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)

Acute anterior uveitis in man is related to Gram negative bacterial infection occurring at sites distant to the eye. This could involve intraocular localization of inflammatory bacterial cell wall constituents. Modulation of the blood-aqueous barrier in rabbit and rat, by muramyl dipeptide (the monomer of peptidoglycan) and lipopolysaccharide (and its monomer lipid A) was studied. The rabbit eye was found to be highly susceptible to MDP and LPS, although without cellular infiltration. In contrast the rat eye was demonstrated to be totally refractory to MDP. The response to LPS in the rat was modest, required high dosages and ocular changes were slow to occur, but cellular infiltration was readily apparent. Since MDP is found in Gram positive (as well as Gram negative) bacterial cell walls it is hypothesized that Gram positive bacteria might also play a role in causing uveitis in man.
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PMID:Modulation of the blood-aqueous barrier by gram positive and gram negative bacterial cell wall components in the rat and rabbit. 231 81

For further characterization of the mechanism involved in the anorexia during bacterial infection, we investigated whether muramyl dipeptide (MDP), the minimal immunologically active structure of gram-positive bacterial cell walls, affects rats' food intake in the same way as lipopolysaccharide (LPS) from E. coli. MDP (1.6 mg/kg body weight = b.wt.) injected intraperitoneally (IP) reduced food intake by decreasing meal frequency without affecting meal size. Indomethacin (2.5 mg/kg b.wt., IP) but not verapamil (5 mg/kg b.wt., IP) attenuated the hypophagic effect of MDP. In further experiments, MDP and LPS (100 micrograms/kg b.wt., IP) both inhibited gastric emptying and indomethacin failed to block this effect of LPS. Hepatic vagotomy did not attenuate the hypophagic effects of MDP or LPS. LPS reduced water intake only when food was available, but reduced food intake also during water deprivation. MDP did not affect water intake. MDP and LPS both had an aversive effect, but LiCl, which was also aversive, failed to reduce feeding under the conditions tested. This questions the role of a conditioned taste aversion in the hypophagia induced by MDP or LPS. The results suggest that a stimulation of eicosanoid synthesis contributes to MDP-induced hypophagia and may therefore also contribute to the anorexia during infection. In contrast, an inhibition of gastric emptying, an activation of hepatic satiety signals or a reduction of water intake, does not seem to be crucial for the hypophagic effects of MDP or LPS.
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PMID:Comparison of the effects of bacterial lipopolysaccharide and muramyl dipeptide on food intake. 238 34

Peripheral blood lymphocytes were incubated with glutaraldehyde-fixed Salmonella bacteria. This resulted in rapid activation of nonspecific cytotoxic potential of the lymphocytes. Both originally noncytotoxic, high-density Percoll-fractionated cells, and cytotoxic natural killer (NK) cell-enriched low-density cells were activated. The induction of originally noncytotoxic cells into activated killer (AK) cells was apparently independent of interferon (IFN), whereas the activation of the NK cell-enriched fractions also involved IFN production. Neither the AK nor NK activity were associated with significant bactericidal activity. The IFN-independent induction of AK activity was not dependent on the O-antigenic polysaccharide part of the lipopolysaccharide (LPS) on the bacterial cell surface, because both smooth (S) strains with differing O-antigenic structures (S-4,12 and S-6,7) and a rough (Re) strain without O-antigen were effective inducers. Isolated LPS, and especially alkali-hydrolyzed (O-deacylated, detoxified) LPS (ALPS) interfered with the induction of cytotoxicity. At concentrations of 10 to 30 micrograms/ml, ALPS totally inhibited the induction of AK activity without affecting the endogenous NK activity. Thus contact with bacteria can lead to the emergence of AK cells, and a bacterial product can effectively block this activation. These phenomena stress the complexity of interactions with host defenses that can take place during bacterial infection.
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PMID:Bacterial induction of human activated lymphocyte killing and its inhibition by lipopolysaccharide (LPS). 241 46

