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      Could Streptococcal Erythrogenic Toxin B Induce Inflammation prior to the Development of Immune Complex Deposits in Poststreptococcal Glomerulonephritis?

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          Acute poststreptococcal glomerulonephritis (APSGN) is a consequence of the immune response to streptococcal antigens with further in situ antigen-antibody interaction and deposition of circulating immune complexes, resulting in the activation of complement and the inflammatory process. These events are related to a previous antibody response. However, early renal events, when circulating streptococcal antigens bind to the kidney during streptococcal infection, remain unknown. Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) are largely produced by nephritogenic streptococci and have high affinity for anionic glomerular structures. Renal deposition of ETB/ETBP makes conceivable a possible interaction between these streptococcal proteins with intrinsic glomerular cells or infiltrating leukocytes. Since ETB/ETBP are chemotactic for leukocytes and capable of inducing proliferation, cytokine and chemokine production, expression of adhesion molecules and apoptosis in renal cells and leukocytes, the early presence of these proteins could be a relevant event before and during antigen-antibody interaction takes place in renal tissues.

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          Most cited references 20

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          Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin.

          When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.
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            Regulation of transendothelial neutrophil migration by endogenous interleukin-8.

            Movement of neutrophils from the bloodstream to inflamed tissue depends on the activation of both the neutrophil and the endothelial cell. Endothelial cells lining the postcapillary venule respond to proinflammatory mediators by expressing adhesion molecules and synthesizing a variety of neutrophil-activating factors. Endothelial cell production of a 77-amino acid variant of interleukin-8 (IL-8) was found to be a requirement for the invasion of neutrophils through a vessel wall model. IL-8 secreted by cytokine- or lipopolysaccharide-stimulated endothelial cells induced the rapid shedding of neutrophil lectin adhesion molecule-1, the up-regulation of leukocyte beta 2 integrins, and the attachment and transmigration of the neutrophils. Thus, endogenous endothelial IL-8 regulates transvenular traffic during acute inflammatory responses.
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              Interleukin 6 is an autocrine growth factor for mesangial cells.

              Interleukin 6 (IL-6) induces the acute phase response, differentiation of B cells, proliferation of T cells, thymocytes, hematopoietic progenitors, hybridoma and plasmacytoma cells. Monocytes, T cells, fibroblasts, epithelial and endothelial cells secrete IL-6. Since IL-6 responsive cell-types may participate in the pathogenesis of glomerular inflammation, we studied the secretion of IL-6 by rat MCs, using the IL-6 dependent hybridoma cell line B9. The results of our studies indicate that MCs secrete IL-6 with a molecular weight of 17-42 kDa and isoelectric point of 4.0 to 5.3 MC-IL-6 activity could be blocked by a polyclonal antimurine-IL-6 antibody. MC express IL-6 mRNA as determined by Northern blot. Furthermore, our data demonstrate that IL-6 acts as an autocrine growth factor for MC. Incubation of subconfluent MC with recombinant IL-6 results in a dose-dependent increase of 3H-thymidine incorporation and number of MCs. Moreover, reverse phase HPLC fractions of MC-CM containing IL-6 activity increase 3H-thymidine incorporation by MC. In addition to its possible paracrine role in mediating the immune response in the glomerulus, MC-IL-6 may also be one of the autocrine signals leading to mesangial cell proliferation in vivo.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                January 2007
                30 November 2006
                : 105
                : 2
                : e41-e44
                aInstituto de Investigaciones Clinicas ‘Dr. Americo Negrette’, Facultad de Medicina, bInstituto de Investigaciones de la Facultad de Odontologia, Facultad de Odontologia, y cCatedra de Inmunologia, Bioanálisis, Universidad del Zulia, Maracaibo, Venezuela
                97602 Nephron Exp Nephrol 2007;105:e41–e44
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 1, References: 41, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/97602


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