Es. The value of host age, particularly in atherosclerosis, suggests that vascular wall aging is often a vital component of disease. Equally essential should be determinants imposed by the tissue environment, as all vasculitides and atherosclerosis share the stringency in tissue tropism, which means that they almost exclusively take place in an anatomically defined part of the vascular tree. Immune cell aging fundamentally 5-HT3 Receptor Antagonist list alterations the functionality of innate and adaptive immune cells. How the tissue aging procedure affects the propensity to attract and retain inflammatory cells within the vessel wall is unexplored. Exploiting the phagocytic ability of macrophages to load them with distinct cargo will offer new avenues for immunomodulatory therapy in restricted tissue web pages.Autoimmunity. Author manuscript; offered in PMC 2015 October 15.Shirai et al.PageAcknowledgmentsThis function was supported by the National Institutes of Health (R01 AR042547, RO1 HL117913, R01 AI044142, RO1 AI108906 and P01 HL058000 to CMW and R01 AI108891 and R01 AG045779 to JJG). Analysis studies informing this function received vital help from the Govenar Discovery Fund.Author Manuscript Author Manuscript Author Manuscript Author Manuscript
Clin Exp Immunol 2001; 123:421Polarized secretion of CXC chemokines by human intestinal epithelial cells in response to Bacteroides fragilis enterotoxin: NF-k B plays a major role inside the regulation of IL-8 expressionJ. M. KI M, Y. K . OH , Y . J. KI M H. B. OH Y. J . CH O Department of Microbiology Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Division of Microbiology, Pochon CHA University College of Medicine, Kyunggi-do, epartment of Science, Joongbu University, Choongnam and aboratory of Bacterial Toxins, Department of Microbiology, National Institute of Well being, Seoul, Korea (Accepted for publication two November 2000)SUMMARY Enterotoxigenic B. fragilis, which produces a ,20 kD heat-labile toxin (BFT), has been related with diarrhoeal diseases and mucosal inflammation. To determine if epithelial cells can contribute to BFTinduced inflammation, we assessed the expression of CXC chemokines by BFT-stimulated human intestinal epithelial cells. BFT stimulation improved expression in the neutrophil chemoattractant and activators ENA-78, GRO-a , and IL-8. Up-regulated chemokine mRNA expression was paralleled by elevated protein levels. Activation from the IL-8 and NF-k B transcriptional reporters was inhibited in cells cotransfected with all the Ik B kinase b and IkBa superrepressor plasmids. Whereas lactate dehydrogenase, which was utilised to monitor cell lysis, was released predominantly in the apical surface, CXC chemokines had been predominantly secreted in the basolateral surface of BFT-treated epithelial cells. The basolateral secretion of CXC chemokines from BFT-stimulated colon epithelial cells suggests that these chemokines can contribute for the inflammatory cell infiltrate inside the underlying intestinal mucosa. Keywords Bacteroides fragilis CXC chemokines epithelial cells NF-k BINTRODUCTION Enterotoxigenic Bacteroides fragilis (ETBF), which produces a ,20-kD heat-labile metalloprotease toxin (B. fragilis PLK3 MedChemExpress enterotoxin, or BFT), has been associated with noninvasive diarrhoeal disease in animals and young young children [1,2]. Also, B. fragilis isolated from the bloodstream as well as other extraintestinal websites (e.g. intra-abdominal abscesses) may well also produce BFT [3,4], but correlations of BFT with severity or.