title: [Effects of interleukin-10 on expression of inflammatory mediators and anti-inflammatory mediators during acute lung injury in rats].
abstract: OBJECTIVE
  To investigate the effects of interleukin-10 (IL-10) on expression of inflammatory mediators and anti-inflammatory mediators during acute lung injury (ALI).
  
  
  METHODS
  Rat model of ALI was reproduced by intratracheal instillation of lipopolysaccharide (LPS) in a dose of 10 mg/kg. Fifty-four male SD rats were randomly divided into control group, LPS group and LPS+IL-10 group, with 18 rats in each group (6 rats at 2, 6 and 24 hours respectively). Arterial gas analysis, the total protein concentration in bronchoalveolar lavage fluid (BALF), the total cell counts and classification in BALF, the lung coefficient, lung pathology were examined. Reverse transcription-polymerase chain reaction (RT-PCR) method was used to determine the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-1ra mRNA in lung tissue.
  
  
  RESULTS
  (1)In LPS group the partial pressure of oxygen in artery (PaO(2)) was progressively decreased, while the lung coefficient, the total protein concentration, the total cell counts in BALF were greatly increased, and lung pathology showed severe polymorphonuclear leukocytes infiltration with bleeding and hyaline membranes formation. In LPS+IL-10 group the values of all above parameters were alleviated. (2)In LPS group TNF-alpha mRNA expression peaked at 2 hours, then decreased sharply; IL-1beta mRNA expression greatly increased at 2 hours, peaked at 6 hours, then decreased; IL-1ra mRNA expression increased and peaked at 6 hours, remaining higher than control group at 24 hours. IL-10 inhibited TNF-alpha mRNA and IL-1beta mRNA expression but showed no effect on IL-1ra mRNA expression.
  
  
  CONCLUSIONS
  (1)ALI is characterized by overwhelming expression of TNF-alpha mRNA, IL-1beta mRNA, while the expression of IL-1ra mRNA is much delayed than TNF-alpha mRNA and IL-1beta mRNA. It suggests that there is an imbalance between inflammatory/anti-inflammatory mediators in the early phase of ALI. (2)IL-10 can inhibit the expression of inflammatory mediators and has no effect on the expression of anti-inflammatory mediators, thus it contributes to the balance between them, ameliorating ALI in rats.
authors.affiliation: Department of Respiratory Medicine in South Building, General Hospital of PLA, Beijing 100853, China. lhxsls@sina.com
authors.forename: Hong-xia
authors.initials: HX
authors.lastname: Li
authors.forename: Jin-chuan
authors.initials: JC
authors.lastname: Zhang
authors.forename: Ya-li
authors.initials: YL
authors.lastname: Zhao
authors.forename: Hao-jie
authors.initials: HJ
authors.lastname: Hao
mesh_terms: D055371:Acute Lung Injury / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000378:metabolism*; D053590:Interleukin 1 Receptor Antagonist Protein / Q000378:metabolism; D016753:Interleukin-10 / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10