title: Spontaneous Recovery of Reflex Voiding Following Spinal Cord Injury Mediated by Anti-inflammatory and Neuroprotective Factors.
abstract: OBJECTIVE
  To investigate the time-dependent changes in expression of cytokines that characterizes the spontaneous recovery of reflex voiding after spinal cord injury (SCI). SCI is known to reorganize the neural circuitry of micturition reflex after injury.
  
  
  METHODS
  Under isoflurane anesthesia, spinal cord of 18 adult female Sprague-Dawley rats was completely transected at the Th9-10 level. Awake cystometry was performed at each time point on controls and 6 SCI animals, and bladder was then harvested for analysis of 29 proteins Millipore kit or enzyme-linked immunosorbent assay. Prophylactic dose of ampicillin 100 mg/kg was administered periodically to all SCI animals.
  
  
  RESULTS
  Spontaneous recovery of voiding after SCI at 12 weeks was evident from increased intercontractile interval and voiding efficiency during cystometry. Expression of proinflammatory interleukins ([IL] IL-1α and IL-1β, IL-2, IL-5, IL-6, IL-18, tumor necrosis factor alpha [TNF-α]) and CXC chemokines (CXCL1, CXCL2, CXCL10), CX3CL1, and CCL2 showed significant elevation at 4 and at 8 weeks with slight decrease at 12 weeks. In contrast, expression of anti-inflammatory IL-10 and neuroprotective factors, CXCL-5, and leptin, was elevated at 8 and at 12 weeks (P < .05). In contrast, expression of CCL3, CCL5, and growth factors (vascular endothelial growth factor, nerve growth factor, epidermal growth factor, granulocyte colony-stimulating factor, and granulocyte macrophage colony-stimulating factor) did not show any significant temporal change after SCI.
  
  
  CONCLUSIONS
  Spontaneous recovery of reflex voiding at 12 weeks was marked by increased endogenous expression of anti-inflammatory cytokine IL-10 and neuroprotective factors, CXCL-5, and leptin, which suggests that pharmacological suppression of inflammation, can hasten the emergence of reflex voiding after SCI.
authors.affiliation: Department of Urology, University of Pittsburgh, Pittsburgh, PA. Electronic address: prt18@pitt.edu.
authors.forename: Pradeep
authors.initials: P
authors.lastname: Tyagi
authors.affiliation: Department of Urology, University of Pittsburgh, Pittsburgh, PA.
authors.forename: Katsumi
authors.initials: K
authors.lastname: Kadekawa
authors.affiliation: Department of Urology, University of Pittsburgh, Pittsburgh, PA.
authors.forename: Mahendra
authors.initials: M
authors.lastname: Kashyap
authors.affiliation: Department of Urology, University of Pittsburgh, Pittsburgh, PA.
authors.forename: Subrata
authors.initials: S
authors.lastname: Pore
authors.affiliation: Department of Urology, University of Pittsburgh, Pittsburgh, PA.
authors.forename: Naoki
authors.initials: N
authors.lastname: Yoshimura
mesh_terms: D000818:Animals; D018925:Chemokines / Q000096:biosynthesis / Q000502:physiology; D005260:Female; D007378:Interleukins / Q000096:biosynthesis / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D012018:Reflex / Q000502:physiology*; D012075:Remission, Spontaneous; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D014554:Urination
chemical_list: D018925:Chemokines; D007378:Interleukins