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)

Infections by coxsackie virus B3 (CVB3) have been reported to be associated with an enhanced influx of mononuclear leukocytes into afflicted tissue. Current evidence indicates that monocytes/macrophages are specifically involved in CVB3-induced myocarditis by maintaining a chronic inflammatory response. To examine susceptibility and reactivity to CVB3, freshly isolated human monocytes were exposed to various virus doses (0.1-10 MOI) in the presence or absence of macrophage-activating lipopolysaccharide (LPS). CVB3 infection alone induced an activation of monocytes as evidenced by enhanced adherence, release of cytokines and secretion of prostaglandin E2 (PGE2). Simultaneous addition of LPS almost entirely suppressed LPS-specific production of tumour necrosis factor alpha (TNF alpha) and PGE2, partially inhibited release of interleukin 1 beta (IL 1 beta) and did not affect interleukin 6 (IL6) synthesis of CVB3-infected monocytes. These data show that CVB3 activates monocytes to cytokine production but renders them unreactive to further activating stimuli. Further studies should determine the extent to which continuous cytokine release from persistently CVB3-infected monocytes, and their apparent unresponsiveness to other stimuli, contribute to chronic myocarditis.
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PMID:Lipopolysaccharide suppresses cytokine release from coxsackie virus-infected human monocytes. 131 6

Infections by Trypanosoma lewisi are characterized by hyporesponsiveness of the immune system during the early phase of parasitaemia. Blastogenic response of normal rat spleen cells to amphiphilic and hydrophilic components of Triton X-114 solubilized epimastigote forms of T. lewisi which characterizes the early phase of infection showed that suppression of responses to mitogens Concanavalin A (Con-A) and lipopolysaccharide (LPS) occurred exclusively with the amphiphilic fraction that consists of integral surface membrane constituents. The Con-A-induced suppression by the amphiphilic constituents was ablated by addition of exogenous IL-2 or by the removal of the adherent cell population in the cultures. This suggests that the integral surface membrane components play an important regulatory role in infections with Trypanosoma lewisi, through complex mechanisms that probably involve the B cells and suppressor macrophages; the suppressor macrophages probably produce a suppressor factor that inhibits the proliferation of T helper cells and subsequently the production of interleukin-2.
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PMID:Cellular responses to phase fractions of Trypanosoma lewisi. 155 27

Observations were made on the differences in cell-mediated immune responses in the mice infected with strongly pathogenic Naegleria fowleri ITMAP 359, weakly pathogenic Naegleria jadini 0400, or non-pathogenic Naegleria gruberi EGB, respectively. Variations in cell-mediated responses and changes in antibody titers according to the duration after infection were noted. Infections were done by dropping 5 microliters saline suspension containing 10 x 10(4) trophozoites cultured axenically in the CGVS medium into the right nasal cavity of ICR mice aging about 6-7 weeks, under the anesthesia by intraperitoneal injection of secobarbital. Following infection, delayed type hypersensitivity(DTH) responses in the footpad and blastogenic responses of the mouse spleen cells using [3H]-thymidine were observed on the day 1, 4, 7, 10 and 14 after infection. For the preparation of amoeba lysates, each of cultured trophozoites were homogenized with an ultrasonicator, and centrifugated at 20,000 g. The supernatants of amoeba lysates were used as the mitogen and antigen for ELISA. Concanavalin A(Con. A) and lipopolysaccharide(LPS) were also used as mitogens in the blastogenic response. 1. The mice infected with N. fowleri showed the mortality rate of 75.7%. The rate was 6.2% for the N. jadini infected group, while no dead mouse was observed for N. gruberi infections. 2. In regard to DTH responses in the N. fowleri infected mice, the level increased in comparison to the control group but declined after 7 days. An increase was also noted for the N. jadini group after 1 day, but gradual decreases were observed through the infection period. In addition, no difference was noted between the N. gruberi infected and control groups. 3. Concerning the blastogenic response of the splenocytes, it increased after 10 days in the experimental group of N. fowleri infection, but the differences were not statistically significant compared with control group. It was evident that N. jadini group was not different from control group either, while there was a tendency of decrease in N. gruberi infected group. In regard to the blastogenic response of the splenocytes by LPS, it was found that the N. fowleri, N. jadini and N. gruberi infected groups had no differences from the control group. 4. The serum antibody titer of N. fowleri and N. jadini infected mice increased from the day 7 and 14 after infection respectively, while the N. gruberi infected mice showed no increase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the cell-mediated immunity in experimental Naegleria spp. infections]. 248 28

