ABSTRACT
Background: Helicobacter pylori produces a gastric mucosal inflammation characterized by neutrophil infiltration, due to the liberation of interleukin-8. Aim: To measure interleukin-8 levels in gastric mucosa samples from cbildren colonized by H. pylori. Patients and methods: Thirty one children that required an upper gastrointestinal endoscopy for diagnostic purpose were studied. Antral biopsies were obtained for pathological study; H. pylori detection using CLO-test and interleukin-8 determination by ELISA. Results: Nine children were not infected by H. pylori. Of these, six had a pathologically normal gastric mucosa and three had a mild chronic gastritis. Twenty two children were infected by H. pylori and all had a chonic gastritis with activity signs in 13. Mucosal interleukin-8 was higher in infected than in non infected children (59.7 (range 6.1-379.7) and 15.8 (range 3.9-104.1) pg/mg respectively p=0.029). Colonized children with an active chronic gastritis had higher interleukin-8 levels than those with an active gastritis (84.4 (range 33-3-379.0) and 26.8 (range 6.1-372.6) pg/ml respectively p=0.04). Conclusions: Stomach colonization by H. pylori is associated with higher mucosal levels of interleukin-8. This phenomenon probably plays a role in the genesis and intensity of gastric mucosal inflammation in cbildren
Subject(s)
Humans , Male , Female , Child, Preschool , Adolescent , Interleukin-8/isolation & purification , Helicobacter pylori/pathogenicity , Gastric Mucosa/pathology , Biopsy , Enzyme-Linked Immunosorbent Assay , Helicobacter Infections/pathology , Gastritis/pathology , Endoscopy, Digestive System , Chronic DiseaseABSTRACT
La presencia de bacterias a nivel de la mucosa de las vías urinarias determina una respuesta inflamatoria. El factor responsable de la invasión de células inflamatorias es la IL6 (interleuquina 6) y los componentes bacterianos inductores son las adhesinas y el LPS de la membrana bacteriana. La actividad inflamatoria no es sólo responsable de los síntomas agudos sino de la eliminación bacteriana. En los estudios experimentales, los animales no reactivos al LPS fueron incapaces de eliminar las bacterias y en embarazadas se ha demostrado que una respuesta menor de IL6 puede relacionarse con la mayor incidencia de pielonefritis (1-4). La respuesta inflamatoria también ha sido relacionada con la producción de IL8 (interleuquina 8). Estudios en humanos han mostrado correlación entre concentración de IL8 urinaria y los recuentos leucocitarios (5).