title: Ulinastatin protects pulmonary tissues from lipopolysaccharide-induced injury as an immunomodulator.
abstract: BACKGROUND
  Organ protection is a routine therapy in patients with severe trauma, infection, and even multiple organ dysfunction syndrome. Appropriate inflammatory response benefits organ function with sepsis. Our aim was to verify the immunoregulatory effects of Ulinastatin (UTI) on lipopolysaccharide (LPS) administrated mice.
  
  
  METHODS
  C57BL/6J mice were subjected to an intraperitoneal injection of LPS and were randomly divided into a LPS control (L group) and an UTI-treated group (U group). Bone marrow-derived dendritic cells (DCs) were prepared from mouse femur bone marrow, and CD40, CD80, CD86, or MHC class II as DC markers were analyzed. The expression of spleen HLA-DR was detected by immunohistochemistry analysis. The alterations of Toll-like receptor 4-MyD88 signal pathway of DCs and pulmonary tissues were also determined. Selectins and adhesion molecules in lungs and serum were detected. The lung injury degree was represented as wet to dry ratios and alveolar thickness.
  
  
  RESULTS
  After LPS administration, the expression of bone marrow-derived DC marker was increased, showing a mature state, while the mature process could be stepped down by UTI. The spleen HLA-DR expression and the activation degree of Toll-like receptor 4-MyD88 signal pathway also demonstrated the immunoregulatory effects of UTI, which could effectively protect the pulmonary tissues from LPS-induced injury.
  
  
  CONCLUSIONS
  Our results demonstrated that UTI reduced LPS-induced pulmonary injury. The mechanism of its action might involve the immunoregulation and the mitigation of excessive inflammatory reaction.
authors: Emergency Department and Surgical Intensive Care Unit, Shanghai 10th People's Hospital, Tongji University School of Medicine, Shanghai, China.
authors: Chengjin
authors: C
authors: Gao
authors: Rongrong
authors: R
authors: Li
authors: Sheng
authors: S
authors: Wang
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000276:immunology / Q000517:prevention & control*; D000818:Animals; D015153:Blotting, Western; D003713:Dendritic Cells / Q000187:drug effects; D019040:E-Selectin / Q000378:metabolism; D005260:Female; D006023:Glycoproteins / Q000494:pharmacology*; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D019007:P-Selectin / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D019040:E-Selectin; D006023:Glycoproteins; D007166:Immunosuppressive Agents; D008070:Lipopolysaccharides; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D019007:P-Selectin; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D019010:Vascular Cell Adhesion Molecule-1; C028665:urinastatin