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)

Interleukin-6 (IL-6) is a pleiotropic cytokine which produces uveitis if administered intraocularly. It has been demonstrated in the aqueous of patients with various uveitis entities. We have investigated the ability of human retinal pigment epithelium (RPE) to produce IL-6 in vitro, both unstimulated, and in the presence of interleukin-1 (IL-1), tumor necrosis factor alpha (TNF), interferon (IFN) gamma, and lipopolysaccharide (LPS). Five human RPE cell lines were cultured over a 6-day period, both unstimulated and in the presence of these cyokines. IL-6 in the supernatants was measured using an ELISA assay. Unstimulated RPE produced small amounts of IL-6. IL-1 at 100 or 10 U/ml markedly upregulated IL-6 production, and TNF at 1000, 100 or 10 U/ml did so to a lesser extent. Neither IFN gamma or LPS alone increased IL-6 expression, but together gave significant upregulation. Thus human RPE can produce IL-6 and may be the source of this cytokine in ocular inflammatory states.
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PMID:Production of interleukin-6 by human retinal pigment epithelium in vitro and its regulation by other cytokines. 142 42

Using 31P-NMR spectroscopy, the authors observed dynamic changes in the organophosphate metabolites in the lenses of two groups of Lewis rats affected by experimental uveitis induced by injecting Salmonella lipopolysaccharide (n = 20) or S-antigen (n = 25). A comparative study was done on the metabolic changes, the degree of inflammation, and histological changes in the rat lenses. Dynamic changes in the organophosphate profile in the lenses were measured by 31P-NMR spectroscopy. Only inorganic phosphate showed a significant increase (p less than 0.05) related to the increased inflammation in the endotoxin group, but the lenses showed no morphological change. Choline phosphate, adenosine triphosphate, and inorganic phosphate increased significantly (p less than 0.01) in the acute stage of inflammation, but a significant decrease (p less than 0.01) was evident from the peak of inflammation, following the histological destruction of the lenses. Our results indicated that in experimental uveitis dynamic changes in the organophosphate profile of the lenses were closely related to the protecting reaction against the stress caused by inflammation. Furthermore, we theorized that the generation of the secondary cataract was associated with the decreased metabolism of the phosphate compounds.
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PMID:[Dynamic changes in the organophosphate metabolites of the lenses affected by endotoxin and S-antigen induced uveitis]. 150 84

The potential role of interleukin-6 (IL-6) was studied as an inflammatory mediator of endotoxin (or lipopolysaccharide [LPS])-induced uveitis (EIU) in the rat. In young Lewis rats, levels of intraocular IL-6, but not serum IL-6, correlated with the severity of uveitis and with aqueous humor protein levels in response to foot pad injections of LPS (P less than 0.001). Adult Lewis rats did not develop uveitis and had no intraocular IL-6, although IL-6 was released systemically. Resistance to EIU and absence of IL-6 levels in the aqueous humor, despite the ability to release serum IL-6, also were observed in brown Norway rats, irrespective of age and weight. Intravitreal injection of as little as 1 ng of human recombinant IL-6 induced uveitis in young Lewis rats. In adult Lewis rats, and in young animals made tolerant to LPS, intravitreal IL-6 still caused substantial leakage of plasma proteins into the anterior chamber but no influx of inflammatory cells. As early as 2 hr after intravitreal injection of IL-6, immunohistochemical analysis showed invasion of the iris, corneal stroma, and anterior chamber by polymorphonuclear leukocytes (PMN) and expression of major histocompatibility complex (MHC) class II antigen in the retina by large cells that were macrophage-marker ED2 negative. This was followed by massive PMN infiltration of the retinal layers and vitreous. The MHC class II antigen expression of ciliary and iris epithelium occurred at a later stage (greater than 8 hr).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endotoxin-induced uveitis in the rat. The significance of intraocular interleukin-6. 154 81

