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IL-8 Receptors (il-8 + receptor)
Selected AbstractsPathogenesis of Helicobacter pylori InfectionHELICOBACTER, Issue 2004Paul Hofman ABSTRACT Research in the last year has provided new insights into the function of the the cag -associated type IV secretion system and the vacuolating toxin VacA. A quite new aspect was disclosed by the finding that Helicobacter pylori in Mongolian gerbils colonizes a very distinct topology in the gastric mucous layer, obviously providing optimal conditions for long-term survival. Further research activities focused on H. pylori ammonia and metal metabolism as well as on bacterial stress defence mechanisms. Differential expression of approximately 7% of the bacterial genome was found at low pH suggesting that H. pylori has evolved a multitude of acid-adaptive mechanisms. VacA was shown to interrupt phagosome maturation in macrophage cell lines as well as to modulate and interfere with T lymphocyte immunological functions. Gastric mucosa as well as the H. pylori -infected epithelial cell line AGS strongly express IL-8 receptor A and B, which might contribute to the augmentation of the inflammatory response. Accumulating evidence implicates genetic variation in the inflammatory response to H. pylori in the etiology of the increased risk of gastric cancer after H. pylori infection. The chronic imbalance between apoptosis and cell proliferation is the first step of gastric carcinogenesis. In this regard, it was demonstrated that coexpression of two H. pylori proteins, CagA and HspB, in AGS cells, caused an increase in E2F transcription factor, cyclin D3, and phosphorylated retinoblastoma protein. Taken together, we now have a better understanding of the role of different virulence factors of H. pylori. There is still a lot to be learned, but the promising discoveries summarized here, demonstrate that the investigation of the bacterial survival strategies will give novel insights into pathogenesis and disease development. [source] Expression of Interleukin-8 Receptor A Predicts Poor Outcome in Patients With Nasopharyngeal Carcinoma,THE LARYNGOSCOPE, Issue 1 2005Toshiyuki Horikawa MD Abstract Objectives/Hypothesis: The authors recently demonstrated that interleukin-8 (IL-8) is induced by Epstein-Barr virus encoding latent membrane protein 1 and that IL-8 is overexpressed in tumor cells and correlates significantly with angiogenesis in nasopharyngeal carcinoma. The present objective was to investigate the expressions and the roles of IL-8 receptors in nasopharyngeal carcinoma. Study Design: Retrospective patient file review and immunohistochemical study of tissues of patients with nasopharyngeal carcinoma. Methods: The authors examined the expressions of two high-affinity IL-8 receptors, IL-8 receptor A (IL8RA) and IL-8 receptor B (IL8RB), in 30 patients with nasopharyngeal carcinoma by immunohistochemical analysis. Results: As expected, both IL-8 receptors were expressed on microvessels in tumor nests and surrounding stroma. Interestingly, they were also abundantly expressed on tumor cells. The expressions of IL8RA and IL8RB had no associations with gender, metastasis, or clinical stage. However, the expression of IL8RA in tumors significantly correlated with a shorter overall survival rate (P = .0045). Although the estimated 5-year overall survival rate for IL8RA-negative patients was 68.2%, that in IL8RA-positive patients was only 33.3%. Conclusion: The study results suggest that the expression of IL8RA in tumor cells becomes an important indicator of poor prognosis in nasopharyngeal carcinoma. [source] Human Fallopian Tube Neutrophils , A Distinct Phenotype from Blood NeutrophilsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2006Jennifer M. Smith Problem, The role of neutrophils in the human Fallopian tube (FT) is unknown. In order to provide insights into their functions in the FT, we systematically compared neutrophils from normal FT and peripheral blood (PB). Method of study, Flow cytometric analysis of surface receptors, granule proteins, and intracellular cytokines expressed by neutrophils from enzymatically