demonstrates that it is possible to increase resistance to GBS-090 lethal infection by BRMs, by potentiating the antibody-independent microbicidal activity of the phagocytes.

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Section: Discussionmentioning

confidence: 90%

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Scaringi

1994

FEMS Immunology and Medical Microbiology

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“…A number ofother cytokines such as TNF and GM-CSF can also induce killing of Listeria, leishmania, and trypanozome by macrophages [25][26][27][28][29]. It is not known if RNI are also involved in cytotoxicity induced by cytokines other than IFN-y.…”

Section: Discussionmentioning

confidence: 99%

Differential mechanisms of intracellular killing ofMycobacterium aviumandListeria monocytogenesby activated human and murine macrophages. The role of nitric oxide

Bermudez

1993

Clinical and Experimental Immunology

109

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SUMMARYMurine peritoneal macrophages activated with interferon-gamma (IFN-y) produce large quantities of nitric oxide and are efficient in the killing of certain intracellular pathogens. To examine the role of this mechanism in the killing of Mycobacterium avium by murine and human macrophages, we infected mouse peritoneal macrophages and human monocyte-derived macrophages with M. avium and Listeria monocytogenes and stimulated the cells with recombinant tumour necrosis factor (TNF), granulocyte-macrophage colony-stimulating factor (GM-CSF) or IFN-y, in the presence or absence of N-monomethyl-L-arginine (NMA) or arginase. Neither competitive inhibition with NMA nor depletion of arginine by arginase had any effect on the inhibition of growth/intracellular killing of M. avium by activated human and murine macrophages. In contrast, activation of murine but not human macrophages infected with L. monocytogenes by IFN-y was significantly inhibited by the addition of NMA/arginase. Furthermore, murine macrophages produced large concentrations of nitric oxide following stimulation with recombinant cytokines, although no significant increase of nitric oxide production was observed with human monocyte-derived macrophages.

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“…Although LPS triggers TNF release from murine peritoneal macrophages in vitro [22.23], no TNF-a was detected in peritoneal exudate or blood from animals of either strain during the first 24 h of a BT-induced inflammatory response. Nakane et al [24] reported comparable findings in Z. (.s7er/o-inrected mice where, despite the fact that no TNF-a was detected (L929 bioassay, <4/i/tnl) in serum or spleen homogenates at any time point, injection of animals with anti-TNF-rv antibody 0-2 h p.i.…”

Section: Discussionmentioning

confidence: 69%

Genetic variation in neutrophil accumulation in mice is not mediated through immigrant regulatory cells

Marley

Hadley

Wakelin

1995

Clinical and Experimental Immunology

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SUMMARYGenetic variation of induced peritoneal neutrophiiia in mice was accompanied by parallel variation in macrophage responses. The timing of the macrophage responses in high responder (C57B1/10) mice indicated a potential role for these cells in mediating the enhanced neutrophil response. However, adoptive transfer of inflammatory macrophages did not induce neuirophilia. Analysis of peritoneal cytokine levels in high and low responder mice further indicated [hat IL-I. lL-3. GM-CSE, G-CSE and interferon-gamma (IFN-7) were not involved in mediating the genetic variation observed. Exogenous tumour necrosis factor-alpha (TNF-a) was effective in inducing the high responder phenotype. despite the absence of detectable TNF-fi in either peritoneal fluid or serum. A role for genetically determined differential expression of endotheiial adhesion molecules in high and low responders is suggested.

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Endogenous tumor necrosis factor (cachectin) is essential to host resistance against Listeria monocytogenes infection

Cited by 316 publications

References 39 publications

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Differential mechanisms of intracellular killing ofMycobacterium aviumandListeria monocytogenesby activated human and murine macrophages. The role of nitric oxide

Genetic variation in neutrophil accumulation in mice is not mediated through immigrant regulatory cells

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