Extraintestinally invasive Escherichia coli (EC) that possess both a complete LPS and K1 capsule evade both complement-mediated bacteriolysis and neutrophil-mediated killing. Since C3H/HeJ mice that are hyporesponsive to LPS were uniquely susceptible to lethal infection with EC of this phenotype, we speculated there was an LPS-initiated host defense mechanism against this pathogenic phenotype. The LPS-normoresponsive C3H/HeN as well as the C3H/HeJ mice cleared these EC from the circulation within 4 h of intravenous administration. Whereas electron micrographs of the liver demonstrated these EC undergoing degeneration within the phagolysosomes of of both macrophages and Kupffer cells of C3H/HeN mice, these EC replicated within these cells of the C3H/HeJ mice. Restoration of anti-EC activity of C3H/HeJ mice occurred with activation of Kupffer cells and peritoneal macrophages in vivo with BCG and in vitro with IFN-gamma, but not with LPS. Pretreatment of C3H/HeJ mice with a combination of recombinant murine IL-1 and TNF-alpha also restored the killing of K1(+)-EC but did not enhance the killing of a K1(-)-EC mutant. These data are consistent with the hypothesis that (a) there is no intrinsic inability of C3H/HeJ phagocytes to kill EC, but (b) an LPS-initiated, cytokine-mediated host defense mechanism is required for such killing. These studies emphasize the importance of bacterial surface characteristics in the interaction with specific host defenses.
A Cross, L Asher, M Seguin, L Yuan, N Kelly, C Hammack, J Sadoff, P Gemski Jr
Title and authors | Publication | Year |
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Febrile-range temperature modifies early systemic tumor necrosis factor alpha expression in mice challenged with bacterial endotoxin
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Escherichia coli msbB gene as a virulence factor and a therapeutic target
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Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2
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Exposure to febrile temperature upregulates expression of pyrogenic cytokines in endotoxin-challenged mice
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American Journal of Physiology - Regulatory, Integrative and Comparative Physiology | 1999 |
Advances in Bladder Research
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1999 | |
Febrile-Range Temperature Modifies Early Systemic Tumor Necrosis Factor Alpha Expression in Mice Challenged with Bacterial Endotoxin
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Infection and immunity | 1999 |
Gamma Interferon Augments Macrophage Activation by Lipopolysaccharide by Two Distinct Mechanisms, at the Signal Transduction Level and via an Autocrine Mechanism Involving Tumor Necrosis Factor Alpha and Interleukin-1
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Infection and immunity | 1999 |
Escherichia coli msbB Gene as a Virulence Factor and a Therapeutic Target
RN Moore, JE Somerville, L Cassiano, RP Darveau |
Infection and immunity | 1999 |
Toll-like receptor-2 mediates mycobacteria-induced proinflammatory signaling in macrophages.
Underhill DM, Ozinsky A, Smith KD, Aderem A |
Proceedings of the National Academy of Sciences | 1999 |