title: Association of prostatic inflammation with down-regulation of macrophage inhibitory cytokine-1 gene in symptomatic benign prostatic hyperplasia.
abstract: OBJECTIVE
  Our previous DNA microarray analyses revealed that the macrophage inhibitory cytokine-1 (MIC-1) gene was significantly down-regulated in symptomatic benign prostatic hyperplasia (BPH) samples. We compared the histopathological features of inflammatory changes in prostate adenoma tissues from individuals with symptomatic and asymptomatic (histological only) BPH using MIC-1 mRNA levels.
  
  
  METHODS
  Prostate adenoma tissues were obtained from 25 patients who underwent transurethral prostatectomy to relieve lower urinary tract symptoms due to BPH and 6 patients with bladder cancer who underwent cystoprostatectomy due to bladder cancer. Inflammatory changes in the prostate were examined histopathologically and immunohistochemically, and classified according to the consensus classification system of the Chronic Prostatitis Collaborative Research Network and International Prostatitis Collaborative Network advocated in 2001 with some modification. MIC-1 mRNA was assessed quantitatively by real-time reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  MIC-1 gene down-regulation was observed in 16 of 25 symptomatic BPH samples (64.0%), whereas MIC-1 mRNA was high in 6 of 6 prostate adenoma samples from patients with bladder cancer (p = 0.0006). MIC-1 gene down-regulation correlated with the grade of glandular/ periglandular inflammatory changes with statistical significance (p = 0.0387). MIC-1 gene down-regulation was found in only 1 of 7 BPH samples with a glandular predominant pattern, whereas it was found in 15 of 24 BPH samples with a mixed type or stromal predominant pattern (p = 0.0373).
  
  
  CONCLUSIONS
  Gland destruction by inflammatory infiltrates, followed by replacement of the stromal component in symptomatic BPH may be induced by the down-regulation of the MIC-1 gene.
authors.affiliation: Department of Urology and Pathology, Faculty of Medicine, Kagawa University, Kita-gun, Kagawa, Japan.
authors.forename: Rikiya
authors.initials: R
authors.lastname: Taoka
authors.forename: Fumio
authors.initials: F
authors.lastname: Tsukuda
authors.forename: Masashi
authors.initials: M
authors.lastname: Ishikawa
authors.forename: Reiji
authors.initials: R
authors.lastname: Haba
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kakehi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016207:Cytokines / Q000235:genetics*; D015536:Down-Regulation; D055436:Growth Differentiation Factor 15; D006801:Humans; D008297:Male; D008875:Middle Aged; D011470:Prostatic Hyperplasia / Q000150:complications / Q000235:genetics* / Q000473:pathology; D011472:Prostatitis / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D016207:Cytokines; C526140:GDF15 protein, human; D055436:Growth Differentiation Factor 15; D012333:RNA, Messenger