title: Increased expression of interferon-inducible protein-10 during surgically induced peritoneal injury.
abstract: Interferon-inducible protein 10 (IP-10) is a key regulator of neutrophils, monocytes, and lymphocytes, cells infiltration whose secretory products play a key role in peritoneal wound healing. The objective of the present study was to determine whether IP-10 is expressed by parietal peritoneum and whether its temporal and spatial expression is altered following surgically induced peritoneal injury during healing. Peritoneal sidewall injuries were induced in mice (N = 60), and the severity of adhesions were graded at 12 hours and 1, 2, 4, and 7 days postsurgery. After collection of peritoneal washes, the injured peritoneum with associated adhesion and intact parietal peritoneum were collected to determine IP-10 mRNA and protein expression using quantitative reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry. Peritoneal injury resulted in adhesion formation with increased severity by day 7 postsurgery. The intact parietal peritoneum expressed IP-10 mRNA, whose level of expression significantly increased following peritoneal injury and reached a maximum at day 4 (p = 0.001), declining to the uninjured control levels by day 7 post-injury. The level of IP-10 in peritoneal washes also increased as a result of peritoneal injury. Immunohistochemically, IP-10 was localized to various inflammatory and immune cells, adhesion fibroblasts, and mesothelial cells, and its intensity increased during the course of wound healing. In conclusion, we showed that parietal peritoneum expresses IP-10 and peritoneal tissue injury results in an elevated level of its expression throughout the early phase of wound healing. The results suggest that IP-10 and its elevated expression may play a role in peritoneal cellular activities that influence the early phases of tissue repair and, possibly, the development of peritoneal adhesions.
authors.affiliation: Department of Obstetrics and Gynecology, Institute for Wound Research, University of Florida, Gainesville, Florida 32610, USA.
authors.forename: Megan
authors.initials: M
authors.lastname: Mrstik
authors.forename: Kristina
authors.initials: K
authors.lastname: Kotseos
authors.forename: Chunfeng
authors.initials: C
authors.lastname: Ma
authors.forename: Nasser
authors.initials: N
authors.lastname: Chegini
mesh_terms: D000818:Animals; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000096:biosynthesis*; D005260:Female; D051379:Mice; D010537:Peritoneum / Q000737:chemistry / Q000276:immunology* / Q000601:surgery*; D013514:Surgical Procedures, Operative / Q000009:adverse effects*; D000267:Tissue Adhesions / Q000276:immunology; D014945:Wound Healing / Q000276:immunology*
chemical_list: D054357:Chemokine CXCL10; D019743:Chemokines, CXC