TY - JOUR
T1 - Microscopic Colitis Evolved Into Inflammatory Bowel Diseases Is Characterized by Increased Th1/Tc1 Cells in Colonic Mucosal Lamina Propria
AU - Li, Ji
AU - Yan, Yuchu
AU - Meng, Ziran
AU - Liu, Shuhong
AU - Beck, Paul L
AU - Ghosh, Subrata
AU - Qian, Jiaming
AU - Gui, Xianyong
PY - 2017/6/9
Y1 - 2017/6/9
N2 - BACKGROUND: An association between microscopic colitis (MC), i.e., lymphocytic colitis (LC) and collagenous colitis (CC), and inflammatory bowel diseases (IBD) has been noticed. A subset of MC cases may evolve into IBD, and IBD in remission may present as MC in a histologic pattern. Moreover, MC and IBD may coexist in different regions of the bowel. A link between MC and IBD in their pathogenesis is, therefore, suggested. Abnormal mucosal immunity is likely the key.METHODS: We reviewed 2324 MC cases in Calgary over 14 years and identified 20 cases evolved into IBD (IBD transformers). 13 of them were further investigated for colonic mucosal lamina propria mononuclear cells (LPMNCs), as opposed to 22 cases whose MC resolved. On their index colonic biopsy immunohistochemistry was performed to detect major T cell subsets characterized by key cytokines and master transcription factors (IFNγ and T-bet for Th1/Tc1, GATA-3 for Th2/Tc2, IL-17 and RORc for Th17/Tc17, FoxP3 for Treg/Tcreg) as well as TNFα(+) cells (partly representing Th1). LPMNCs positive for each marker were counted (average number per high-power field).RESULTS: IBD transformers had increased IFNγ(+), T-bet(+), TNF-α(+), and GATA-3(+) LPMNCs compared to the MC-resolved cases. The LC-to-IBD subgroup had increased IFNγ(+) and GATA-3(+) cells compared to the LC-resolved subgroup. The CC-to-IBD subgroup had increased T-bet(+), TNF-α(+), and GATA-3(+) cells compared to the CC-resolved subgroup. Among MC-resolved patients, more TNF-α(+) and RORc(+) cells were seen in LC than in CC.CONCLUSION: Th1/Tc1- and TNFα-producing cells, and likely a subset of Th2/Tc2 cells as well, may be involved in the MC-to-IBD transformation.
AB - BACKGROUND: An association between microscopic colitis (MC), i.e., lymphocytic colitis (LC) and collagenous colitis (CC), and inflammatory bowel diseases (IBD) has been noticed. A subset of MC cases may evolve into IBD, and IBD in remission may present as MC in a histologic pattern. Moreover, MC and IBD may coexist in different regions of the bowel. A link between MC and IBD in their pathogenesis is, therefore, suggested. Abnormal mucosal immunity is likely the key.METHODS: We reviewed 2324 MC cases in Calgary over 14 years and identified 20 cases evolved into IBD (IBD transformers). 13 of them were further investigated for colonic mucosal lamina propria mononuclear cells (LPMNCs), as opposed to 22 cases whose MC resolved. On their index colonic biopsy immunohistochemistry was performed to detect major T cell subsets characterized by key cytokines and master transcription factors (IFNγ and T-bet for Th1/Tc1, GATA-3 for Th2/Tc2, IL-17 and RORc for Th17/Tc17, FoxP3 for Treg/Tcreg) as well as TNFα(+) cells (partly representing Th1). LPMNCs positive for each marker were counted (average number per high-power field).RESULTS: IBD transformers had increased IFNγ(+), T-bet(+), TNF-α(+), and GATA-3(+) LPMNCs compared to the MC-resolved cases. The LC-to-IBD subgroup had increased IFNγ(+) and GATA-3(+) cells compared to the LC-resolved subgroup. The CC-to-IBD subgroup had increased T-bet(+), TNF-α(+), and GATA-3(+) cells compared to the CC-resolved subgroup. Among MC-resolved patients, more TNF-α(+) and RORc(+) cells were seen in LC than in CC.CONCLUSION: Th1/Tc1- and TNFα-producing cells, and likely a subset of Th2/Tc2 cells as well, may be involved in the MC-to-IBD transformation.
KW - Journal Article
KW - microscopic colitis
KW - lymphocytic colitis
KW - collagenous colitis
KW - inflammatory bowel disease
KW - lamina propria mononuclear cells
KW - T lymphocytes
KW - mucosal immunity
U2 - 10.1007/s10620-017-4636-5
DO - 10.1007/s10620-017-4636-5
M3 - Article
C2 - 28597107
SN - 0163-2116
JO - Digestive Diseases and Sciences
JF - Digestive Diseases and Sciences
ER -