The etiology and the physiopathology of acute anterior uveitis (AAU) is not well understood yet. However, two major predisposing factors have been identified: a bacterial infection especially with gram negative organisms (functioning as a trigger) and a genetic background, in particular the expression of HLA B-27 tissue antigen. We report the case of a young woman returning from travel to the Far East with her partner. Both presented simultaneously a gastrointestinal infection with fever and diarrhea. Despite extensive investigations, the infectious agent was never identified because of early empirical antibiotic therapy. A few days later, the patient developed AAU of a moderate grade in both eyes. HLA B-27 testing was positive for her, but not for her partner. Experimental research, based on a animal model such as endotoxin-induced uveitis (EIU), gives us some insight into the possible pathogenic mechanisms of AAU. Footpad injection of endotoxin (lipopolysaccharide component of the wall of gram negative), produce an acute anterior uveitis in rats. Extensive histologic analysis of other organs shows that the anterior segment of the eye is the only structure involved. Intensity of inflammation varies in different rat strains, stressing the importance of the genetic background. The similarity of the animal model to AAU will contribute to orient clinical research towards identifying more thoroughly the possible infectious agent at the origin of AAU and possibly to develop a prophylactic therapy.
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PMID:[Acute anterior uveitis: para-infectious hypothesis in predisposed individuals]. 161 44

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

The histological localization and biochemical properties of the autoantigens relevant to experimental autoimmune ophthalmitis and thyroiditis were studied using sera from mice hyperimmunized with the corresponding tissue extract of syngeneic mice and Klebsiella O3 lipopolysaccharide (KO3 LPS) as a potent adjuvant. Specific antigens were detected in the lens of the eyeball by immunofluorescence test with sera from mice in which ophthalmitis had been induced and the antigens were lenticular proteins with molecular weights (MW) of 15,000 (15K) to 25K, and 45K. The lenticular proteins with MW of 15K to 25K correspond to the subunits of crystalline. These findings clearly demonstrated that our experimental model for autoimmune ophthalmitis was classified as the lens-induced uveitis. The colloids of the thyroid follicles and the follicular cells were markedly stained by sera from mice in which thyroiditis had been induced. One of the autoantigens detected in the thyroid gland was biochemically consistent with a thyroglobulin subunit. It was also shown that these autoantigens detected in the present study were organ-specific but not species-specific. The nature of autoantigens in the eye and the thyroid gland is discussed.
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PMID:Characterization of autoantigens relevant to autoimmune ophthalmitis and thyroiditis in mice immunized with the syngeneic tissue extracts and Klebsiella O3 lipopolysaccharide. 350 32

Uveitis can be induced by systemic or intravitreal administration of endotoxin (lipopolysaccharide, LPS). In this study we correlated the expression of class II antigens (la in rat) of the Major Histocompatibility Complex (MHC), with this experimental model of uveitis. Ia antigen was detected by immunohistochemistry using the Avidin-Biotin-Peroxidase Complex (ABC) method and the monoclonal antibody OX6. Ia antigen was not expressed in normal eyes. However, Ia was expressed in the anterior uvea epithelial cells in all eyes with LPS induced uveitis. This study demonstrates that the ocular Ia expression is a localized process in the anterior uvea in response to systemic or intravitreal LPS. This response appears to be distinct from the action of LPS on macrophage Ia expression, where LPS has been shown to inhibit the induction of Ia antigen in macrophages by gamma interferon.
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PMID:Expression of class II antigen in endotoxin induced uveitis. 353 20

Uveitis could be a reaction to bacterial debris disseminated to the eye from extraocular sites of infection. In this study, we relate the composition of several bacterial components to their inflammatory properties in the eye. Groups of rabbits were injected intravitreously with peptidoglycan-polysaccharide (PG-PS) complexes isolated from group A streptococci, Escherichia coli lipopolysaccharide (LPS), or synthetic muramyl dipeptide (MDP). The lipid A region of LPS and the glycan backbone of PG are chemical analogues; MDP is the minimal biologically active subunit of PG. All of these molecules elicited uveitis as observed both clinically and histologically. The MDP elicited an acute inflammation characterized by a heterophil and monocyte infiltrate that subsided within 16 days. The PG-PS and LPS elicited chronic inflammation characterized by mononuclear and lymphocyte infiltration and severe necrosis of the retina.
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PMID:Experimental uveitis. Elicited by peptidoglycan-polysaccharide complexes, lipopolysaccharide, and muramyl dipeptide. 637 57

