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of the study. MH and BH drafted the manuscript. All authors read and approved the final manuscript.”
“Background Histophilus somni (Haemophilus somnus) is a host-specific, gram-negative coccobacillus, and an opportunistic pathogen of cattle and sometimes sheep buy AZD4547 that is responsible for a variety of systemic infections, including meningoencephalitis, pneumonia, myocarditis, septicemia, and reproductive failure [1, 2]. Hallmarks of H. somni infection include septicemia, by which the organism can disseminate to various tissues such as the brain, heart, and joints [1–3], and adherence to and inflammation of vascular Liothyronine Sodium endothelial cells [4, 5]. Pathogenic isolates of H. somni share many virulence attributes with human-specific mucosal pathogens that are designed to resist host defense mechanisms. For example, the structure of the lipooligosaccharide (LOS) of H. somni is remarkably similar to that of Neisseria gonorrhoeae, including an outer core that mimics the structure of lacto-N-neotetraose on the glycosphingolipid of mammalian cells [6–8]. Furthermore, like Haemophilus

influenzae, the H. somni LOS outer core undergoes a high rate of phase variation due to variable number tandem repeats in the genes that encode for the LOS glycosyl transferases [9, 10]; the LOS is also decorated with N-acetylneuraminic acid (Neu5Ac or sialic acid) and phosphorylcholine, which can contribute to resistance to host defenses and adaptation to specific host sites [11, 12]. Other H. somni virulence attributes include immunoglobulin mTOR inhibitor binding proteins [13, 14], cell adhesions [3], resistance to the bactericidal activity of serum [15], survival in and inhibition of the oxidative burst of phagocytic cells [16–19], toxicity to epithelial cells [20, 21], and induction of apoptosis of endothelial cells [22–24].