Absence of formyl peptide receptor 1 causes endometriotic lesion regression in a mouse model of surgically-induced endometriosis
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Roberta Fusco1, Ramona D’amico1, Marika Cordaro1, Enrico Gugliandolo1, Rosalba Siracusa1, Alessio Filippo Peritore1, Rosalia Crupi1, Daniela Impellizzeri1, Salvatore Cuzzocrea1,2 and Rosanna Di Paola1
1Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
2Department of Pharmacological and Physiological Science, Saint Louis University, St. Louis, MO, USA
Salvatore Cuzzocrea, email: email@example.com
Rosanna Di Paola, email: firstname.lastname@example.org
Keywords: endometriosis; Fpr1; mouse; inflammasome; knockout
Received: May 24, 2018 Accepted: July 13, 2018 Published: July 31, 2018
Endometriosis is a female disease in which endometrial tissues grows outside the uterus. Patients showed alterations in endocrine and immune systems. Endometriotic lesions are characterized by deregulated interaction between immune cells and tissue cells. The formyl peptide receptor 1 (Fpr1) is expressed by both immune and stromal cells including epithelial cells. We investigated the development of the physiopathology of the surgically-induced endometriosis in Fpr1 KO mice compared to WT animals. Operated Fpr1 KO mice showed lower duration of uterine pain behaviors, lower size of developed cysts and reduced mast cell numbers. Immunohistochemical analyses indicated changes in NGF, VEGF and ICAM-1 expression associated with the pathology, which were reduced in absence of the Fpr1 gene. Molecular analyses indicated that in absence of Fpr1 there was reduced neutrophils accumulation and nitrosative stress formation, NF-κB translocation into the nucleus as well as NRLP3 inflammasome signalling. Fpr1 gene deletion caused reduction of resistance to the apoptosis, assessed by TUNEL assay. We underline the pathogenic role of Fpr1 in experimental endometriosis, which is the result of modulation of immune cell recruitment, suggesting it as a new target to control the pathologic features of endometriotic lesions.
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