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Identified virulence factors of Haemophilus: Endotoxin


LOS  

Related genes: kdtA; lic2A; licA; licB; licC; licD; rfaD; rfaE;
Keywords: Endotoxin;
Characteristics:
lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence.
lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-α(1-4)β-Gal LPS structure.
But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid.
Structure features:
Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS.
Lack O-antigen.
Functions:
Major immunogen.
LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals.
LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments.
Mechanism:
lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region).
Phase-variable gene lic3A encodes an α-2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum.
References:
Weiser JN, Pan N, 1998. Adaptation of Haemophilus influenzae to acquired and innate humoral immunity based on phase variation of lipopolysaccharide. Mol. Microbiol. 30(4):767-775.
Rao VK, et al., 1999. Molecular determinants of the pathogenesis of disease due to non-typable Haemophilus influenzae. FEMS Microbiol. Rev. 23(2):99-129.
Hood DW, et al., 1999. Sialic acid in the lipopolysaccharide of Haemophilus influenzae: strain distribution, influence on serum resistance and structural characterization. Mol. Microbiol. 33(4):679-692.
Erwin AL, et al., 2000. Role of lipopolysaccharide phase variation in susceptibility of Haemophilus influenzae to bactericidal immunoglobulin M antibodies in rabbit sera. Infect. Immun. 68(5):2804-2807.
Swords WE, et al., 2000. Non-typeable Haemophilus influenzae adhere to and invade human bronchial epithelial cells via an interaction of lipooligosaccharide with the PAF receptor. Mol. Microbiol. 37(1):13-27.
Humphries HE, High NJ, 2002. The role of licA phase variation in the pathogenesis of invasive disease by Haemophilus influenzae type b. FEMS Immunol. Med. Microbiol. 34(3):221-230.
Bouchet V, et al., 2003. Host-derived sialic acid is incorporated into Haemophilus influenzae lipopolysaccharide and is a major virulence factor in experimental otitis media. Proc. Natl. Acad. Sci. USA. 100(15):8898-8903.








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