A deep rough type structure in Bordetella bronchiseptica lipopolysaccharide modulates host immune responses

F. SISTI ; J. FERNÁNDEZ, ; S.C. HIGGINS; A. CASABUONO,; A. COUTO,; K. H. G. MILLS; D.HOZBOR

MICROBIOLOGY AND IMMUNOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2011 vol. 55 p. 847 - 854

0385-5600

The present authors have previously obtained the Bordetella bronchiseptica mutant BbLP39, whichcontains a deep-rough lipopolysaccharide (LPS) instead the wild type smooth LPS with O antigen. Thismutant was found to be altered in the expression of some proteins and in its ability to colonize mouselungs.Particularly, inBbLP39the expression ofpertactinisdecreased.Todifferentiate the contributionofeachbacterial componenttotheobservedphenotype,heremicedefective in theLPSsensing receptorTLR4(TLR4-defective mice) were used. In contrast to wild-type mice, infection of TLR4-defective mice withBbLP39 resulted in lung infection, which persisted for more than 10 days post-challenge. Comparativeanalysis of the immune responses induced by purifiedmutant andwild type LPSs showed that themutantLPS induced significantly higher degrees of expression of TNF-α and IL-10mRNA than did thewild type.UVmatrix-assisted laser desorption/ionization time-of-flight (MALDITOF) mass spectrometry analysisrevealed that both LPSs had the same penta-acylated lipid A structure.However, the lipid A fromBbLP39contained pyrophosphate instead of phosphate at position 1. This structural difference, in addition tothe lack of O-antigen in BbLP39, may explain the functional differences between BbLP39 and wild typestrains.