Escape from Immune Surveillance byCapnocytophaga canimorsus

Abstract

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.

NMR-based Structural Analysis of the Complete Rough-type Lipopolysaccharide Isolated from Capnocytophaga canimorsus

“…The main fraction (pool 2, yield 1.45 mg) (Fig. 2) represented the purified and complete rough-type LPS of C. canimorsus (3). The third fraction, pool 3 (yield 0.62 mg), was free lipid A as determined by ESI-MS ([M] ϭ 1717.308 units).…”

Molecular Characterization of Capnocytophaga canimorsus and Other Canine Capnocytophaga spp. and Assessment by PCR of Their Frequencies in Dogs

“…Although our two dog strains were in the least common group, more dog strains need to be cultured and typed to see whether all C. canimorsuspositive dogs can infect patients with this pathogen. A toxin produced by some strains could be a virulence factor (7); however, we could not confirm its presence (data not shown), and in a recent publication a toxin was not found (21). Recently, some potential virulence mechanisms for C. canimorsus have been revealed.…”

“…Recently, some potential virulence mechanisms for C. canimorsus have been revealed. It was shown that human macrophages incubated with C. canimorsus failed to produce tumor necrosis factor alpha, interleukin-1␣ (IL-1␣), IL-6, Il-8, and gamma interferon; that TLR-4 could not be activated by the reference strain; and that even tumor necrosis factor alpha release by another pathogen, Yersinia enterocolitica, was impaired by live C. canimorsus (21). The resistance to phagocytosis of C. canimorsus by macrophages and the blocking of the ability of macrophages to kill other bacteria also were demonstrated by the same group of investigators (17), as well as its resistance to killing by complement and polymorphonuclear leukocytes (22).…”

Transcriptional expression levels of chicken collectins are affected by avian influenza A virus inoculation

“…In mammals, an up regulation of collectins has frequently been observed in both bacterial and viral infections (Murray et al, 2002;Grubor et al, 2004), which is usually interpreted as a direct response of the host to increase its defense against the incoming pathogens. A down regulation of collectins upon infection is less frequently reported, but could reflect a survival strategy of the pathogen to overcome the host's hostile environment, as has been described for other innate immune proteins such as Tolllike receptors and defensins (Wang et al, 2000;Shin et al, 2007). However, whether this applies to AIV in the chicken lung and why the altered expression of chicken (col)lectins is tissue specific is not clear at this moment and requires further investigation.…”