Pseudomonas aeruginosa is a gram-negative pathogen, versatile and opportunistic in terms of its genetics, metabolic potential, and mechanisms of virulence. This versatility enables it to respond to variable and frequently adverse environmental conditions. Considered by many to be an aerobic organism, it is capable of growing anaerobically if certain substrates are available, for example, nitrates or arginine. Diversity of mechanisms of genetic exchange, including transformation, transduction, and conjugation, help P. aeruginosa adapt to changing conditions by acquiring new genetic information. Genetic manipulations have been exploited in recent years to study the basic biology of this bacterial species and the roles of its numerous virulence factors. Recently, transposon mutagenesis techniques and recombinant DNA methods (cloning) have been used to study some of the virulence factors of P. aeruginosa. The pathogenesis of P. aeruginosa infections is multifactorial, as manifested by the numerous toxins, or virulence factors, it produces and the variety of diseases it causes. P. aeruginosa is invasive and toxigenic. Infections appear to occur in stages: bacterial adherence, colonization, invasion and dissemination, and systemic or toxemic disease. Virulence factors can contribute to one or several stages of pathogenesis. Surface factors, including pili, lipopolysaccharide, and polysaccharide slime (alginate), probably contribute to the first two stages. Polysaccharide slime and lipopolysaccharide may also contribute to other processes later in the course of infection. Toxins, including exotoxin A and phospholipase C (hemolysin), and proteases of P. aeruginosa may contribute to tissue damage and dissemination. They may also aid in the procurement of nutrients required by the bacteria in the early stages of infection. The significance of the different virulence factors probably depends on the infection. Alginate production and phospholipase C are likely to have special significance in respiratory infections, particularly in cystic fibrosis.
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PMID:Pseudomonas aeruginosa: biology, mechanisms of virulence, epidemiology. 300 72

Infections with the intestinal flagellates Giardia muris and Spironucleus muris are accompanied by a depression in the ability of mice to mount an immune response to a thymus-dependent antigen (sheep red blood cells) but not to a thymus-independent antigen (TNP-lipopolysaccharide). The number of splenic IgM plaque-forming cells and haemagglutination titres, of both IgM and IgG, to sheep red blood cells decreased between days 10 and 21, which correlated with the time of maximal trophozoite levels in the small intestine. The number of background IgM plaque-forming cells to sheep red blood cells or DNP was not significantly different from controls in either infection. No evidence for systemic macrophage activation was associated with these infections. In fact, adherent peritoneal exudate cells (PEC) from infected mice were slightly less cytostatic against target tumour cells than adherent PEC from normal mice, at a time when the parasites were being eliminated from the small intestine.
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PMID:Immunodepression in Giardia muris and Spironucleus muris infections in mice. 636 68

An aroA mutant of gonococcal strain MS11 was constructed (JKD298) and compared with the wild-type (JKD288). The requirement of JKD298 for aromatic compounds, typical of an aroA mutant, was demonstrated using defined media. Other than the expected auxotrophy, no further differences could be demonstrated between the parent and the aroA mutant. SDS-PAGE analysis of protein and lipopolysaccharide (LPS) profiles showed no differences between the strains. Bactericidal assays using human and guinea-pig normal sera showed that both strains were serum sensitive and were similarly converted to serum resistance by in vitro sialylation using CMP-NANA. Infectivity experiments in guinea-pig subcutaneous chambers showed considerably reduced virulence of the aroA JKD298, which could only infect chambers at very high doses. Established infections by either strain elicited a strong PMN response in which similar proportions of each strain were seen intracellularly. Infections by JKD298 provoked a strong antibody response as detected by ELISA using whole sonicated gonococci. This is the first demonstration of attenuation of Neisseria gonorrhoeae by introduction of a defined mutation in a metabolic gene.
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PMID:Neisseria gonorrhoeae strain MS11 harbouring a mutation in gene aroA is attenuated and immunogenic. 841 27

