title: [Activation of innate and specific immune responses in hemolytic uremic syndrome (HUS)-patients].
abstract: The central role of the immune system is the preservation of the health against several pathogenic microbes and injury agents. However, on special conditions defensive mechanisms triggered towards the foreign agent can damage the host. Clinical and experimental evidence indicate that inflammatory reaction triggered by the main components of Shiga toxin (Stx)-producing Escherichia coil (STEC), participate in the evolution to the complete form of HUS. When children are diagnosed of HUS, they present evidence that have suffered a very strong and early inflammatory response. These features include: the presence of a marked neutrophilia, the polymorfonuclear leucocytes (PMN) are "deactivated or exhausted" and the monocytes are differentiated towards an inflammatory phenotype (CD14-reduced and CD16-enhanced membrane expression). In addition, HUS-patients show a marked reduction in the absolute and relative number of leucocytes carrying the receptor (CX3CR1) for the chemokine "Fractalkine" (FKN, CX3CL1), which are the classic monocytes and Natural Killer cells (NK). All these cells express a high cytotoxic potencial. The chemokine FKN is expressed in endothelial and epithelial renal cells, and is involved in the pathogenic mechanism of different nephropathies. Noteworthy, we found a significant correlation between the severity of the renal damage (as days of anuria) and the alterations described above. Finally, the protective role of specific immune response, mainly through the antibody production with Stx-neutralizing capacity, is discussed.
authors.affiliation: División Immunología, Instituto de Investigaciones Hematológicas (IIHEMA), Academia Nacional de Medicina, Ciudad de Buenos Aires. mspalermo@hematologia.anm.edu.ar
authors.forename: Marina S
authors.initials: MS
authors.lastname: Palermo
authors.forename: Gabriela C
authors.initials: GC
authors.lastname: Fernandez
authors.forename: Maria Victoria
authors.initials: MV
authors.lastname: Ramos
authors.forename: Leticia
authors.initials: L
authors.lastname: Bentancor
authors.forename: Romina
authors.initials: R
authors.lastname: Fernandez Brando
authors.forename: Graciela I
authors.initials: GI
authors.lastname: Dran
authors.forename: Martin A
authors.initials: MA
authors.lastname: Isturiz
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D054428:Chemokine CX3CL1 / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000276:immunology / Q000472:pathogenicity; D004927:Escherichia coli Infections / Q000276:immunology; D005346:Fibroblast Growth Factors / Q000276:immunology; D006463:Hemolytic-Uremic Syndrome / Q000276:immunology* / Q000628:therapy; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology; D051189:Murinae; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D006435:Renal Dialysis; D022621:Shiga Toxin / Q000037:antagonists & inhibitors / Q000276:immunology / Q000633:toxicity*
chemical_list: D015703:Antigens, CD; C515538:CX3CL1 protein, human; D054428:Chemokine CX3CL1; D016207:Cytokines; D005346:Fibroblast Growth Factors; D022621:Shiga Toxin