title: Alterations in Th17 and the Respective Cytokine Levels in Helicobacter pylori-Induced Stomach Diseases.
abstract: BACKGROUND
  Infections by Helicobacter can cause the stimulation of sophisticated immune response in mucosal immunity. Among the different lymphocytes, Th17 plays an important role in the defense against H. pylori and may cause gastritis and peptic ulcer due to the increased activation of Th17 and cytokine changes.
  
  
  OBJECTIVE
  To find a relationship between Th17 and IL-17A, IL-21, IL-22, IL-23, TGF-β in the patients with H. pylori infection having signs including gastritis and peptic ulcer.
  
  
  METHODS
  A total of 36 samples from the patients [24 Hp+ and 12 Hp- cases] with dyspepsia symptoms were collected. The percentage of Th17 was measured by flow cytometry. The levels of Th17-associated cytokines in the sera and supernatants of peripheral blood mononuclear cells (PBMCs) which were stimulated with the H. pylori antigen, phytohemagglutinin (PHA), or Dynabeads were measured by ELISA.
  
  
  RESULTS
  Patients were divided into two groups of having either H. pylori infected (peptic ulcer, gastritis (mild, moderate)) or being uninfected. The percentage of Th17 in the patients with peptic ulcer and gastritis was significantly higher than their uninfected counterparts (p ≤ .001). The serum levels of IL-17A, IL-23, and TGF-β in the peptic ulcer and gastritis groups were significantly higher compared with the corresponding levels in the uninfected population (p < .05). A significant association of TGF-β, IL-21, and Th17 was observed with low levels of IL-17A in the mild gastritis patients (p < .05). Significantly higher levels of IL-22, IL-17A, IL-23, and higher Th17 frequencies were detected in the moderate gastritis patients, as compared with the uninfected patients (p ≤ .001).
  
  
  CONCLUSIONS
  It can be concluded that among the cytokines associated with Th17, the two cytokines of IL-21 and TGF-β play a more critical role in peptic ulcer and gastritis in the individuals infected with H. pylori. Furthermore, inflammation varies depending on the type of the cytokine and its secreted level.
authors.affiliation: Prof. Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Seyedeh Azra
authors.initials: SA
authors.lastname: Shamsdin
authors.affiliation: Prof. Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Abdolvahab
authors.initials: A
authors.lastname: Alborzi
authors.affiliation: Prof. Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Manoochehr
authors.initials: M
authors.lastname: Rasouli
authors.affiliation: Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Mohamad Kazem
authors.initials: MK
authors.lastname: Hosseini
authors.affiliation: Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Kamran
authors.initials: K
authors.lastname: Bagheri Lankrani
authors.affiliation: Prof. Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
authors.forename: Mehdi
authors.initials: M
authors.lastname: Kalani
mesh_terms: D000328:Adult; D000368:Aged; D016207:Cytokines / Q000032:analysis*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000473:pathology*; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D018928:Immunity, Mucosal; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000473:pathology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines
keywords: Helicobacter pylori; IL-17A; IL-21; IL-22; IL-23; TGF-β; Th17