Es. The significance of host age, especially in atherosclerosis, suggests that vascular wall aging is really a essential component of illness. Equally critical has to be determinants imposed by the tissue environment, as all vasculitides and atherosclerosis share the stringency in tissue tropism, which means that they practically exclusively happen in an anatomically defined a part of the vascular tree. Immune cell aging fundamentally alterations the functionality of innate and adaptive immune cells. How the tissue aging method affects the propensity to attract and retain inflammatory cells in the vessel wall is unexplored. Exploiting the phagocytic potential of macrophages to load them with certain cargo will deliver new avenues for immunomodulatory therapy in restricted tissue sites.Autoimmunity. Author manuscript; obtainable in PMC 2015 October 15.Shirai et al.PageAcknowledgmentsThis work was supported by the National Institutes of Well being (R01 AR042547, RO1 HL117913, R01 AI044142, RO1 AI108906 and P01 HL058000 to CMW and R01 AI108891 and R01 AG045779 to JJG). Research studies informing this perform received vital assistance 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 PKCĪ¼ review fragilis enterotoxin: NF-k B plays a significant function in 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 Overall health, Seoul, Korea (Accepted for publication 2 November 2000)SUMMARY Enterotoxigenic B. fragilis, which produces a ,20 kD heat-labile toxin (BFT), has been related with diarrhoeal illnesses and mucosal inflammation. To identify if epithelial cells can contribute to BFTinduced inflammation, we assessed the expression of CXC chemokines by BFT-stimulated human intestinal epithelial cells. BFT stimulation increased expression from 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 together with the Ik B kinase b and IkBa superrepressor plasmids. Whereas lactate dehydrogenase, which was used to monitor cell lysis, was released predominantly in the apical surface, CXC chemokines have been predominantly secreted from the PAR2 supplier 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 to the inflammatory cell infiltrate inside the underlying intestinal mucosa. Keywords and phrases Bacteroides fragilis CXC chemokines epithelial cells NF-k BINTRODUCTION Enterotoxigenic Bacteroides fragilis (ETBF), which produces a ,20-kD heat-labile metalloprotease toxin (B. fragilis enterotoxin, or BFT), has been connected with noninvasive diarrhoeal illness in animals and young youngsters [1,2]. Also, B. fragilis isolated in the bloodstream as well as other extraintestinal internet sites (e.g. intra-abdominal abscesses) may also create BFT [3,4], but correlations of BFT with severity or.