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

Sexually differentiated responses occur in molecular, cellular, physiologic, and organismic aspects of immune-system function in relation to acquired and innate immunities. These sex differences apparently include activational effects, which depend on gonadal hormone levels in adults, and lifelong effects, which arise directly from genetic differences or organizational effects of gonadal hormones early in development that lead to lifelong sex differences. Sex differences in immune function also can have great biological significance. Despite this, the mechanisms of these effects rarely have been analyzed extensively. This is especially true of anorexia during illness or disease. Therefore, this review briefly considers 1) the biological mechanisms of sex differences; 2) sex differences in immune function; 3) clinical and experimental data related to sex differences in four diseases or disease models that involve anorexia, Crohn's inflammatory-bowel disease, cancer, turpentine inflammation, and lipopolysaccharide bacteremia; and 4) sex differences in anorexia after interleukin-1 administration.
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PMID:Sex differences in disease anorexia. 1139 14

OK-432 has been used clinically as a biological response modifier for cancer therapy. We investigated here the protective effects of OK-432 against endotoxic shock and infectious death caused by Pseudomonas aeruginosa and Salmonella enteritidis in mice and proposed a possible mechanism. Pretreatment of OK-432 reduced the lethality of lipopolysaccharide (LPS)-induced endotoxic shock in D-(+)-galactosamine-sensitized C3H/HeN mice. OK-432 did not affect the TNFalpha production in blood, but it did decrease the susceptibility to TNFalpha. Furthermore, an acceleration of LPS clearance from blood was detected. The pretreatment of OK-432 also decreased the lethality of mice in bacterial infection caused by P. aeruginosa and S. enteritidis. The rapid decrease of the viable bacteria from the circulating blood and in spleen and liver in mice was observed in a manner similar to LPS clearance. These findings indicate that the protective effect of OK-432 against the endotoxemia and bacteremia may depend on an up-regulation of clearance of LPS and bacteria and the augmented resistance to TNFalpha.
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PMID:Protective effect of OK-432 on mice against endotoxemia and infection with Pseudomonas aeruginosa and Salmonella enteritidis. 1149 17

The ability of cefoxitin, clindamycin, imipenem, meropenem, metronidazole and piperacillin-tazobactam to cause gram-negative anaerobic bacteria to release endotoxin and the influence of such liberated endotoxin on antibiotic efficacy were investigated in in-vivo experiments in animal models. Experimental infections in various animal models (mice, hamster and infant rats) with cultures of wild and reference strains of Bacteroides fragilis group and Fusobacterium spp. were carried out by injecting these animals with different inocula (10(6), 10(7) and 10(8) cfu/ml) of the bacterial suspension, Appropriate doses of the test antibiotics were then injected and the plasma lipopolysaccharide (endotoxin) release measured by the Limulus Amoebocyte Lysate (LAL) Assay. Evidence of worsening of the outcome of the infections post-therapy was assessed, including histopathological changes in the internal organs. Infection with generalized septicemia was established with F. nucleatum in the mice and hamster models while with the B. fragilis group, infections only led to intra-abdominal abscess formation. Plasma endotoxin release was higher in animals infected with F. nucleatum than B. fragilis and was unrelated to the bacterial inoculum. Imipenem, meropenem and cefoxitin, in that order, induced the highest levels of endotoxin activities in the animal model, particularly following F. nucleatum infection. Histological examination of the internal organs of various animals showed variation in the pattern of histopathological changes; grades 3-4 inflammatory changes in the liver were observed in the Fusobacterium-infected animals that were treated with the carbapenems and cefoxitin. Therapy with the other antibiotics did not exacerbate anaerobic sepsis. In this study, bacteremia did not lead to massive endotoxin release and antibiotic therapy appeared not to have negatively influenced the outcome of most of the gram-negative anaerobic infections, except for infections caused by Fusobacterium spp. However, it is conceivable that if the gastrointestinal tract is the source of the endotoxin in patients with systemic inflammatory response syndrome, then the obligate anaerobes like Bacteroides and Fusobacterium species, which are members of the gut flora, may play a major role in the unfavorable outcome of antibiotic therapy in some of these infections.
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PMID:Influence of in-vivo endotoxin liberation on anti-anaerobic antimicrobial efficacy. 1176 Feb 15