Infections in cystic fibrosis (CF) due to Burkholderia cepacia are challenging due to their resistance to antibiotics. We explored a new strategy for increasing the permeability of B. cepacia using cationic agents, including amino compounds, to reduce the MICs of standard antibiotics. Twenty-eight B. cepacia isolates from four CF centres in North America and four non-CF B. cepacia were examined by standard microtitre broth dilution methods for susceptibility to a variety of antibiotics in the presence of non-inhibitory concentrations of diaminoacetone (DAA), methylglyoxal bis-guanylhydrazone (MGBH), chlorpromazine (CPZ) and prochlorperazine (PCPZ). The proportion of isolates with greater than four-fold reductions in MIC in the presence of 0.3 mM CPZ or 0.4 mM PCPZ were 90% and 94% for gentamicin, 80% and 83% for tobramycin, 45% and 17% for ceftazidime, and 35% and 17% for amifloxacin. CPZ showed the same degree of reduction in the MIC of azithromycin in 79% strains (MIC50 reduced to 16 from > or = 256 mg/L). Non-CF B. cepacia showed a greater than four-fold reduction in MIC with CPZ for gentamicin, tobramycin and azithromycin and two-fold reduction for ceftazidime. Little or no reduction in MIC was seen with DAA or MGBH for any antibiotic. Addition of magnesium ions to the medium competitively inhibited any MIC reduction effect seen with the cationic agents. CPZ and PCPZ appeared to enhance the permeability of B. cepacia to antibiotics based upon ionic charge characteristics of the antibiotic. No significant differences were seen in outer membrane protein and lipopolysaccharide profiles between the culture treated with CPZ and the respective control culture of strain B. cepacia ATCC 13945. The fluorescent probe 1N-phenylnaphthylamine had no increased access across the outer membrane in the presence of CPZ for B. cepacia ATCC 13945. However, thin-section electron microscopy revealed separation between the outer membrane and the rest of the cytoplasm accompanied by a widening of the periplasmic space. These data provide a rationale for investigating amino compounds as potential permeability-increasing agents against B. cepacia.
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PMID:Enhancement of Burkholderia cepacia antimicrobial susceptibility by cationic compounds. 933 85

Infections are frequent complications in end-stage renal failure patients undergoing hemodialysis (HD), and peripheral blood monocytes are important cells in host defense against infections. The majority of circulating monocytes express high levels of lipopolysaccharide receptor antigen CD14 and are negative for the immunoglobulin Fcgamma receptor type III (CD16). We studied the occurrence of a minor subpopulation coexpressing low levels of CD14 together with CD16 in HD patients. In healthy controls CD14+ CD16+ monocytes account for 8% +/- 4% of CD14+ monocytes, with an absolute number of 29 +/- 14 cells/microl. In stable HD patients the CD14+ CD16+ subpopulation was significantly elevated (14% +/- 3%, or 66 +/- 28 cells/microl), while the number of CD14(++) monocytes (monocytes strongly positive for CD14) remained constant. In HD patients suffering from chronic infections a further rise in CD14+ CD16+ monocytes was observed (128 +/- 71 cells/microl; P < 0.01) such that this subpopulation constituted 24% of all blood monocytes. In contrast, numbers of CD14++ cells did not change compared to those for stable HD patients, indicating that the CD14+ CD16+ monocyte subpopulation was selectively expanded. During acute infections the CD14+ CD16+ cell subpopulation always expanded. A whole-blood assay revealed that CD14+ CD16+ monocytes exhibited a higher phagocytosis rate for Escherichia coli bacteria than CD14++ monocytes, underlining their role during host defense. In addition, CD14+ CD16+ monocytes expressed higher levels of major histocompatibility complex (MHC) class II antigens (HLA-DR, -DP, and -DQ) and equal amounts of MHC class I antigens (HLA-ABC). Thus, CD14+ CD16+ cells constitute a potent phagocytosing and antigen-presenting monocyte subpopulation, which is expanded during acute and chronic infections commonly observed in chronic HD patients.
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PMID:Expanded CD14+ CD16+ monocyte subpopulation in patients with acute and chronic infections undergoing hemodialysis. 959 48

