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.