Klebsiella pneumoniae is a common cause of gram-negative bacterial nosocomial pneumonia. Two surface polysaccharides, lipopolysaccharide (LPS) O side chain and capsular polysaccharide (CPS), are critical for the microorganism in causing sepsis, but little is known about their role in pneumonia. To investigate their contribution in the pathogenesis of K. pneumoniae pneumonia, we characterized the host response to bacterial challenge with a highly virulent clinical isolate or with isogenic insertion-duplication mutants deficient in CPS or LPS O side chain in a murine model of pneumonia. Animals challenged intratracheally with the wild-type or LPS O side chain-deficient strain developed pneumonia and became bacteremic before death. Extensive lung lesions as well as pleuritis, vasculitis, and edema were observed by histopathological examination, and polymorphonuclear infiltration was also demonstrated. In contrast, none of the animals challenged with the unencapsulated strain developed pneumonia or bacteremia. Examination of tissue from this group did not identify lung lesions, and none of the infected animals died. Analysis of the early host defense mechanisms that contributed to the clearance of the unencapsulated mutant showed that the levels of C3 deposited on the unencapsulated mutant surface were threefold higher than those for the wild-type and LPS O side chain-deficient strains. Furthermore, phagocytosis of the unencapsulated mutant by human alveolar macrophages (AM) was more efficient than that of the wild-type and LPS O side chain-deficient strains. We conclude that CPS, but not LPS O side chain, is essential for Klebsiella pneumonia because it modulates the deposition of C3 and protects the microorganisms against human AM phagocytosis.
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PMID:Molecular analysis of the contribution of the capsular polysaccharide and the lipopolysaccharide O side chain to the virulence of Klebsiella pneumoniae in a murine model of pneumonia. 1195 99

Periodontal disease is a significant cause of alveolar bone resorption resulting ultimately in the loss of teeth. Inflammation of the periodontal tissues is initiated by bacteria of the oral micro-flora. Invading micro-organisms stimulate both protective and destructive inflammatory-immune responses involving cytokine release syndrome, chemokines, arachidonic acid metabolites, reactive oxygen and nitrogen intermediates, and matrix melloproteinases. The local infection may affect general health in two ways. First, transient bacteremia from the oral focus may result in metastatic infection in remote organs of susceptible hosts, such as bacterial endocarditis in patients with congenital or acquired heart diseases. Second, lipopolysaccharide and inflammatory mediators are not only involved in local tissue destruction but have the potential to modulate the course of cardiovascular, chronic obstructive lung and autoimmune diseases, diabetes mellitus and preterm birth. Epidemiologic observations, awaiting further verification by controlled prospective trials, underline the impact of oral health on general well-doing.
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PMID:[Periodontal disease and general health--literature review]. 1198 Apr 26

Inner-core lipopolysaccharide (LPS) from Neisseria meningitidis is under investigation as a vaccine for prevention of meningococcal disease caused by N. meningitidis serogroup B (NmB). We investigated the functional activity of murine monoclonal antibody (MAb) B5 that recognizes a highly conserved (galE) LPS epitope. Three patterns of MAb reactivity were observed in N. meningitidis by Western blot, depending on the relative prevalence of sialylated, nonsialylated, and/or truncated LPS glycoforms. Three representative N. meningitidis strains (8047, M986, and 2996) were investigated with MAb B5 in functional assays in vitro and in vivo. MAb B5 completely protected infant rats against bacteremia caused by 8047, partially protected against 2996, and had no protective activity against M986. Thus, an inner-core LPS epitope can be a target for protective immunity, but the affinity of MAb B5 may only be sufficient to mediate protection against NmB strains possessing at least some truncated glycoforms.
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PMID:Highly conserved Neisseria meningitidis inner-core lipopolysaccharide epitope confers protection against experimental meningococcal bacteremia. 1269 1

There has been a dramatic increase in the number of reported cases of infection due to Vibrio vulnificus in Taiwan. Although the organism has been etiologically implicated in a variety of clinical syndromes, most cases of V. vulnificus infection are categorized as primary bacteremia, skin and soft tissue infection. The mortality was up to 50% in septic patients, most of them dying within 48 h of admission. In most of the cases involving V. vulnificus infection have underlying disease, particularly liver cirrhosis. The pathogenesis may attribute to several virulent factors, such as lipopolysaccharide, capsular lipopolysaccharide, cytolysin, metalloprotease and siderophore. Tetracycline was suggested as the drug of choice based on an animal study. Our previous in vitro data showed that cefotaxime and minocycline acted synergistically in inhibiting V. vulnificus. Furthermore, another in vivo animal study indicated that therapy using combined with cefotaxime and minocycline was distinctly more advantageous than therapy with the single antibiotic regimen for the treatment of severe experimental murine V. vulnificus infection. Recently, we also demonstrated that the newer fluoroquinolones, as single agents were as effective as the combination therapy both in vitro and in vivo.
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PMID:Vibrio vulnificus infection: clinical manifestations, pathogenesis, and antimicrobial therapy. 1288 57

