ReviewThe role of cytokines and adhesion molecules in the development of inflammatory injury
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Supplementation with Astragalus polysaccharides alters Aeromonas-induced tissue-specific cellular immune response
2014, Microbial PathogenesisCitation Excerpt :These findings parallel those in other studies, e.g. those of [15,16,28–30]. The histopathological alterations in Aeromonas-infected group may also be due to the toxic effects of bacterial secretions, e.g. LPS, which cause a higher level of hepatic polymorphonuclear cell infiltration and ensuing necrosis [16,31] and, together with secondary organ damage as a result of the release of lytic enzymes and oxygen radicals [32]. Liver sections of the A. hydrophila group showed swelling of the hepatocytes, with the presence of vacuolated cytoplasm and a marked narrowing of the hepatic sinusoids.
In vivo and in vitro inhibitory effects of a traditional Chinese formulation on LPS-stimulated leukocyte-endothelial cell adhesion and VCAM-1 gene expression
2012, Journal of EthnopharmacologyCitation Excerpt :These endothelial cell-associated molecules facilitate the rolling, adhesion, and emigration of circulating leukocytes across the endothelial cell barrier to sites of inflammation by a multistep process. Endothelial activation, defined as up-regulation of cell adhesion molecules, constitutes a critical initial step in the recruitment of leukocytes to foci of inflammation (Hoover et al., 1978; Shanley et al., 1995; Parent and Eichacker, 1999). The expression of cell adhesion molecules (CAMs) is known to be stimulated by lipopolysaccharide (LPS), or proinflammatory cytokines such as tumor necrosis factor (TNF) and interleukin (IL)-1 (Aird, 2003).
Dietary flavonoid apigenin inhibits high glucose and tumor necrosis factor α-induced adhesion molecule expression in human endothelial cells
2010, Journal of Nutritional BiochemistryNF-κB and P38 MAPK Inhibition Improve Survival in Endotoxin Shock and in a Cecal Ligation and Puncture Model of Sepsis in Combination With Antibiotic Therapy
2009, Journal of Surgical ResearchCitation Excerpt :SN-50 also attenuates LPS induced IL-1 and TNF-α response in alveolar epithelial cells and can also attenuate inflammation in a carrageenin-induced rat hind paw model [19, 20]. The beneficial effects of NFκB inhibition in models of endotoxin shock have been clearly demonstrated, with survival rates varying depending on the specific inhibitor used [21, 22]. However the effects of NFκB inhibition in polymicrobial models of sepsis are variable and conflicting, with some studies showing benefit and others harm [23, 24].