scholarly journals P166 Decreased expression of elafin in peripheral blood and intestinal mucosa in inflammatory bowel disease

2017 ◽  
Vol 11 (suppl_1) ◽  
pp. S161-S161
Author(s):  
W. Zhang ◽  
G. Teng ◽  
H. Wang ◽  
Y. Tian ◽  
Y. Zheng
2018 ◽  
Vol 214 (8) ◽  
pp. 1095-1104 ◽  
Author(s):  
Xu-Feng Pei ◽  
Long-Lei Cao ◽  
Fang Huang ◽  
Xu Qiao ◽  
Jie Yu ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Luisa Guidi ◽  
Carla Felice ◽  
Annabella Procoli ◽  
Giuseppina Bonanno ◽  
Enrica Martinelli ◽  
...  

Treg modulation has been hypothesized as one of the mechanisms by which antitumor necrosis factorα(TNFα) agents exert their action in rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). However, data in IBD are still conflicting. We evaluated CD4+CD25+FOXP3+(Tregs) by flow cytometry in peripheral blood from 32 adult IBD patient before (T0) and after the induction of anti-TNFαtherapy (T1). Eight healthy controls (HCs) were included. We also evaluated the number of FOXP3+cells in the lamina propria (LP) in biopsies taken in a subset of patients and controls. Treg frequencies were significantly increased in peripheral blood from our patients after anti-TNFαtherapy compared to T0. T1 but not T0 levels were higher than HC. The increase was detectable only in clinical responders to the treatment. A negative correlation was found among delta Treg levels and the age of patients or disease duration and with the activity score of Crohn’s disease (CD). No significant differences were found in LP FOXP3+cells. Our data suggest the possibility that in IBD patients the treatment with anti-TNFαmay affect Treg percentages and that Treg modifications may correlate with clinical response, but differently in early versus late disease.


2020 ◽  
Vol 26 (11) ◽  
pp. 1658-1668 ◽  
Author(s):  
Daniele Corridoni ◽  
Thomas Chapman ◽  
Agne Antanaviciute ◽  
Jack Satsangi ◽  
Alison Simmons

Abstract The intestinal mucosa represents a unique environment where the coordinated function of diverse epithelial, mesenchymal, and immune cells maintains a physiologically balanced environment in the presence of gut microbiota. The intestinal mucosa plays a central role in the pathogenesis of inflammatory bowel disease (IBD), yet the molecular and cellular composition of this diverse environment is poorly understood. However, the recent advent of multimodal single-cell technologies, including single-cell RNA sequencing (scRNA-seq), now provides an opportunity to accurately map the tissue architecture, characterize rare cell types that were previously overlooked, and define function at a single-cell level. In this review, we summarize key advances in single-cell technology and provide an overview of important aspects of computational analysis. We describe emerging data in the field of IBD and discuss how the characterization of novel intestinal mucosa cell populations is reshaping our understanding of this complex disease. We conclude by considering the potential clinical applications, including the definition of novel drug targets and the opportunity for personalization of care in this exciting new era of precision medicine.


2019 ◽  
Vol 13 (7) ◽  
pp. 873-883 ◽  
Author(s):  
Elena Lo Presti ◽  
Roberto Di Mitri ◽  
Filippo Mocciaro ◽  
Anna Barbara Di Stefano ◽  
Nunzia Scibetta ◽  
...  

Abstract Background and Aims Inflammatory bowel disease [IBD] is a complex chronic inflammatory disease of the human gut with no clear aetiology. Traditionally, dysregulated adaptive immune responses play an important role even though accumulating evidence suggests a role also for innate immunity. Because of the well-known plasticity of γδ T cells, we investigated their percentage occurrence, phenotypic features and effector functions in the intestinal mucosa of early-onset and long-standing IBD patients, as compared to healthy subjects. Methods Fresh biopsies from 30 Crohn’s disease and ulcerative colitis patients were obtained and digested, and cells were analysed by flow cytometry. Results We found a reduced frequency of Vδ1 T cells in tissue from early and late IBD patients (2.24% and 1.95%, respectively, vs 5.44% in healthy tissue) but an increased frequency of Vδ2 T cells in the gut of late IBD patients (3.19% in late patients vs 1.5% in early patients and 1.65% in healthy tissue). The infiltrating Vδ2 T cells had predominant effector memory and terminally differentiated phenotypes and produced elevated levels of tumour necrosis factor-α [TNF-α] and interleukin-17 [IL-17]. The frequency of tissue Vδ2 T cells correlated with the extent of the inflammatory response and the severity of IBD. Conclusion Our study shows that tissue Vδ1 T cells are decreased in IBD patients while Vδ2 T cells are increased in the gut of IBD patients and contribute to TNF-α production. Moreover, we identify an as yet unappreciated role of Vδ2 T cells in IL-17 production in the gut of long-standing IBD patients, suggesting that they also participate in the chronic inflammatory process.


1998 ◽  
Vol 114 ◽  
pp. A1009
Author(s):  
G. Kim ◽  
T. Wu ◽  
W. Havran ◽  
R. Boismenu ◽  
M. Poleski

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