Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The outcome of the early stages of a neisserial infection is determined by receptor-mediated events that culminate in the attachment and invasion of human mucosal tissues. The factors participating in this process, including pili, opacity proteins (Opa), and perhaps lipopolysaccharide (LPS), are subject to complex genetic controls that allow these factors to be produced in multiple forms. Antigenic variation allows the pathogenic Neisseriae to evade the human immune response, and facilitates their interaction with a variety of different cells and tissues of the human host. One of the major genetic mechanisms causing antigenic variation is transformation, which allows virulence genes to be exchanged and recombined between independent Neisseria strains within multiply infected individuals. A number of other factors, such as IgA protease, alpha-factor, and the meningococcal capsule are also implicated in pathogenesis and render the pathogenic Neisseriae an excellent model for the investigation of bacterial virulence.
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PMID:Pathogenic neisseriae--a model of bacterial virulence and genetic flexibility. 208 68

The early stages of an infection with pathogenic Neisseriae are determined by receptor-mediated events that finally lead to the attachment and invasion of human mucous tissues. The factors participating in this process, the pili, OPA proteins, and perhaps lipopolysaccharide (LPS), are subject to complex genetic changes that enable the pathogens to produce multiple variant forms of these factors. Antigenic variation of the pathogenic Neisseriae permits both, the escape from the human immune response and the interaction with different cells and tissues of the human host. One of the intrinsic mechanisms of antigenic variation, i.e. genetic transformation, allows exchange and recombination of virulence genes between independent Neisseria strains in multiply infected individuals. Factors, such as IgA protease, alpha-factor, and the meningococcal capsule are attributed with further striking properties, and thus render the pathogenic Neisseriae as an excellent model for the investigation of bacterial virulence.
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PMID:[Pathogenic neisseriae--model of bacterial virulence and genetic flexibility]. 257 Jul 47

Haemophilus influenzae are small, gram-negative, rod-shaped bacteria. Because of their special growth requirements, they do not grow on usual blood agar media, but flourish on the mucosal membranes of the human respiratory tract where they adhere to the epithelial cells by fimbriae (a potential vaccine component). Nasopharyngeal carriage of Haemophilus influenzae is very common, and in healthy carriers the bacteria are usually unencapsulated. The outer membrane of Haemophilus influenzae contains lipopolysaccharide (of so called R form, without O antigen) and major outer membrane proteins. The lipopolysaccharide is a virulence determinant. An extracellular enzyme, IgA protease, is another potential virulence determinant. The outer membrane of Haemophilus influenzae is a rather ineffective barrier towards antibiotics, and thus the major determinants of antibacterial resistance in Haemophilus influenzae are plasmid-coded enzymes that inactivate the antibiotic, and changes in the target molecules.
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PMID:Unencapsulated Haemophilus influenzae--what kind of pathogen? 290 69