title: [B7-H3 monoclonal antibody attenuates the inflammation and tissue injury in mice with cerulein-induced acute pancreatitis].
abstract: OBJECTIVE
  To explore the effect of B7-H3 monoclonal antibody (mAb) on cerulein-induced acute pancreatitis (AP).
  
  
  METHODS
  Mice were randomly divided into three groups: control group, AP group and B7-H3 mAb treatment group. AP was induced in mice by intraperitoneal injections of cerulein. B7-H3 mAb was administered to the mice by subcutaneous injection 1 hour before the injections of cerulein. The blood, pancreas and lung tissues of the mice were collected 6, 12 and 24 hours after cerulein induction. Expression of B7-H3 protein was detected in the pancreas tissues of the control and AP groups by Western blotting and immunohistochemistry. Serum activities of amylase and lipase were tested by VITROS 5600 Integrated System. The pancreas wet-dry mass ratio was used to value the edema of pancreas. Pathological changes of pancreas and lung tissues were evaluated by HE staining. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β were detected by ELISA in all groups.
  
  
  RESULTS
  The level of B7-H3 protein increased in the pancreas tissues of the AP group after successful induction of cerulein, and reached the peak at 12 hours. Serum activities of amylase and lipase in the AP group were significantly higher than those in the control group, while decreased obviously after the intervention of B7-H3 mAb. H&E staining showed that evident inflammation appeared in pancreas and lung tissues of the AP group, and the inflammation and wet-dry mass ratio were markedly reduced in the treatment group. The levels of proinflammatory factors TNF-α, IL-6 and IL-1β in the AP group showed a time-dependent increase, and peaked at 12 hours, while in the treatment group were relatively lower.
  
  
  CONCLUSIONS
  B7-H3 is over-expressed in cerulein-induced AP. Anti-B7-H3 mAb can attenuate the inflammation and alleviate the injury of pancreas and lung tissues.
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital, Soochow University, Suzhou 215006, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Zhuang
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital, Soochow University, Suzhou 215006, China. *Corresponding author, E-mail: xcf150709@163.com.
authors.forename: Chunfang
authors.initials: C
authors.lastname: Xu
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D060887:B7 Antigens / Q000037:antagonists & inhibitors* / Q000276:immunology / Q000378:metabolism; D015153:Blotting, Western; D002108:Ceruletide; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008049:Lipase / Q000097:blood; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000911:Antibodies, Monoclonal; D060887:B7 Antigens; C486038:Cd276 protein, mouse; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002108:Ceruletide; D008049:Lipase; D000681:Amylases