Escape from Immune Surveillance byCapnocytophaga canimorsus
Autor: | Guy R. Cornelis, Cécile Paroz, Hwain Shin, Manuela Mally, Marina Kuhn |
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Rok vydání: | 2007 |
Předmět: |
Down-Regulation
Biology Nitric Oxide p38 Mitogen-Activated Protein Kinases Microbiology Proinflammatory cytokine Interferon-gamma Mice Dogs Immune system Interferon Interleukin-1alpha medicine Animals Humans Immunology and Allergy Interleukin 8 Chemokine CCL4 Cells Cultured Toll-like receptor Virulence Tumor Necrosis Factor-alpha Macrophages Interleukin-8 Capnocytophaga canimorsus Macrophage Inflammatory Proteins biology.organism_classification Mice Inbred C57BL Toll-Like Receptor 4 Infectious Diseases Immunology TLR4 Tumor necrosis factor alpha Gram-Negative Bacterial Infections Capnocytophaga medicine.drug |
Zdroj: | The Journal of Infectious Diseases. 195:375-386 |
ISSN: | 1537-6613 0022-1899 |
Popis: | Capnocytophaga canimorsus, a commensal bacterium from dogs' mouths, can cause septicemia or meningitis in humans through bites or scratches. Here, we describe and characterize the inflammatory response of human and mouse macrophages on C. canimorsus infection. Macrophages infected with 10 different strains failed to release tumor necrosis factor (TNF)- alpha and interleukin (IL)-1 alpha . Macrophages infected with live and heat-killed (HK) C. canimorsus 5 (Cc5), a strain isolated from a patient with fatal septicemia, did not release IL-6, IL-8, interferon- gamma , macrophage inflammatory protein-1 beta , and nitric oxide (NO). This absence of a proinflammatory response was characterized by the inability of Toll-like receptor (TLR) 4 to respond to Cc5. Moreover, live but not HK Cc5 blocked the release of TNF- alpha and NO induced by HK Yersinia enterocolitica. In addition, live Cc5 down-regulated the expression of TLR4 and dephosphorylated p38 mitogen-activated protein kinase. These results highlight passive and active mechanisms of immune evasion by C. canimorsus, which may explain its capacity to escape from the host immune system. |
Databáze: | OpenAIRE |
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