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

Bacterial adhesion is probably a prerequisite for colonization of mucous membranes, but adhesion to the bronchial mucosa has not been studied in detail. We investigated adhesion of respiratory pathogens to bronchial epithelial cells, and asked whether chronic bronchitis had an influence on bacterial adhesion. Oropharyngeal and bronchial cells were collected during bronchoscopy from 14 healthy nonsmokers, 22 smokers with nonobstructive chronic bronchitis, and 19 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD). Patients with a forced expiratory volume in one second (FEV1) less than 50% predicted were excluded. Adhesion of highly adherent test strains of H. influenzae and S. pneumoniae to these cells were studied. The test strains of H. influenzae and S. pneumoniae were found to adhere well to both oropharyngeal and bronchial cells. H. influenzae showed a higher degree of adhesion both to ciliated and goblet cells from the patients with nonobstructive bronchitis than to cells from the healthy nonsmokers. No corresponding difference was found for S. pneumoniae. The patients with COPD did not differ from the controls in their adhesion values. Our results indicate that bacterial adhesion is of importance for the colonization and retention of H. influenzae in the human airways. For S. pneumoniae the role of adhesion is more uncertain.
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PMID:Bacterial adhesion to oropharyngeal and bronchial epithelial cells in smokers with chronic bronchitis and in healthy nonsmokers. 782 81

Eight strains of Haemophilus influenzae were tested for binding to human vitronectin. All strains adhered to vitronectin-coated glass slides but no binding was detected using soluble vitronectin, suggesting that surface association of vitronectin is a prerequisite. Vitronectin binding was not likely to be mediated by fimbriae as non-fimbriated and fimbriated isogenic strains adhered equally. Adhesion could be blocked by heparin, which is also known to block vitronectin binding to Staphylococcus aureus. However, no blocking was achieved with sialic acid-rich glycoproteins such as fetuin and mucin contrasting with Helicobacter pylori for which sialic acid seems to play an important role. With Streptococcus pneumoniae binding was detected both with soluble and surface-associated vitronectin and could not be blocked by heparin. Our results suggest that H. influenzae, Streptococcus pneumoniae and Helicobacter pylori all use distinct modes to interact with vitronectin.
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PMID:Interaction of vitronectin with Haemophilus influenzae. 1242 74

Adhesion to the respiratory epithelium plays an important role in Haemophilus influenzae infection. The distribution of H. influenzae adhesins in type b and nontypeable strains has been characterized, but little is known about the prevalence of these factors in non-type b encapsulated strains. We analyzed 53 invasive type a, type e, and type f strains for the presence of hap, hia, hmw, and hif genes; Hap, Hia, and HMW1/2 adhesins; and hemagglutinating pili. The hap gene was ubiquitous, and homologs of hmw and hia were present in 7 of 53 (13.2%) and 45 of 53 (84.9%) strains, respectively. Hap was detected in 28 of 45 (62.2%) hap(+) strains, HMW1/2 was detected in 5 of 7 (71.4%) hmw(+) strains, and Hia was detected in 31 of 45 (68.8%) hia(+) strains. The hif gene cluster was present in 26 of 53 strains (49.1%), and 21 of 26 hif(+) strains (80.8%) agglutinated (HA) red blood cells. Nine isolates exhibited HA but lacked the hif gene cluster. The distribution of adhesin genes correlated with the genetic relatedness of the strains. Strains belonging to one type a clonotype and the major type e clonotype possessed hia but lacked the hif cluster. Strains belonging to the second type a clonotype possessed both hia and hif genes. All type f strains belonging to the major type f clonotype possessed hia and lacked hifB. Although the specific complement of adhesin genes in non-type b encapsulated H. influenzae varies, most invasive strains express Hap and Hia, suggesting these adhesins may be especially important to the virulence of these organisms.
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PMID:Prevalence and distribution of adhesins in invasive non-type b encapsulated Haemophilus influenzae. 1265 75

The blood-cerebrospinal fluid (CSF) barrier physiologically protects the meningeal spaces from bloodborne bacterial pathogens, due to the existence of specialized junctional interendothelial complexes. A few bacterial pathogens are able to reach the subarachnoidal space and cause bacterial meningitis in humans, a rare but dreadful disease. Surprisingly, most of them are extracellular commensals of the nasopharynx (Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenzae) or of the digestive tract (Escherichia coli and Streptococcus agalactiae). The particular ability of these pathogens to induce meningitis is related to virulence factors that allow them to escape host innate immunity, to multiply within the serum, and to interact closely with the endothelial front line of defense of the blood-CSF barrier. In vitro studies using microvascular brain endothelial cell lines have shown that induced transcytosis may be a common route used by H. influenzae, S. pneumoniae, E. coli and S. agalactiae to reach the CSF. N. meningitidis is a strict human pathogen that interacts very tightly with endothelial cells. Adhesion of the meningococcus is mediated by type IV pili that induce a localized remodeling of the sub cortical cytoskeleton, leading to the formation of endothelial membrane protrusions that anchor bacterial colonies at the endoluminal face of the endothelial cell membrane, allowing a better resistance to blood flow. Recent work has shown that N. meningitidis is also able to recruit the polarity complex Par3/Par6/aPKC that re-routes endothelial cell adhesion molecules of interendothelial junctions, opening a paracellular route for bacteria to cross the endothelial barrier.
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PMID:Mechanisms of meningeal invasion by a bacterial extracellular pathogen, the example of Neisseria meningitidis. 2002 34