Expressão da Anexina A1, seu receptor FPR2/Alx e Citocinas inflamatórias na endometriose peritoneal e no peritônio saudável

INTRODUCTION: Endometriosis is a disease characterized by the presence of \nextrauterine endometrial implants. Its etiopathogenesis isn’t fully understood, it’s \nbelieved that immunological and hormonal factors influence the peritoneal \nenvironment, preventing the elimination of refluxed endometrial cells during the \nmenstrual period. In addition, endometriosis has been reported as an inflammatory \nprocess and some studies have demonstrated the inflammatory resolutive mediators \ninvolvement in endometrial physiology and suggest that they may be involved in the \nendometriosis progression by anti-inflammatory and antiangeogenic action. \nOBJECTIVE: To characterize Annexin A1 (ANXA1), FPR2/ALX and cytokines \nexpression in peritoneal endometriosis and to clarify their role in its etiology. \nMETHODS: A laboratory analysis was performed human samples with forty women \nin reproductive age (22 patients with endometriosis and 18 control women) that had \nundergone laparoscopic surgery. Peritoneal biopsy e fluid aspirations from \nendometriosis and control samples were analyzed for the expression of ANXA1, \nFPR2/ALX and cytokines. ANXA1 and FPR2 / ALX levels were measured by \nWestern blotting and interleukin 1ß (IL-1ß), 4 (IL-4), 6 (IL-6) e 10 (IL-10) were \nquantified by enzyme-linked immunosorbent assay (ELISA). \nRESULTS: The present study identified the presence in human peritoneal tissue of \nANXA1 and FPR2 / ALX both in healthy condition and in women with peritoneal \nendometriosis, however, was lower in endometriosis samples than in control \nsamples. By quantifying the IL-6 and IL-1β cytokines in the peritoneal fluid by ELISA, \nthis study identified a higher IL-6 concentration in endometriosis group, but no \nsignificative difference in IL-1ß levels. In all samples, levels of IL-4 and IL-10 \ncytokines were below the detection level of the method used. \nCONCLUSION: These results indicate that the reduction of the inflammatory \nresolution mediators may be responsible for the inflammatory process perpetuation, \nmaintenance and worsening of endometriosis.