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Infect. Immun. doi:10.1128/IAI.00028-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Viable Haemophilus somnus induce myosin light chain kinase-dependent decrease in brain endothelial cell monolayer resistance

Comparative Biomedical Sciences Graduate Program, University of Wisconsin-Madison, Madison WI; Johns Hopkins University School of Medicine, Baltimore MD

^* To whom correspondence should be addressed. Email: czuprync{at}svm.vetmed.wisc.edu.

	Abstract

Haemophilus somnus causes thrombotic meningoencephalitis (TME) in cattle. Our laboratory has previously reported that H. somnus has the ability to adhere to, but not invade, bovine brain endothelial cells (BBEC) in vitro. The goal of this study was to determine if H. somnus alters brain endothelial cell monolayer integrity in vitro, in a manner that would be expected to contribute to inflammation of the central nervous system (CNS). Monolayer integrity was monitored by measuring trans-endothelial electrical resistance (TEER) and albumin flux. BBEC incubated with H. somnus underwent rapid cytoskeletal rearrangement, significant increases in albumin flux, and reductions in TEER. Decreased monolayer TEER was preceded by phosphorylation of the myosin regulatory light chain, and was partially dependent on TNF- and myosin light chain kinase, but not IL-1. Neither heat killed H. somnus, formalin-fixed H. somnus nor purified lipooligosaccharide altered monolayer integrity within a 2 hr incubation period, whereas conditioned media from H. somnus-treated BBEC caused a modest reduction in TEER. The data from this study support the hypothesis that viable H. somnus alters integrity of the blood-brain barrier by promoting contraction of BBEC and increasing paracellular permeability of the CNS vasculature.