Bacterial surface carbohydrates are important pathogenic factors in gram-negative pneumonia infections. Among these factors, O antigen has been reported to protect pathogens against complement-mediated killing. To examine further the role of O antigen, we insertionally inactivated the gene encoding a galactosyltransferase necessary for serotype O1 O-antigen synthesis (wbbO) from Klebsiella pneumoniae 43816. Analysis of the mutant lipopolysaccharide by sodium dodecyl sulfate-polyacrylamide gel electrophoresis confirmed the absence of O antigen. In vitro, there were no detectable differences between wild-type K. pneumoniae and the O-antigen-deficient mutant in regard to avid binding by murine complement C3 or resistance to serum- or whole-blood-mediated killing. Nevertheless, the 72-h 50% lethal dose of the wild-type strain was 30-fold greater than that of the mutant (2 x 10(3) versus 6 x 10(4) CFU) after intratracheal injection in ICR strain mice. Despite being less lethal, the mutant organism exhibited comparable intrapulmonary proliferation at 24 h compared to the level of the wild type. Whole-lung chemokine expression (CCL3 and CXCL2) and bronchoalveolar inflammatory cell content were also similar between the two infections. However, whereas the wild-type organism produced bacteremia within 24 h of infection in every instance, bacteremia was not seen in mutant-infected mice. These results suggest that during murine pneumonia caused by K. pneumoniae, O antigen contributes to lethality by increasing the propensity for bacteremia and not by significantly changing the early course of intrapulmonary infection.
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PMID:The Klebsiella pneumoniae O antigen contributes to bacteremia and lethality during murine pneumonia. 1497 47

A hallmark of Bartonella henselae is persistent bacteremia in cats despite the presence of a vigorous host immune response. To understand better the long-term survival of B. henselae in cats, we examined the feline humoral immune response to B. henselae outer membrane (OM) proteins in naturally and experimentally infected cats. Initially, a panel of sera (n = 42) collected throughout North America from naturally infected cats was used to probe B. henselae total membranes to detect commonly recognized antigens. Twelve antigens reacted with sera from at least 85% of cats, and five were recognized by sera from all cats. To localize these antigens further, OMs were purified on discontinuous sucrose density step gradients. Each membrane fraction (OM, hybrid or inner membrane [IM]) contained less than 1% of the total malate dehydrogenase activity (soluble marker), indicating very little contamination by cytoplasmic proteins. FtsI, an integral IM cell division protein, was used to identify the low-density fraction (rho = 1.13 g/cm3) as putative IM (<5% of the total FtsI localized to the high-density fraction) while lipopolysaccharide (LPS) and Pap31, a homolog of the Bartonella quintana heme-binding protein A (HbpA), defined the high-density fraction (rho = 1.20 g/cm3) as putative OM. Additionally, little evidence of cross-contamination between the IM and OM was evident by two-dimensional gel electrophoresis. When purified OMs were probed with feline sera, antigenic proteins profiles were very similar to those observed with total membranes, indicating that many, but not all, of the immunoreactive proteins detected in the initial immunoblots were OM components. Interestingly, two-dimensional immunoblots indicated that B. henselae LPS and members of the Hbp family of proteins did not appear to stimulate an humoral response in any infected cats. Seven proteins were recognized by at least 70% of sera tested, but only three were recognized by all sera. Nanospray-tandem mass spectrometry was used to identify OM components, including the immunodominant OM proteins. Recognition of the nonimmunogenic nature of the major OM components, such as LPS, and identification of the predominant immunogens should elucidate the mechanisms by which B. henselae establishes persistent bacteremic infections within cats. Additionally, the common antigens may serve as potential feline vaccine candidates to eliminate the pathogen from its animal reservoir.
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PMID:Predominant outer membrane antigens of Bartonella henselae. 1515 10

Coronary artery disease results from an inflammatory process in blood vessels of afflicted individuals. This process is accelerated with diabetes for reasons that are largely unknown. Recent evidence indicates that infection at sites remote from the heart leads to bacteremia and endotoxemia, thereby stimulating systemic inflammation, which represents an important risk factor for atherosclerosis. We examined the inflammatory response of the heart/aorta of diabetic db/db mice that develop type II diabetes. Subcutaneous inoculation of lipopolysaccharide was used to mimic a local infection. This stimulated an up-regulation of adhesion molecules, cytokines, and chemokines via an endotoxemia that was significantly more rapid and more pronounced in the diabetic compared with normal mice. The 13- to 30-fold induction of key proinflammatory molecules in the heart/aorta of diabetic mice even exceeded that at the site of inoculation. Given that infection, bacteremia, and endotoxemia are relatively frequent events in humans, these results identify a putative mechanism for increased cardiovascular heart disease in diabetes.
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PMID:Influence of diabetes on the exacerbation of an inflammatory response in cardiovascular tissue. 1528 96


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