|Leite, F - UNIV. OF WI, MADISON, WI|
|Brown, F - UNIV. OF WI, MADISON, WI|
|Sylte, M - UNIV. OF WI, MADISON, WI|
|Czuprynski, C - UNIV. OF WI, MADISON, WI|
Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 3, 2000
Publication Date: N/A
Interpretive Summary: Pneumonic pasteurellosis is a common and severe disease of beef and dairy cattle. The causative agent, Pastuerella haemolytica, causes a massive influx of white blood cells into lung tissues which sickens or kills the calf. It was found that lung inflammation increases the calf's susceptibility to the bacterium and that the calf may actually amplify the deadly effects of the Pasteurella. This information helps to better understand the cause of this disease and may lead to effective strategies for disease control.
Technical Abstract: The influx and death of polymorphonuclear leukocytes within the infected lung are hallmarks of bovine pasteurellosis. Recent reports have shown that the Pasteurella haemolytica leukotoxin (LKT) and other RTX toxins bind beta(2)-integrins on target cells. In this study, we demonstrate that exposure of bovine neutrophils to recombinant bovine interleukin-1beta aupregulates beta(2)-integrins (CD11a/CD18), which in turn enhance the binding and amplify the biological effects of partially purified LKT on these cells. LKT binding and cytotoxicity were inhibited by addition of an anti-integrin antibody (CD11a/CD18). These findings help to clarify the early events that occur in bovine pasteurellosis and support the hypothesis that inflammatory mediators might increase the severity of pasteurellosis by causing upregulation of beta(2)-integrins that serve as an LKT receptor on bovine neutrophils.