dispersed FT and PB was performed. Results, Fallopian tube neutrophils expressed significantly higher levels of CD64, human class II histocompatibility antigen DR (HLA-DR), , -interferon, and vascular endothelial growth factor than those from PB. Fewer FT neutrophils expressed IL-8 receptors compared to PB, while more expressed the receptor for the bacterial-derived chemoattractant formyl-Met-Leu-Phe (fMLP). The number of FT neutrophils containing the granule proteins matrix metalloproteinase-9, lactoferrin, and myeloperoxidase was decreased versus PB. Conclusion, Fallopian tube neutrophils exhibit a phenotype distinct from PB neutrophils, suggesting functional activation of innate immune defense in the female reproductive tract as well as a potential role in maintaining normal FT physiology. [source] Expression of Interleukin-8 Receptor A Predicts Poor Outcome in Patients With Nasopharyngeal Carcinoma,THE LARYNGOSCOPE, Issue 1 2005Toshiyuki Horikawa MD Abstract Objectives/Hypothesis: The authors recently demonstrated that interleukin-8 (IL-8) is induced by Epstein-Barr virus encoding latent membrane protein 1 and that IL-8 is overexpressed in tumor cells and correlates significantly with angiogenesis in nasopharyngeal carcinoma. The present objective was to investigate the expressions and the roles of IL-8 receptors in nasopharyngeal carcinoma. Study Design: Retrospective patient file review and immunohistochemical study of tissues of patients with nasopharyngeal carcinoma. Methods: The authors examined the expressions of two high-affinity IL-8 receptors, IL-8 receptor A (IL8RA) and IL-8 receptor B (IL8RB), in 30 patients with nasopharyngeal carcinoma by immunohistochemical analysis. Results: As expected, both IL-8 receptors were expressed on microvessels in tumor nests and surrounding stroma. Interestingly, they were also abundantly expressed on tumor cells. The expressions of IL8RA and IL8RB had no associations with gender, metastasis, or clinical stage. However, the expression of IL8RA in tumors significantly correlated with a shorter overall survival rate (P = .0045). Although the estimated 5-year overall survival rate for IL8RA-negative patients was 68.2%, that in IL8RA-positive patients was only 33.3%. Conclusion: The study results suggest that the expression of IL8RA in tumor cells becomes an important indicator of poor prognosis in nasopharyngeal carcinoma. [source] Down-regulation of CXCR1 and CXCR2 expression on human neutrophils upon activation of whole blood by S. aureus is mediated by TNF-,CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2001I. Tikhonov It was suggested that bacterial products can inhibit the expression of leucocyte chemokine receptors during sepsis and affect leucocyte functions in septic syndrome. Superantigens and toxins produced by Staphylococcus aureus are capable of activating leucocytes via binding to MHC-II antigens on monocytes and T-cell receptor molecules on T lymphocytes. It was recently shown that staphylococcal enterotoxins directly down-regulate the expression of CC chemokine receptors on monocytes through binding to MHC class II molecules. We studied the effects of killed S. aureus on the expression of interleukin-8 receptors, CXCR1 and CXCR2, on polymorphonuclear leucocytes (PMN), which are known to lack the expression of MHC-II antigens. It was shown that S. aureus down-regulated the cell-surface expression of CXCR1 and CXCR2 on PMN in the whole blood and total blood leucocyte fraction containing PMN and monocytes, but did not modulate IL-8 receptor expression in purified PMN suspension. Antibody to TNF-, abrogated down-regulation of IL-8 receptors induced by S. aureus. In contrast, LPS reduced CXCR1 and CXCR2 expression in purified PMN and whole blood in a TNF-,-independent manner. We further showed that TNF-,-induced decrease of CXCR1 and CXCR2 expression was associated with lower IL-8 binding and lower CXCR1 and CXCR2 mRNA levels, and was abrogated by protease inhibitors. We suggest that during septicemia, S. aureus may inhibit neutrophil responsiveness to IL-8 and other CXC chemokines via TNF-,- mediated down-regulation of CXCR1 and CXCR2. [source] |