Host response to bovine respiratory pathogens

Abstract

AbstractBovine respiratory disease (BRD) involves complex interactions amongst viral and bacterial pathogens that can lead to intense pulmonary inflammation (fibrinous pleuropneumonia). Viral infection greatly increases the susceptibility of cattle to secondary infection of the lung with bacterial pathogens likeMannheimia haemolyticaandHistophilus somni. The underlying reason for this viral/bacterial synergism, and the manner in which cattle respond to the virulence strategies of the bacterial pathogens, is incompletely understood. Bovine herpesvirus type 1 (BHV-1) infection of bronchial epithelial cellsin vitroenhances the binding ofM. haemolyticaand triggers release of inflammatory mediators that attract and enhance binding of neutrophils. An exotoxin (leukotoxin) released fromM. haemolyticafurther stimulates release of inflammatory mediators and causes leukocyte death. Cattle infected withH. somnifrequently display vasculitis. Exposure of bovine endothelial cells toH. somniior its lipooligosaccharide (LOS) increases endothelium permeability, and makes the surface of the endothelial cells pro-coagulant. These processes are amplified in the presence of platelets. The above findings demonstrate that bovine respiratory pathogens (BHV-1,M. haemolyticaandH. somni) interact with leukocytes and other cells (epithelial and endothelial cells) leading to the inflammation that characterizes BRD.