title: Gelsolin is depleted in post-shock mesenteric lymph.
abstract: BACKGROUND
  Gelsolin is a plasma protein that functions to depolymerize actin filaments preventing capillary plug formation following tissue injury. It also functions to mediate the inflammatory response by binding proinflammatory lipids such as lysophosphatidic acid, sphingosine-1-phosphate and phosphoinositides. Clinically, reduced gelsolin concentrations have been associated with increased mortality in critically ill, trauma, and burn patients. We have previously shown that following hemorrhagic shock with splanchnic hypoperfusion, mesenteric lymph contains lipid components that cause neutrophil and EC activation and that protein concentrations are severely diluted due to resuscitation. We hypothesized that lipid binding proteins such as gelsolin may be depleted after trauma/hemorrhagic shock leading to increased lipid bioactivity.
  
  
  METHODS
  Shock was induced in SD rats by controlled hemorrhage and the mesenteric duct cannulated for lymph collection. Resuscitation was performed by infusing 2x SB volume in NS over 30 min, followed by 1/2 SB volume over 30 min, then 2x SB volume in NS over 60 min. Pre and post-shock lymph was loaded at equal protein concentrations on 2D-gels, followed by trypsin digestion and identification with mass spectrometry (MS-MS). Proteomics data were confirmed with Western blotting then quantitated by densitometry. Analysis of variance was used evaluate statistical data.
  
  
  RESULTS
  Gelsolin decreased in mesenteric lymph following hemorrhagic shock.
  
  
  CONCLUSIONS
  Gelsolin is found at high levels (comparable to plasma) in mesenteric lymph. Following hemorrhagic shock, gelsolin levels decrease significantly, possibly due to consumption by the actin scavenging system. The magnitude of this change in concentration could release lipid bioactivity and predispose the lung and other organs to capillary injury.
authors.affiliation: Department of Surgery, University of Colorado Health Science, Denver, Colorado 80204, USA.
authors.forename: Janeen R
authors.initials: JR
authors.lastname: Jordan
authors.forename: Ernest E
authors.initials: EE
authors.lastname: Moore
authors.forename: Sagar S
authors.initials: SS
authors.lastname: Damle
authors.forename: Phillip
authors.initials: P
authors.lastname: Eckels
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Johnson
authors.forename: Jonathan P
authors.initials: JP
authors.lastname: Roach
authors.forename: Jasmina S
authors.initials: JS
authors.lastname: Redzic
authors.forename: Kirk C
authors.initials: KC
authors.lastname: Hansen
authors.forename: Anirban
authors.initials: A
authors.lastname: Banerjee
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D003627:Data Interpretation, Statistical; D004195:Disease Models, Animal; D005440:Fluid Therapy; D018260:Gelsolin / Q000378:metabolism*; D008196:Lymph / Q000378:metabolism*; D008297:Male; D013058:Mass Spectrometry; D008643:Mesentery / Q000378:metabolism; D040901:Proteomics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000378:metabolism* / Q000628:therapy
chemical_list: D000199:Actins; D018260:Gelsolin