Lipooligosaccharide P-k (Gal alpha 1-4Gal beta 1-4Glc) epitope of Moraxella catarrhalis is a factor in resistance to bactericidal activity mediated by normal human serum
A. Zaleski et al., Lipooligosaccharide P-k (Gal alpha 1-4Gal beta 1-4Glc) epitope of Moraxella catarrhalis is a factor in resistance to bactericidal activity mediated by normal human serum, INFEC IMMUN, 68(9), 2000, pp. 5261-5268
Moraxella catarrhalis is a respiratory pathogen responsible for acute bacte
rial otitis media in children and exacerbation of chronic bronchitis in adu
lts. M. catarrhalis strains are frequently resistant to the bactericidal ac
tivity of normal human serum. In order to determine if the lipooligosacchar
ide (LOS) of M. catarrhalis has a role in serum resistance, the UDP-glucose
-4-epimerase (galE) gene was identified, cloned, and sequenced and a deleti
on/insertion mutation was introduced into M. catarrhalis strain 2951. GalE
enzymatic activity, measured in whole-cell lysates, was ablated in M. catar
rhalis 2951 galE. Mass spectrometric analysis of LOS isolated with hot phen
ol-water confirmed that strain 2951 produced a type A LOS. These studies sh
owed that the LOS from 2951 galE had lost two hexose residues due to the ga
lE mutation and that the resultant LOS structure lacked the (Gal alpha 1-4G
al beta 1-4Glc) P-k epitope found on M. catarrhalis 2951. Wild-type M. cata
rrhalis 2951 is resistant to complement-mediated serum bactericidal activit
y. In contrast, a greater than 2-log(10)-unit reduction in CFU occurred aft
er incubation of 2951 galE in either 50 or 25% pooled human serum (PNHS), a
nd CFU in 10% PNHS decreased by about 1 log(10) unit. These studies suggest
that the P-k epitope of the LOS may be an important factor in the resistan
ce of M. catarrhalis to the complement-mediated bactericidal effect of norm
al human serum.