title: rhPLD2 suppresses chronic inflammation reactions in a guinea pig asthma model.
abstract: BACKGROUND
  Asthma is a complex inflammatory disorder of the airways, and research on alternative therapeutic strategies has attracted attention. This study aimed at hypersusceptibility and toxicity of recombinant human phospholipase D2 (rhPLD2) in guinea pigs. We determined the behavioral responses in the model of immediate hypersensitivity animals and changes of eosinophil levels following use of the drugs. Special attention was given to the effects of rhPLD2 in vivo on the guinea pig with chronic persistent asthma and the mechanism involved.
  
  
  METHODS
  To investigate the effect of rhPLD2 on the expression of protein kinase C (PKC), and to examine the activity of signal transducer and activator of transcription 1 and 5a in the lung of the guinea pig with chronic asthma. Guinea pigs with chronic asthma were divided into five groups: a saline group, a dexamethasone 5.0 mg group, and rhPLD2 (1.5, 2, or 3 mg) groups. Non-sensitized animals were as normal control group. PKC expression was measured by immunohistochemistry, alterations of STAT1 and STAT5a were detected by TransAM transcription factor assay kits.
  
  
  RESULTS
  rhPLD2 (3.0 mg) decreased PKC expression to baseline and inhibited STAT1 activity compared with that of the saline group (p < 0.01).
  
  
  CONCLUSIONS
  The rhPLD2 may suppress the chronic inflammatory reaction through down-regulating PKC expression and STAT1/STAT5a activity in the lung. The rhPLD2 may be a suitable therapeutic target for asthma.
authors.affiliation: Immunology Dept. and Center of Neuroscience, Fujian Medical University, Fuzhou, Fujian 350004, China.
authors.forename: Li-Qiong
authors.initials: LQ
authors.lastname: Cai
authors.forename: Jie-ying
authors.initials: JY
authors.lastname: Zhang
authors.forename: Chuan-Xing
authors.initials: CX
authors.lastname: Yu
authors.forename: Ling
authors.initials: L
authors.lastname: Zhu
mesh_terms: D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000378:metabolism; D002908:Chronic Disease; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects; D004353:Drug Evaluation, Preclinical; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006168:Guinea Pigs; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D010739:Phospholipase D / Q000494:pharmacology*; D011493:Protein Kinase C / Q000096:biosynthesis; D011994:Recombinant Proteins / Q000494:pharmacology*; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050799:STAT5 Transcription Factor / Q000378:metabolism
chemical_list: D011994:Recombinant Proteins; D050794:STAT1 Transcription Factor; D050799:STAT5 Transcription Factor; D011493:Protein Kinase C; C105606:phospholipase D2; D010739:Phospholipase D