Paradoxical effect of pilus expression on binding of antibodies by Haemophilus influenzae

Gilsdorf, Janet R.; Tucci, Michelle; Forney, Larry J.; Watson, Wendy; Marrs, Carl F.; Hansen, Eric J.

doi:10.1128/iai.61.8.3375-3381.1993

Cited by 8 publications

(1 citation statement)

References 26 publications

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“…As for the role of pili, data from Gutierrez et al (26) suggest that infant rats inoculated with piliated H. influenzae b, either intranasally, intravenously, or intraperitoneally, had decreased levels of bacteremia compared to rats inoculated with nonpiliated variants. In addition, piliated H. influenzae organisms bind (and are killed by) antibodies directed against nonpilus surface antigens more effectively than do nonpiliated organisms (24). Furthermore, piliated H. influenzae stimulates enhanced opsonization-dependent phagocytosis by neutrophils as determined by chemiluminescence (62).…”

Section: Functional Characterization Of H Influenzae Pilimentioning

confidence: 99%

Role of pili in Haemophilus influenzae adherence and colonization

1997

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Haemophilus influenzae was first recognized as an important pathogen in 1892, when it was isolated from throat swab specimens and mistakenly identified as the causative agent of influenza (45). Humans are the only natural reservoir for this bacterium, which is found, most commonly, on respiratory mucosal surfaces and, occasionally, in the female genital tract. Up to 50 to 80% of healthy individuals are colonized with nontypeable H. influenzae, which possesses no capsular polysaccharide and fails to react with standard typing sera; fewer than 5% are colonized with strains of serotypes a through f, which possess one of six antigenically and biochemically distinct polysaccharide capsules. For reasons that are not entirely clear, children are more likely to be colonized with H. influenzae than are adults (63). In addition to asymptomatic mucosal colonization, H. influenzae causes a wide spectrum of clinical infections (63). Organisms possessing the type b capsule are highly virulent in nonimmune hosts (primarily young, unvaccinated children) and may cause bacteremia and invasive infections such as meningitis, epiglottitis, pneumonia, septic arthritis, and buccal cellulitis. Nonencapsulated H. influenzae strains as well as those possessing the non-b capsules a and c through f rarely cause bacteremia or invasive infections in healthy hosts. A unique exception is the Brazilian purpuric fever strain of nontypeable H. influenzae biogroup aegyptius, which apparently does not possess a polysaccharide capsule and yet has caused outbreaks of bacteremia, sepsis, and vascular collapse and death in young children, primarily in Brazil (44). Nonencapsulated organisms, however, commonly cause localized respiratory tract infections such as otitis media, sinusitis, bronchitis, and pneumonia (41, 63). Although asymptomatic in most individuals, H. influenzae colonization of the respiratory mucosa is the first step in a series of events that may lead to infection (1, 53). In respiratory organ culture tissues infected with H. influenzae, the bacterium is closely associated with mucus, damaged epithelium, and nonciliated cells (12, 13, 30). Furthermore, these organisms invade both cultured epithelial cells (31, 56) and mononuclear, macrophage-like cells within human adenoid tissue (16); survival of the bacterium within cells lining the respiratory mucosa may play a role in prolonged H. influenzae colonization of the respiratory tract. It is not clear whether H. influenzae nasopharyngeal colonization in humans results in immunity and, thus, protection against subsequent infection by the colonizing organism. In infant rats, however, H. influenzae type b nasopharyngeal colonization without bacteremia failed to protect animals against challenge, whereas colonized animals that were also bacteremic were protected (19). COLONIZATION AND ADHERENCE FACTORS OF H.

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Section: Functional Characterization Of H Influenzae Pilimentioning

confidence: 99%