You are here: Home Published Research Susceptibility of nontypeable Haemophilus influenzae to human beta-defensins is influenced by lipooligosaccharide acylation.

Timothy D Starner, W. E Swords, Michael A Apicella, and Paul B McCray (2002)

Susceptibility of nontypeable Haemophilus influenzae to human beta-defensins is influenced by lipooligosaccharide acylation.

Infection and immunity, 70(9):5287–5289.

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.

Acylation, Acyltransferases, Anti-Bacterial Agents, Bacterial Proteins, Drug Resistance, Bacterial, Genes, Bacterial, Genetic Complementation Test, Haemophilus influenzae, Humans, In Vitro Techniques, Lipid A, Lipopolysaccharides, Mutation, beta-Defensins
Acylation, Acyltransferases, Anti-Bacterial Agents, Bacterial Proteins, Drug Resistance, Bacterial, Genes, Bacterial, Genetic Complementation Test, Haemophilus influenzae, Humans, In Vitro Techniques, Lipid A, Lipopolysaccharides, Mutation, beta-Defensins
 
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