Infections are associated with a specific behavioral pattern that includes hypomotility, hypophagia, increased sleep, decreased libido, and decreased exploration. This behavioral response is considered adaptive and important for the survival of the animal. A similar behavioral pattern was observed following treatment with endotoxin (lipopolysaccharide [LPS]) and cytokines, such as interleukin-1 (IL-1). Because the secretion of these cytokines is induced by LPS and infections, it is possible that they mediate the behavioral responses to infection. We have studied ingestive behavior and locomotor activity in mice following infection with influenza virus, or injection of LPS, IL-1, or IL-6. A lethal dose of influenza virus, LPS, IL-1a and IL-1b each decreased the intake of sweetened condensed milk and 24-hour food pellet intake and decreased locomotor activity. Mouse IL-6 was ineffective. A sublethal dose of influenza virus decreased food pellet intake and locomotor activity, but did not significantly alter milk intake. Indomethacin prevented the behavioral responses to IL-1, and attenuated those to LPS, but had only a very small effect on those to influenza virus. Similar results were obtained with the IL-1-receptor antagonist (IL-1ra); it completely prevented the responses to IL-1, attenuated those to LPS, but, even after chronic high dose administration, attenuated the effects of influenza virus infection only slightly. Our results suggest that while IL-1 may play an important role in the responses to infection, IL-6 does not. Moreover, IL-1 cannot be the only factor contributing to the altered behavior of LPS-injected or influenza virus-infected mice.
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PMID:The role of cytokines in infection-related behavior. 962 84

Pseudomonas aeruginosa causes a variety of diseases in humans including lung and ocular infections. Infections of the cornea are usually associated with wearing contact lenses and can result in loss of vision. This study aimed to determine the effect of carbon or nitrogen limitation on the adhesion to contact lenses of a strain of Ps. aeruginosa isolated from contact lens-related corneal inflammation. Cells were grown in a continuous culture apparatus in varying levels of glucose or ammonia to effect nutrient limitation. Adhesion to contact lenses was measured as total counts and viable counts. The cell surface hydrophobicity and charge were measured using adhesion to surface-modified Sepharose. Changes in lipopolysaccharide were determined using 1D SDS-PAGE and changes in cell-surface proteins were measured using 2D gel electrophoresis. The more the cultures were nitrogen limited, the greater the increase in adhesion to unworn hydrogel contact lenses 0.3 x 10(3) - 2.2 x 10(3) cells/mm2 on Etafilon A lenses. Cells that were carbon limited showed a greater increase in adhesion to contact lenses when the lenses had been coated in artificial tears. It appeared that lipopolysaccharide may have been involved in the constitutive adhesion to unworn lenses that occurred during C-limitation, whereas changes in the outer membrane proteins contributed to the increased adhesion under nitrogen limitation, or the change in adhesion that occurred to carbon-limited cells using contact lenses coated in artificial tears. Nine cell-surface proteins appeared during nitrogen limitation with kDa/pI of 75/4.8, 4.9, 5.0; 62/5.6; 89/6.5; 38/6.4; 28/1.5; 18/6.4; 12/4.5. Any or all of these may have been involved in the increased adhesion and further experiments are underway to examine this possibility.
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PMID:Effect of nutrient limitation on adhesion characteristics of Pseudomonas aeruginosa. 1038 43


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