Nontypeable Haemophilus influenzae (NTHI) lipooligosaccharide htrB mutants exhibited greater than 45-fold-increased sensitivity to human beta-defensin 2 (HBD-2) compared to the wild type. Complementation by htrB in trans to acylation competence reversed this increased sensitivity. In contrast, NTHI was more susceptible to HBD-3 and showed no changes in sensitivity as a result of lipooligosaccharide mutations in oligosaccharide and lipid A biosynthesis genes.
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Starner et al. (2002) studied this question.
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