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)

We examined the effect of lipopolysaccharide (LPS) on dextran bead-induced lung granulomas using LPS responder (C3H/HeN) and nonresponder (C3H/HeJ) mice. LPS augmented granuloma sizes, TNF-alpha and N-acetyl-beta-D-glucosaminidase levels of lung extracts in C3H/HeN, but not in C3H/HeJ mice. Granuloma macrophages of C3H/HeN mice produced higher levels of superoxide anion and TNF-alpha than those of C3H/HeJ mice. Taken together with our previous report that macrophages and macrophage-derived cytokines are essential for the development of lesions, the present results suggest that activation of macrophages plays an important role in the development and augmentation of pulmonary granulomas.
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PMID:Augmentation of pulmonary foreign body granulomatous inflammation in mice by lipopolysaccharide: involvement of macrophage activation and tumor necrosis factor-alpha. 131 16

Effective bone biomaterials provide structural support for bone regeneration and elicit minimal inflammatory or toxic effects in vivo. Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) is a bacterially derived biodegradable polymer that possesses suitable mechanical strength for use as a bone biomaterial and has a slow rate of degradation in biological environments. Our previous in vitro study showed that many PHBV preparations are contaminated with bacterial lipopolysaccharide, and we developed a purification procedure to substantially remove it. Here, we have evaluated the in vivo biocompatibility of PHBV purified by H(2)O(2) treatment and solvent extraction. We utilized a murine tibial defect model consisting of a hole drilled through the diameter of the tibial diaphysis into which nonporous cylindrical plugs of purified PHBV were implanted. The animals were sacrificed at 1 week and 4 weeks postsurgery, and tibiae were examined using histological staining. The PHBV implant induced a mild inflammatory response 1 week after injury, which persisted for 4 weeks. Granuloma type tissues formed only when the implant protruded into the overlaying tissue. Woven bone formation occurred adjacent to the implant, which gave rise to lamellar bone and stabilized the implant indicating that the PHBV did not affect this process. Our data validated the murine defect model and indicate that solid PHBV induces a mild tissue reaction with bone deposition adjacent to the implant with no fibrous tissue present at 4 weeks post surgery.
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PMID:Responses in vivo to purified poly(3-hydroxybutyrate-co-3-hydroxyvalerate) implanted in a murine tibial defect model. 1906 68

Although the etiology of sarcoidosis is unknown, genetic susceptibility has been demonstrated. Granuloma formation is a key feature in the pathophysiology of sarcoidosis and Crohn's Disease, raising the possibility that these diseases share common pathogenetic pathways. An association between sarcoidosis and the protein "CD14", a molecule that is part of the lipopolysaccharide (LPS) cell surface receptor complex, has been suggested. In the current study we evaluated the CD14 gene promoter 159 C-->T polymorphic site and soluble CD14 levels in a cohort of 74 sarcoidosis patients compared to 85 healthy controls. We further sought to identify correlations between clinical phenotype, specific genotypes and soluble CD14 levels. We found the TT genotype to be more prevalent in the sarcoidosis patient group than in controls (p=0.03). Serum levels of soluble CD14 were higher in the sarcoidosis patients (p=0.001). Within the patient cohort, CC homozygous patients presented at an older age with milder disease as assessed with the SAC score, longer time to diagnosis, and less impairment of pulmonary function tests. Our study suggests a role of CD14 in the pathogenesis of sarcoidosis, and a clinical phenotype-genotype association. Further mechanistic and epidemiologic studies are needed in order to establish the specific role of CD14 in the etiology, pathogenesis and clinical phenotype of sarcoidosis.
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PMID:Association between CD14 gene polymorphisms and disease phenotype in sarcoidosis. 2043 Jun 3