Nonlethal thermal injury in mice results in rapid death by immediate injection of 10(3) viable P. aeruginosa in the skin of the burn sites. Resistance to the lethal burn combined with P. aeruginosa infection developed 24 h after initial thermal injury and reached maximal effect 7 days later; it then continued for at least 21 days. The optimal survival was achieved when the first thermal injury was made for 7 seconds at 350 degrees C. Increased resistance, but for a short period could also be obtained by injection of lipopolysaccharide (LPS) 1-4 days prior to the burn-P. aeruginosa infection. However, when the LPS was injected immediately after the burn-infection, the lethal effect was increased. The induction of late protection after thermal injury and bacterial infection was demonstrated with P. aeruginosa organisms only. Under similar schedule of thermal injury resistance was not induced by infection with Semliki forest virus. On the contrary viral infection increased the susceptibility of burned mice to a fatal outcome. Immune or natural antibodies were not elevated in the sera of post burn mice. Furthermore, delayed type hypersensitivity response, as evaluated by a footpad weight assay was inhibited and this inhibition persisted at least for 7 days post burn. The thymus weight and its lymphoid cell content in thermally injured mice decreased significantly 7 days post burn, whereas the weight of the spleen increased and it contained fewer lymphocytes per gram tissue. We suggest that endotoxin entering the systemic circulation post-burn might be one of the factors contributing to the early sensitivity and the late protection against the fatal P. aeruginosa burn-infection.
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PMID:Thermal injury-induced non-specific resistance to fatal Pseudomonas aeruginosa burn-infection in mice. 255 18

Periodontal disease is thought to be initiated by a bacterial infection and subsequently developed by immunopathological mechanisms thorough host-parasite interactions. The macrophage and lymphocyte are the major functional cell types in the lesion of the disease and participate in tissue destruction and alteration of the periodontal connective tissue as well as in host defense mechanisms. However, the detailed implications of macrophages in development of the disease is still unclear. The aim of this study was to gain more understanding of the functional role of macrophages in periodontal disease. In this study, we examined the inducing effects of sonicated extracts from some gram-negative and gram-positive bacteria associated with the pathogenesis of periodontal disease, including Bacteroides gingivalis, Fusobacterium nucleatum, Haemophilus actinomycetemcomitans, and Actinomyces viscosus, on activation of macrophage functions and IL-1 production by the macrophages from the mouse peritoneum. At a dose as low as 1 microgram/ml (dry weight) sonicated extracts from B. gingivalis induced an increase in acid phosphatase activity and in glucose consumption of mouse peritoneal macrophages in vitro. A significant increase in the acid phosphatase and in glucose consumption was observed in the cultures at 24 h and 48 h, respectively, after the addition of the sonicate. Sonicated extracts from A. viscosus, a gram-positive bacterium, as well as B. gingivalis, F. nucleatum, and H. actinomycetemcomitans, gram-negative ones, were able to induce the increase in acid phosphatase activity and in glucose consumption of the macrophages. These periodontopathic bacteria were found to strongly induce IL-1 production by the macrophages as early as 24 h after addition of the sonicates. A significant increase in the IL-1 production was observed at a dose of 1 microgram/ml of the sonicates. The inducing ability was equivalent to 1 microgram/ml Escherichia coli lipopolysaccharide. The highest production of IL-1 was observed in the macrophages treated with H. actinomycetemcomitans among these sonicates. Sonicated extracts from both gram-negative and gram-positive bacteria were able to induce the IL-1 production by macrophages from C3H/HeJ mice, which are LPS low-responders. These results suggest that periodontopathic bacteria have potent ability to induce macrophage activation and IL-1 production and that the activated macrophages may play an important role in development of periodontal disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Inducing effect of periodontopathic bacteria on activation of macrophage functions and production of interleukin-1 by mouse peritoneal macrophages]. 260 96

Bovine uterine defense mechanisms during physiological and pathological conditions have been reviewed in this article. The initial uterine defense against bacterial infection is phagocytosis by uterine leucocytes (mainly neutrophils). The reported literature showed that very little work has been done on immunoglobulins and their role in the bovine uterine defense mechanisms; however, some investigators have found a positive correlation between gamma-globulin and the development of uterine infection after calving. Many explanations exist for the difference in susceptibility of the uterus to infection during the different phases of estrous cycle; however, most of the reports agreed that the uterine defense mechanism is inadequate during diestrus. The abnormal puerperium effects uterine defense mechanisms adversely and prolongs the time to complete uterine involution. Future treatment may utilise natural antimicrobial substances such as proteins or peptides derived from PMN, chemoattractant substances such as E. coli lipopolysaccharide or a bacteria-free filtrate of streptococci. Specific hyperimmunserum could also be used as opsonin for refractory cases of uterine bacterial infections.
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PMID:Bovine uterine defense mechanisms: a review. 269 49

