Disease relevance of traH

• Biological activity, lipoprotein-binding behavior, and in vivo disposition of extracted and native forms of Salmonella typhimurium lipopolysaccharides [1].
• Bacterial lipoprotein induces resistance to Gram-negative sepsis in TLR4-deficient mice via enhanced bacterial clearance [2].
• LP release was not unique to E. coli [3].
• Lipoprotein (LP) is a major component of the outer membrane of bacteria in the family Enterobacteriaceae [3].
• Humoral and cell-mediated immunity in mice to a 17-kilodalton lipoprotein of Francisella tularensis expressed by Salmonella typhimurium [4].

High impact information on traH

• Sites of tissue binding and uptake in vivo of bacterial lipopolysaccharide-high density lipoprotein complexes: studies in the rat and squirrel monkey [5].
• The alveolar epithelium is lined by surfactant, a lipoprotein complex that both reduces surface tension and mediates several innate immune functions including bacterial aggregation, alteration of alveolar macrophage function, and regulation of bacterial clearance [6].
• Using a newly constructed minitransposon with a phoA reporter gene in a Salmonella enteritidis phoN mutant, we have identified an iron- and pH-inducible lipoprotein gene sfbA, which is a component of a novel ABC-type transporter system required for virulence [7].
• The YfgL Lipoprotein Is Essential for Type III Secretion System Expression and Virulence of Salmonella enterica Serovar Enteritidis [8].
• In a previous paper, we provided evidence that two functional copies of the lipoprotein gene (lppA and lppB) located on the chromosome of Salmonella enterica serovar Typhimurium contributed to bacterial virulence [9].

Chemical compound and disease context of traH

• The role of lipopolysaccharide in sepsis is well studied; however, the contribution of other bacterial outer membrane components, such as Braun (murein) lipoprotein (Lpp), is not well defined [10].
• Biosynthesis and assembly of envelope lipoprotein in a glycerol-requiring mutant of Salmonella typhimurium [11].
• ApbE is a lipoprotein in Salmonella typhimurium, and mutants unable to make this protein have a reduced ability to make thiamine (vitamin B(1)) and require it as a supplement for optimal growth in minimal glucose medium [12].
• Vaccines consisting of acetone-killed Salmonella typhimurium were supplemented with a synthetically prepared lipopeptide derivative of bacterial lipoprotein, Pam3Cys-Ser-Ser-Asn-Ala [13].

Biological context of traH

• We constructed a serovar Typhimurium strain with deletions in both copies of the lpp gene (lpp1 and lpp2) by marker exchange mutagenesis [10].
• These studies provided the first evidence of the relative contributions of Lpp and lipid A acylation to Salmonella pathogenesis [9].
• The genome of Salmonella enterica serovar Typhimurium harbors two copies of the lipoprotein (lpp) gene [10].
• We therefore tested whether the lack of motility of Salmonella mutants defective in lipoprotein biogenesis is a result of inability to modify FlgH [14].
• Altered expression patterns in the absence of Dam methylation were also found for the chemotaxis genes cheR (repressed by Dam) and STM3216 (activated by Dam) and for the Braun lipoprotein gene, lppB (activated by Dam) [15].

Anatomical context of traH

• Activation of murine macrophages by lipoprotein and lipooligosaccharide of Treponema denticola [16].
• Polyclonal activation of B-lymphocytes in vivo by Salmonella typhimurium lipoprotein [17].
• The motility of the mutant was impaired, despite the finding that the number of flagella was similar in the lpp double knockout mutant and the WT serovar Typhimurium [10].
• A 17-kDa lipoprotein, TUL4, of the facultative intracellular bacterium Francisella tularensis is one of several membrane proteins that induce an in vitro response in T cells from F. tularensis-primed humans [4].
• The integrity of the cell membrane and the secretion of the effector proteins through the type III secretion system were not affected in the lpp double-knockout mutant [10].

Associations of traH with chemical compounds

• The pilN product was shown to be a lipoprotein by an experiment using globomycin [18].
• Treatment of bacteria with the antibiotic ceftazidime significantly enhanced LP release [3].
• Conversely, sodium deoxycholate (0.15 g/dl), which disaggregates LPS, greatly increased binding of LPS to HDL in the absence of lipoprotein-free plasma [19].
• We found that calcium chloride (1 mM), an agent which prevents LPS disaggregation, inhibited binding of LPS to HDL by interfering with the modification of LPS by lipoprotein-free plasma [19].
• Lipopolysaccharide and lipoprotein were identified easily as discrete precipitates when they were solubilized with Triton X-100 [20].

Analytical, diagnostic and therapeutic context of traH

• Quantitative immunoprecipitation experiments indicated that essentially all of the apo-SAA was bound to lipoprotein particles containing apo-A-I [21].
• Removal of the main impurities, lipopolysaccharide (LPS) and lipoprotein, was accompanied by loss of protective capacity in passive immunization experiments [22].
• Global gene expression of a murein (Braun) lipoprotein mutant of Salmonella enterica serovar Typhimurium by microarray analysis [23].
• Composition and structure of lipopolysaccharide-human plasma low density lipoprotein complex. Analytical ultracentrifugation, 31P-NMR, ESR and fluorescence spectroscopy studies [24].

References