World Journal of Gastroenterology · 2014 · 40 citations · 28 references
Life SciencesImmunologyMolecular BiologyGene ExpressionInflammationInnate ImmunityCytokine BiologyGastrointestinal InflammationInflammatory BiomarkersInflammatory Bowel DiseaseInflammatory SignalingToll-like ReceptorsClinical RemissionDifferential Transcript ExpressionMicrorna In InflammationToll-like Receptor SignalingToll-like Receptor Signaling CascadesToll-like Receptor Signaling PathwaysToll-like Receptor-mediated Innate Immune ResponseToll-like Receptors In Inflammation
AIM: To investigate Toll-like receptor (TLR) signaling regulators in microscopic and ulcerative colitis patients. METHODS: Total RNA and microRNA were isolated from fresh frozen colonic biopsies of non-inflamed controls and patients with active or in-remission collagenous colitis (CC), lymphocytic colitis (LC), or ulcerative colitis (UC). We compared expressions of interleukin-1 receptor-associated kinase (IRAK)-2, IRAK-M, interleukin (IL)-37, microRNA (miR)-146a, miR-155, and miR-21 using quantitative real time reverse transcription polymerase chain reaction. RESULTS: IRAK-M expression was increased in LC patients with active disease in histopathological remission (LC-HR; P = 0.02) and UC patients (P = 0.01), but no differences in IRAK-2 expression were detected compared to controls. miR-146a, -155 and -21 expressions were increased in LC-HR (P = 0.04, 0.07, and 0.004) and UC (P = 0.02, 0.04 and 0.03) patients. miR-146a and miR-21 expressions were significantly enhanced in UC patients compared to UC remission (UC-R; P = 0.01 and 0.04). Likewise, active CC patients showed significantly increased expression of miR-155 (P = 0.003) and miR-21 (P = 0.006). IL-37 expression was decreased in both CC (P = 0.03) and LC (P = 0.04) patients with a similar trend in UC patients but not statistically significant, whilst it was increased in UC-R patients compared to controls (P = 0.02) and active UC (P = 0.001). CONCLUSION: The identification of differentially expressed miRNAs, IL-37, and IRAK-M suggests different pathophysiologic mechanisms in various disease stages in LC, CC, and UC.
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Konstantin D. Taganov, Mark Boldin, Kuang‐Jung Chang et al. · Proceedings of the National Academy of Sciences · 2006 · 4.3K citations · Full text
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