Virulent strains of the bovine opportunistic pathogen Haemophilus somnus (Histophilus somni) cause multi-systemic diseases in cattle. One of the reported virulence factors that H. somnus may use to persist in the host is resistance to intracellular killing. We report here that H. somnus significantly (P < 0.001) inhibited production of superoxide anion (O2-) by bovine mammary and alveolar macrophages as well as by polymorphonuclear leukocytes. Inhibition of O2- was time- and dose-dependent and did not occur after incubation with Escherichia coli, H. influenzae, or Brucella abortus. Non-viable H. somnus, purified lipooligosaccharide, or cell-free supernatant from mid-log phase cultures did not inhibit O2- production, indicating that O2- inhibition required contact with live H. somnus. Furthermore, preincubation of phagocytic cells with cytochalasin B to prevent phagocytosis did not decrease the ability of H. somnus to inhibit O2- production. Some H. somnus isolates from the prepuce of healthy bulls were less capable or incapable of inhibiting macrophage O2- production compared to isolates tested from disease sites. Our results suggest that inhibition of O2- may be an important virulence factor exploited by pathogenic strains of H. somnus to resist killing by professional phagocytic cells.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.micpath.2004.08.002 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!