Changes of cytokine levels in a mouse model of post-infectious irritable bowel syndrome

Abstract

BackgroundIrritable 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.MethodsC57BL/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.ResultsLevels 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.ConclusionsThe 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.

Peroxiredoxin 1 as an inflammatory marker in diarrhea‐predominant and postinfectious irritable bowel syndrome

“…17,[32][33][34] Continuous inflammatory responses in intestinal tissues are considered as the prominent pathological features of IBS, especially IBS-D and PI-IBS. 16,33,[35][36][37] PRDX1 is associated with some tumors [21][22][23]38 and especially associated with colorectal cancer caused by chronic inflammation. 39,40 However, few studies have examined the relationship between PRDX1 and intestinal inflammation.…”

“…35 Arjuna P provided evidence for subclinical intestinal mucosal inflammation in patients with IBS-D in a tropical setting. 35 Arjuna P provided evidence for subclinical intestinal mucosal inflammation in patients with IBS-D in a tropical setting.…”

“…In all IBS patients, the serum PRDX1 (r = .335, P < .001) and TNF-α 16,33,[35][36][37] PRDX1 is associated with some tumors [21][22][23]38 and especially associated with colorectal cancer caused by chronic inflammation. 39,40 However, few studies have examined the relationship between PRDX1 and intestinal inflammation.…”

Corticotropin‐releasing factor induces inflammatory cytokines via the NLRP6‐inflammatory cytokine axis in a murine model of irritable bowel syndrome

“…After that, the mice were given either 400 μL sterile normal saline, or 400 μL C. butyricum containing 5 × 10 8 CFU/mL via oral gavage daily for 7 days. The mice were then scored for abdominal withdrawal reflex to determine visceral sensitivity using the colorectal distension assay by two blinded investigators for each pressure (20, 40, 60, and 80 mmHg) for five times . The mean score was calculated and recorded.…”

“…The mice were then scored for abdominal withdrawal reflex to determine visceral sensitivity using the colorectal distension assay by two blinded investigators for each pressure (20, 40, 60, and 80 mmHg) for five times. [15][16][17][18] The mean score was calculated and recorded.…”