The ability of primed human polymorphonuclear leukocytes (PMNLs) to respond metabolically to stimulation with formylmethionyl-leucyl-phenylalanine (FMLP) was investigated. Cells isolated from an aseptic inflammatory reaction and from patients with a severe bacterial infection as well as cells that had been treated with a bacterial lipopolysaccharide were investigated. When these cells were compared to peripheral blood cells isolated from healthy controls, they were found to be metabolically primed, i.e., the cells gave rise to an increased chemiluminescence response to subsequent stimulation with the peptide. It was also shown that proportionally more of the activity generated from the primed PMNL was of an intracellular origin compared with that obtained from nonprimed cells. The biological effects induced by radicals produced extracellularly and intracellularly are discussed.
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PMID:Relationship between intracellularly and extracellularly generated oxygen metabolites from primed polymorphonuclear leukocytes differs from that obtained from nonprimed cells. 275 87

Patients with systemic lupus erythematosus experience clinical exacerbation during superimposed bacterial infection. Previous studies in mice indicated that heightened immune phenomena during exposure to bacterial lipopolysaccharide (LPS) appear to be related, in part, to polyclonal B cell activation, to abnormal disposal of immune complexes (IC), and to increased localization of IC in tissues. To investigate whether such effects were reversible, we administered bacterial LPS to C57BL/6 mice for 5 weeks. Control mice received vehicle alone. We then discontinued LPS, and 6 weeks later LPS and control mice were challenged with a subsaturating dose of radiolabeled IC; the removal of IC from the circulation, their localization in the liver, spleen, and kidney were determined. In comparison to values in control mice, in mice previously exposed to LPS, serologic features of polyclonal B cell activation persisted; liver uptake of pathogenic IC (greater than Ag2Ab2) was normal, but removal of small size IC (less than or equal to Ag2Ab2) from the circulation was delayed; localization of IC in the kidneys was enhanced, and pathologic proteinuria developed. The effects of repeated exposure to bacterial LPS are partially reversible, but they last long after LPS is discontinued and may contribute to altered disposal of IC, enhanced organ localization of IC, and organ dysfunction.
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PMID:Defective disposal of immune complexes and polyclonal B cell activation persist long after exposure to bacterial lipopolysaccharide in mice. 281 Dec 99

Bacterial infection of the mouse urinary tract is followed by the recruitment of leukocytes to the mucosal surface. This study examined the bacterial components involved in the induction of this response. Escherichia coli of serotype O75:K5:H- expressing adhesins specific for the Gal alpha 1-4Gal beta- (Gal, galactose) and mannose-containing receptors were instilled into the urinary bladder of lipopolysaccharide responder (C3H/HcN) and lipopolysaccharide nonresponder (C3H/HeJ) mice. The inflammation was quantitated as the number of leukocytes excreted into the urine at various times after infection. The response was first shown to depend on the Lps genotype of the mouse. The leukocyte excretion that occurred within 24 h after infection of C3H/HeN mice was absent in C3H/HeJ mice. The components triggering the response were present on both live and Formalin-killed bacterial cells, and the response was mimicked by intravesical inoculation of isolated lipid A. Pretreatment of bacteria with soluble receptor oligosaccharides resulted in inhibition of attachment in vitro and of the inflammation in vivo. A direct synergy between adhesins specific for Gal alpha 1-4Gal beta receptors and lipid A was demonstrated. Mixtures of these components induced a leukocyte response higher than the sum of the responses to each component alone. These results suggest that the inflammation induced by gram-negative bacteria in the urinary tract can be triggered at the level of the epithelial cells by endotoxin presented by an attaching bacterial cell and that intact function at the Lps locus of the host is required for this to occur.
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PMID:Induction of inflammation by Escherichia coli on the mucosal level: requirement for adherence and endotoxin. 289 44

Serologic recognition of common lipopolysaccharide core antigens has been related to enhanced resistance to gram-negative bacterial disease in several species. Class-specific titers (IgG, IgM) were determined by direct ELISA, using intact Escherichia coli (J5) as a plate antigen. Serum samples were obtained from 224 neonatal swine between the ages of 36 and 60 hours. The mean (+/- SEM) log10 IgG titer against gram-negative core antigens was 1:1,713 +/- 0.4718 and the mean log10 IgM titer was 1:202 +/- 0.5644. The IgG titer was directly related with litter size, birth weight, and serum total IgG concentration; IgM titer was directly related with dam parity and serum total IgG concentration.
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PMID:Humoral recognition of lipopolysaccharide core antigens of gram-negative bacteria in neonatal swine. 291 17


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