TY  - JOUR
AU  - Bao, H.-F.
AU  - She, C.-H.
AU  - Hou, C.-C.
AU  - Ji, D.-N.
AU  - Hu, D.
AU  - Zou, J.
AU  - Shen, Y.
AU  - Jian, L.-L.
AU  - Cai, J.-F.
AU  - Ye, J.-F.
AU  - Luo, D.
AU  - Ma, H.-F.
AU  - Guan, J.-L.
TI  - PLK1-activating IFI16–STING–TBK1 pathway induces apoptosis of intestinal epithelial cells in patients with intestinal Behçet's syndrome
JF  - FEBS JOURNAL
J2  - FEBS J
PY  - 2024
SN  - 1742-464X
DO  - 10.1111/febs.17147
UR  - https://m2.mtmt.hu/api/publication/34995700
ID  - 34995700
N1  - Export Date: 12 June 2024; CODEN: FJEOA
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Zhu, F.
AU  - Yang, T.
AU  - Ning, M.
AU  - Liu, Y.
AU  - Xia, W.
AU  - Fu, Y.
AU  - Wen, T.
AU  - Zheng, M.
AU  - Xia, R.
AU  - Qian, R.
AU  - Li, Y.
AU  - Sun, M.
AU  - Liu, J.
AU  - Tian, L.
AU  - Zhou, Q.
AU  - Yu, X.
AU  - Peng, C.
TI  - MiR-146a alleviates inflammatory bowel disease in mice through systematic regulation of multiple genetic networks
JF  - FRONTIERS IN IMMUNOLOGY
J2  - FRONT IMMUNOL
VL  - 15
PY  - 2024
SN  - 1664-3224
DO  - 10.3389/fimmu.2024.1366319
UR  - https://m2.mtmt.hu/api/publication/34995711
ID  - 34995711
N1  - Export Date: 12 June 2024
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Peng, Shuai
AU  - Shen, Lei
AU  - Yu, Xiaoyun
AU  - Wu, Jing
AU  - Zha, Lanlan
AU  - Xia, Yuan
AU  - Luo, Hesheng
TI  - miR-200a attenuated oxidative stress, inflammation, and apoptosis in dextran sulfate sodium-induced colitis through activation of Nrf2
JF  - FRONTIERS IN IMMUNOLOGY
J2  - FRONT IMMUNOL
VL  - 14
PY  - 2023
PG  - 14
SN  - 1664-3224
DO  - 10.3389/fimmu.2023.1196065
UR  - https://m2.mtmt.hu/api/publication/34367526
ID  - 34367526
N1  - Export Date: 28 November 2023
AB  - Introduction: Oxidative stress and inflammatory responses are critical factors in ulcerative colitis disease pathogenesis. Nuclear factor erythroid 2-related factor 2 (Nrf2) modulates oxidative stress and suppresses inflammatory responses, and the protective benefits of Nrf2 activation have been associated with the therapy of ulcerative colitis. MicroRNA-200a (miR-200a) could target Kelch-like ECH-associated protein 1 (Keap1) and activate the Nrf2-regulated antioxidant pathway. Nevertheless, whether miR-200a modulates the Keap1/Nrf2 pathway in dextran sulfate sodium (DSS)-induced colonic damage is unknown. Here, our research intends to examine the impact of miR-200a in the model of DSS-induced colitis.Methods: Prior to DSS intervention, we overexpressed miR-200a in mice for four weeks using an adeno-associated viral (AAV) vector to address this problem. ELISA detected the concentration of inflammation-related cytokines. The genes involved in inflammatory reactions and oxidative stress were identified using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot, and immunofluorescence. Moreover, we applied siRNAs to weakened Nrf2 expression to confirm the hypothesis that miR-200a provided protection via Nrf2.Results: The present study discovered miR-200a down-regulation, excessive inflammatory activation, enterocyte apoptosis, colonic dysfunction, and Keap1/Nrf2 antioxidant pathway inactivation in mouse colitis and NCM460 cells under DSS induction. However, our data demonstrated thatmiR-200a overexpression represses Keap1 and activates the Nrf2 antioxidant pathway, thereby alleviating these adverse alterations in animal and cellular models. Significantly, following Nrf2 deficiency, we failed to observe the protective benefits of miR-200a against colonic damage.Discussion: Taken together, through activating the Keap1/ Nrf2 signaling pathway, miR-200a protected against DSS-induced colonic damage. These studies offer an innovative therapeutic approach for ulcerative colitis.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Infantino, Claudia
AU  - Francavilla, Roberta
AU  - Vella, Adriana
AU  - Cenni, Sabrina
AU  - Principi, Nicola
AU  - Strisciuglio, Caterina
AU  - Esposito, Susanna
TI  - Role of Vitamin D in Celiac Disease and Inflammatory Bowel Diseases
JF  - NUTRIENTS
J2  - NUTRIENTS
VL  - 14
PY  - 2022
IS  - 23
PG  - 14
SN  - 2072-6643
DO  - 10.3390/nu14235154
UR  - https://m2.mtmt.hu/api/publication/33590034
ID  - 33590034
N1  - Export Date: 24 January 2023
AB  - Vitamin D (VD) is a pro-hormone that has long been known as a key regulator of calcium homeostasis and bone health in both children and adults. In recent years, studies have shown that VD may exert many extra-skeletal functions, mainly through a relevant modulation of the innate and adaptive immune system. This has suggested that VD could play a fundamental role in conditioning development, clinical course, and treatment of several autoimmune disorders, including celiac disease (CD) and inflammatory bowel diseases (IBDs). The main aim of this review is to evaluate the relationships between VD, CD, and IBDs. Literature analysis showed a potential impact of VD on CD and IBDs can be reasonably assumed based on the well-documented in vitro and in vivo VD activities on the gastrointestinal tract and the immune system. The evidence that VD can preserve intestinal mucosa from chemical and immunological damage and that VD modulation of the immune system functions can contrast the mechanisms that lead to the intestinal modifications characteristic of gastrointestinal autoimmune diseases has suggested that VD could play a role in controlling both the development and the course of CD and IBDs. Administration of VD in already diagnosed CD and IBD cases has not always significantly modified disease course. However, despite these relevant problems, most of the experts recommend monitoring of VD levels in patients with CD and IBDs and administration of supplements in patients with hypovitaminosis.
LA  - English
DB  - MTMT
ER  -