title: Intestinal Barrier Dysfunction: A Novel Therapeutic Target for Inflammatory Response in Acute Stanford Type A Aortic Dissection.
abstract: BACKGROUND
  Intestinal barrier dysfunction would lead to a rigorous inflammatory reaction due to the translocation of intestinal lumen-derived bacteria and endotoxins. The aim of the present study was to investigate whether intestinal barrier dysfunction occurs in patients with acute Stanford type A aortic dissection (ATAAD) and to determine its potential relationship with the plasma levels of several inflammatory biomarkers in the progression of ATAAD.
  
  
  METHODS
  Serum samples from a total of 46 patients with ATAAD and 36 healthy volunteers were prospectively collected and analyzed. The serum levels of diamine oxidase (DAO), lactate dehydrogenase (LDH), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and C-reactive protein (CRP) were measured using colorimetric assay, enzyme-linked immunosorbent assay, and immunoturbidimetric assay.
  
  
  RESULTS
  Serum levels of DAO, LDH, IL-6, TNF-α, and CRP in patients with ATAAD were significantly higher than those in healthy participants. A significantly positive correlation between DAO activity and IL-6 (r = .56, P < .001), TNF-α (r = .63, P < .001), and CRP (r = .53, P < .001) was observed. Moreover, the activity of DAO correlated negatively with the Pao 2/fraction of inspired oxygen (Fio 2) ratio (r = -.39, P = .007).
  
  
  CONCLUSIONS
  Intestinal barrier dysfunction, reflected by an increased level of serum DAO, may play an important role in the development of systemic inflammatory responses in patients with ATAAD. Therefore, strategies of preserving a normal intestinal barrier function may open new horizons in the treatment of inflammation-related adverse events in the setting of ATAAD.
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Jun
authors.initials: J
authors.lastname: Gu
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Hong
authors.initials: H
authors.lastname: Qian
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Yingkang
authors.initials: Y
authors.lastname: Shi
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Eryong
authors.initials: E
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Yingqiang
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Zhenghua
authors.initials: Z
authors.lastname: Xiao
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Zhi
authors.initials: Z
authors.lastname: Fang
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Minghua
authors.initials: M
authors.lastname: Zhong
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China.
authors.forename: Hongwei
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Cheng du, Sichuan, People's Republic of China mengwei11111@gmail.com.
authors.forename: Wei
authors.initials: W
authors.lastname: Meng
mesh_terms: D000328:Adult; D000368:Aged; D006631:Amine Oxidase (Copper-Containing) / Q000097:blood; D000784:Aortic Dissection / Q000097:blood* / Q000175:diagnosis / Q000276:immunology; D001014:Aortic Aneurysm / Q000097:blood* / Q000175:diagnosis / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008875:Middle Aged; D010539:Permeability; D011237:Predictive Value of Tests; D011446:Prospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000175:diagnosis / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D007770:L-Lactate Dehydrogenase; D006631:Amine Oxidase (Copper-Containing)
keywords: C-reactive protein; acute Stanford type A aortic dissection; diamine oxidase; inflammatory mediator; interleukin-6; intestinal barrier dysfunction; tumor necrosis factor α