Endometriosis is charactertized by ectopic endometrial tissue associated with inflammation, fibrosis and pelvic pain. Endometrios often occurs together with or is mistaken for interstitial cystitis (IC), a sterile inflammatory condition of the urinary bladder. Both conditions are referred to as chronic pelvic pain syndrome (CPPS), with a combined estimated prevalence of about 1 per 1000 women in the USA. These conditions are often exacerbated by acute stress; yet, there has been little effort to investigate any common pathophysiological factors involved.
One reason for the apparent complexity is the expanding interactions between neuromodulators, immune molecules and hormones in these syndromes. We have shown that biopsies of affected endometriosis and IC sites are characterized by an increased number of activated mast cells in areas intensely stained postive for corticotropin releasing hormone (CRH). Moreover, mast cells secrete large amounts of CRH and also express CRH receptors (CRH-R), indicating autocrine effects. However, these processes have not been studied to date. We hypothesize that local CRH or Urocortin (Ucn) activate mast cells, which contribute to inflammation, sensory nerve sensitization and fibrosis. Our proposed studies will generate information that will help our understanding of the pathophysiology of endometriosis and its comorbidity with IC.
Researchers involved in this project:
Prof. Pio Conti, Professor of Immunology and General Pathology, University of Chieti, Italy.
Theoharis C. Theoharides, Professor of Pharmacology and Internal Medicine, Tufts University, School of Medicine, Boston, MA, USA.
One reason for the apparent complexity is the expanding interactions between neuromodulators, immune molecules and hormones in these syndromes. We have shown that biopsies of affected endometriosis and IC sites are characterized by an increased number of activated mast cells in areas intensely stained postive for corticotropin releasing hormone (CRH). Moreover, mast cells secrete large amounts of CRH and also express CRH receptors (CRH-R), indicating autocrine effects. However, these processes have not been studied to date. We hypothesize that local CRH or Urocortin (Ucn) activate mast cells, which contribute to inflammation, sensory nerve sensitization and fibrosis. Our proposed studies will generate information that will help our understanding of the pathophysiology of endometriosis and its comorbidity with IC.
Researchers involved in this project:
Prof. Pio Conti, Professor of Immunology and General Pathology, University of Chieti, Italy.
Theoharis C. Theoharides, Professor of Pharmacology and Internal Medicine, Tufts University, School of Medicine, Boston, MA, USA.