title: Changes of cytokine levels in a mouse model of post-infectious irritable bowel syndrome.
abstract: BACKGROUND
  Irritable bowel syndrome (IBS) is a highly prevalent functional gastrointestinal disorder. Post-infectious IBS (PI-IBS) is caused by an acute gastrointestinal infection preceding the onset of symptoms. However, the pathophysiology of PI-IBS is not clear, and the purpose of this study was to investigate the probable immune mechanisms of PI-IBS.
  
  
  METHODS
  C57BL/6 mice were randomly assigned to either an infection group or a control group. Mice in the infection group were infected with Trichinella spiralis to establish a model of PI-IBS (500 Trichinella), while control mice received only salt solution. Visceral sensitivity of colorectal distention in mice was evaluated by abdominal withdrawal reflex scores and intestinal inflammation was assessed using hematoxylin-eosin staining; at day 56 post-infection, the mRNA and protein levels of specific cytokines in the gut segments were detected using reverse-transcription polymerase chain reaction and enzyme-linked immunoabsorbent assay.
  
  
  RESULTS
  Levels of interferon γ and interleukin (IL)-17 in the PI-IBS group were significantly increased in the duodenum and ileum, and IL-10 was decreased in the jejunum, ileum, and colon compared with control mice. However, the expression level of IL-1β was not significantly different between the two groups.
  
  
  CONCLUSIONS
  The present study suggests that the local low-grade inflammation and immune activation that are an important component of the pathophysiology of PI-IBS are primarily induced and maintained by specific cytokines.
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 4000 l6, China. yblyl9527@126.com.
authors.forename: Bo
authors.initials: B
authors.lastname: Yang
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 4000 l6, China. chqxchzh@163.com.
authors.forename: Xuchun
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Department of Gastroenterology, Hainan Provincial People's Hospital, Haikou, 570311, China. yangbo7552@126.com.
authors.forename: Cheng
authors.initials: C
authors.lastname: Lan
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology; D043183:Irritable Bowel Syndrome / Q000276:immunology* / Q000378:metabolism / Q000469:parasitology; D051379:Mice; D008810:Mice, Inbred C57BL; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017160:Trichinella spiralis; D014235:Trichinellosis / Q000150:complications*
chemical_list: D015415:Biomarkers; D016207:Cytokines; C556062:IL10 protein, mouse; D020381:Interleukin-17; D053583:Interleukin-1beta; D016753:Interleukin-10; D007371:Interferon-gamma