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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion to mucosal cells is an important virulence attribute of bacterial pathogens colonizing these sites. Bacteria of the upper respiratory system, such as members of the genus Bordetella, have well-defined adhesins. The main adhesin of B. pertussis is the filamentous hemagglutinin which can be used by other bacteria for attachment. The main adhesin of B. bronchiseptica is the bovine erythrocyte hemagglutinin. In both Bordetella species the presence of fimbriae does not appear critical to adhesion. In contrast, atrophic rhinitis (AR)-producing strains of Pasteurella multocida colonize poorly the pig's nasal mucosa. We performed an in vitro trial using newborn pigs' turbinate explants and showed that two toxigenic strains (serotype D fimbria + and serotype A fimbria -) were adherent when observed by scanning electron microscopy (SEM). Intranasal inoculation of both six week old and newborn SPF pigs with various strains of P. multocida also resulted in colonization. Adhesion was best achieved by toxigenic strains, regardless of possession of fimbria, hemagglutinin or capsular serotype. Colonization was more abundant and constant in tonsils. Nasal colonization was sporadic and sparse. Colonization of trachea and lung was only observed with serotype A strains. The results showed that toxigenic P. multocida can colonize the upper respiratory tract, especially the tonsils, of pigs.
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PMID:Bacterial adhesion to mucosal surfaces with special reference to Pasteurella multocida isolates from atrophic rhinitis. 214 99

Adhesion molecules on respiratory epithelial cells play a critical role in inflammatory cell recruitment and accumulation at sites of inflammation. Bordetella pertussis colonizes the human respiratory tract by infecting epithelial cells, leading to an inflammatory response. In this study, the role of bacterial factors in the expression of intercellular adhesion molecule-1 (ICAM-1) on human respiratory epithelial cells was investigated in response to B. pertussis. Flow cytometry and real time RT-PCR analysis showed that BEAS-2B human bronchial epithelial cells expressed increased levels of ICAM-1 mRNA and surface protein in response to B. pertussis infection. Filamentous hemagglutinin (FHA) played a role in this response because of the impaired capability of a FHA-deficient isogenic strain. A mutant strain in which an Arg-Gly-Asp (RGD) site of FHA had been changed to Arg-Ala-Asp had diminished ability to up-regulate ICAM-1 expression. RGD sequence-associated up-regulation of ICAM-1 expression was also observed in primary normal human bronchial epithelial cells. Pretreatment of cells with integrin antagonists such as RGD-containing peptide and antibody against very late antigen-5 (VLA-5) inhibited the up-regulation of ICAM-1 expression, suggesting the participation of VLA-5 integrin in this response. Pertussis toxin (PT) prevented the up-regulation of ICAM-1 expression because a PT-deficient mutant strain induced higher levels of ICAM-1 mRNA and surface protein than the parental strain. Consistent with this, purified PT suppressed the up-regulation of epithelial ICAM-1 expression. These findings demonstrate that B. pertussis FHA up-regulates ICAM-1 expression on respiratory epithelial cells through interaction of its RGD site with host cell VLA-5 integrin, and that PT impairs this response.
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PMID:Bordetella pertussis infection of human respiratory epithelial cells up-regulates intercellular adhesion molecule-1 expression: role of filamentous hemagglutinin and pertussis toxin. 1222 Sep 88