A single intraperitoneal dose of endotoxin (lipopolysaccharide or LPS) induces an acute inflammatory response in the uveal tract of rats. This inflammation is characterized by a breakdown of the blood/aqueous barrier within 3 hr after the LPS and the subsequent development of clinical disease and a cellular infiltrate. Early change in vascular permeability, clinical, and pathological changes were dose dependent with the two highest doses (100 micrograms or 500 micrograms) producing more severe pathology. Clinical and histopathologic abnormalities peaked at 24 hr and were resolving by 48 hr. Although clinical and histologic changes correlated well, the degree of breakdown of the blood/aqueous barrier at 3 hr failed to predict the extent of the cellular exudate measured by either clinical or histologic criteria. In addition, pharmacologic suppression of the early vascular permeability changes with indomethacin, cyproheptadine, or both agents failed to protect the animals consistently from subsequently developing significant clinical disease or cellular infiltrates on histopathology. LPS-induced uveitis in the rat provides a simple, reproducible model for ocular inflammation without requiring direct eye manipulation. The mediators responsible for the early vascular permeability in this model appear to be distinct from the mediators primarily responsible for the subsequent cellular exudate.
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PMID:Endotoxin-induced uveitis in the rat: observations on altered vascular permeability, clinical findings, and histology. 651

Monocytes and retinal pigment epithelial cells are intimately associated in membranes of eyes with proliferative vitreoretinopathy and in certain types of uveitis. The goal of this study was to determine whether monocytes modulate cytokine expression in retinal pigment epithelial cells, and if so, to identify the monocyte products responsible for this effect. Cultured human retinal pigment epithelial cells were exposed to varying concentrations of monocyte-conditioned medium from unstimulated human monocytes for 1-48 hr, or from monocytes prestimulated with lipopolysaccharide. mRNA expression of interleukin-1 beta, interleukin-6, interleukin-8, melanoma growth stimulating activity/gro alpha and gamma, macrophage colony stimulating factor, transforming growth factor-beta 2, basic fibroblast growth factor and activin beta A chain was determined by reverse transcription polymerase chain reaction. Protein secretion of selected cytokines, interleukin-1 beta, interleukin-6, interleukin-8, macrophage colony stimulating factor and transforming growth factor-beta 2 was measured in RPE-conditioned medium by ELISA. Retinal pigment epithelial cells constitutively expressed mRNA for interleukin-6, macrophage colony stimulating factor, transforming growth factor-beta 2, basic fibroblast growth factor and activin beta A chain. Interleukin-1 beta, melanoma growth stimulating activity/gro alpha and gamma and interleukin-8 were not expressed under basal conditions. Stimulated monocyte-conditioned medium markedly induced mRNA of all cytokines except basic fibroblast growth factor and transforming growth factor-beta 2 in a dose- and time-dependent manner. Unstimulated monocyte-conditioned medium was a less potent inducing agent, but still enhanced mRNA expression of interleukin-6, interleukin-8 and melanoma growth stimulating activity/gro alpha. Stimulated monocyte-conditioned medium also induced a time-dependent increase in interleukin-6, Interleukin-8, macrophage colony stimulation factor and transforming growth factor-beta 2, but not interleukin-1 beta protein secretion (p < 0.05 for all time points). Neutralizing antibodies to interleukin-1 beta, or tumour necrosis factor alpha, but not interleukin-1 alpha, significantly reduced cytokine mRNA expression induced by stimulated monocyte-conditioned medium. The combination of all three neutralizing antibodies almost entirely eliminated monocyte-induced mRNA expression and protein production of all cytokines studied. Activated monocytes secrete a heterogeneous mixture of products that together strongly induce expression of multiple cytokines in human retinal pigment epithelial cells. Most if not all of the inducing effect can be accounted for by interleukin-1 beta and tumour necrosis factor alpha. Because cytokines have been implicated in proliferative vitreoretinopathy and uveitis, monocyte-mediated cytokine expression by RPE cells may serve to initiate and perpetuate these diseases.
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PMID:Monocyte-induced cytokine expression in cultured human retinal pigment epithelial cells. 761 19


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