Premium
Intestine mucosal IL‐22 is reduced following oral probiotic administration: implications on epithelial barrier repair
Author(s) -
Rigby Rachael Jane,
Thagia Imtiyaz,
Pattisson Charlotte,
Ng Siew,
Kamm Michael,
Knight Stella C
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.944.2
Subject(s) - probiotic , in vitro , interleukin , intestinal mucosa , stimulation , ulcerative colitis , cytokine , medicine , biology , immunology , gastroenterology , biochemistry , genetics , disease , bacteria
Interleukin‐22 (IL‐22) is known to play a key regulatory role at mucosal surfaces including the gut. IL‐22 receptor is predominantly expressed on intestinal epithelial cells (IEC) and evidence suggests that IL‐22 can promote intestinal inflammation and mucosal healing. This study demonstrates a role of probiotics in reducing mucosal IL‐22 and investigates the functional role of IL‐22 on IEC in vitro . Rectal biopsies were obtained from active ulcerative colitis patients immediately prior to probiotic (VSL#3) oral administration and approx. 2 months post‐exposure. Biopsies were cultured in complete medium overnight, supernatant collected and spontaneous IL‐22 secretion measured using ELISA. Effects of varying IL‐22 concentration (100ngml −1 –1ngml −1 ) were tested in vitro using both cancer (SW480) and non‐transformed IEC lines. Stimulation was carried out for 48h (proliferation) or 2h (mRNA). A significant reduction in IL‐22 secreted from mucosal biopsies was detected following probiotic treatment (n=9; p<0.03). In our system, addition of IL‐22 to in vitro IEC cultures did not significantly change proliferation rates (n=12, per concentration). IL‐22 induced moderate increases in SOCS3 and TNFα mRNA at the 50ng and 10ng/ml doses. The long‐term effects of IL‐22 on IEC and the predominant source of IL‐22 in the intestinal mucosa will now be investigated.