WCRB2014 POSTER PRESENTATIONS (1) (335 abstracts)
Fibrotic remodeling and duct obstruction are major patho-physiological mechanisms in bacterial epididymitis in mice
Vera Michel 1 , Sudhanshu Bhushan 1 , Ralf Middendorff 1 , Kate L Loveland 2 , David D de Kretser 2 , Mark P Hedger 2 & Andreas Meinhardt 1
1Justus Liebig University Giessen, Germany; 2Monash University, Clayton, Victoria, Australia
Introduction: Bacterial epididymitis is a common disorder in urological outpatient clinics and usually results from ascending infections originating in the urinary tract often involving uropathogenic E. coli (UPEC) as causative pathogen. In 40% of patients with acute epididymitis, impaired semen parameters persist even after antibiotic treatment. Members of the TGFβ cytokine superfamily, such as activin A, have recently been identified in the epididymis and are critical mediators of inflammation and fibrosis. Inhibition of activin action by follistatin has emerged as a potential therapy, because it modulates inflammation and fibrosis.
Materials and methods: Activin signaling molecules and fibrotic markers were investigated by immunohistochemistry and qRT-PCR in an acute epididymitis model by infecting mice with the uropathogenic isolate UPEC CFT073 for 3d and 7d.
Results and discussion: At 3d post-infection, epididymides showed a leukocytic infiltration and decreased sperm numbers in the lumen, but no or mild interstitial fibrosis. At 7d post-infection, ductal obstruction and massive fibrotic remodeling was visible especially in the cauda region. Concomitant elevation of epididymal smooth muscle actin (SMA) and collagen 1α mRNA expression accompanied the fibrosis. At 3d post-infection, a strong increase (>20-fold) in mRNA expression of inhibin subunit-α (Inha), activin receptor (ActvR)IIB and SMA were detected in the cauda, whilst no changes were observed in activin subunits (Inhba, Inhbb), ActvRI and follistatin. Of note, Inhba mRNA, SMA and collagen 1α were all increased considerably at 7d post-infection, raising the possibility of a causative link between the increase in activin and the fibrotic damage in acute epididymitis.
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ISSN 2052-1472 (online)
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