AI Article Synopsis

Article Abstract

Indoleamine 2,3-dioxygenase (IDO) catalyzes the first step in the degradation of tryptophan, an essential amino acid. During inflammation IDO can be induced in different cell types resulting in local tryptophan depletion. This inhibits T cell proliferation and may induce apoptosis. High expression of IDO was previously found in inflammatory bowel disease and is thought to represent a mechanism for downregulation of the local immune response. Our aim is to investigate the expression pattern of IDO in normal and inflamed murine and human intestinal mucosa. Immunohistochemical staining for IDO was performed on paraffin sections of colon of two mouse models for colitis and their controls and on paraffin sections of human ileum and colon in normal and two different inflammatory conditions, namely inflammatory bowel disease and diverticulitis. IDO immunohistochemistry showed similar results in murine and human tissue. In normal, as well as in inflamed mucosa, some mononuclear cells, fibroblasts and endothelial cells were positive for IDO. In inflamed mucosa a specific expression pattern of epithelial IDO was found where epithelial cells flanking ulcers or bordering crypt abscesses showed high IDO expression. Moreover, in human intestinal inflammation, IDO was expressed in ulcer associated cell lineage. Since bacterial invasion is more pronounced in erosions and in crypt abscesses and since IDO activity and the resulting local tryptophan depletion can cause growth arrest of several tryptophan-dependent microorganisms, IDO expression in the vicinity of interruptions of the epithelial barrier may point to a role for IDO as a local anti-infectious agent. Furthermore, expression of IDO at the margin of ulcerations and in the reparative ulcer-associated cell lineage suggests involvement of IDO in repair processes.

Download full-text PDF

Source
http://dx.doi.org/10.1177/039463200802100205DOI Listing

Publication Analysis

Top Keywords

ido
15
expression pattern
12
intestinal mucosa
8
indoleamine 23-dioxygenase
8
inflammation ido
8
local tryptophan
8
tryptophan depletion
8
expression ido
8
inflammatory bowel
8
bowel disease
8

Similar Publications

Chimeric antigen receptor (CAR) T-cell therapy plays a critical role in the treatment of B-cell hematologic malignancies. The combination of PD-1 inhibitors and CAR-T has shown encouraging results in treating patients with relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL). However, there are still cases where treatment is ineffective.

View Article and Find Full Text PDF

The helminth Trichinella spiralis, through its excretory-secretory (ES L1) products, induces immune regulatory mechanisms that modulate the host's immune response not only to itself, but also to bystander antigens, foreign or self in origin, which can result in the alleviation of inflammatory diseases. Under the influence of ES L1, dendritic cells (DCs) acquire a tolerogenic phenotype and the capacity to induce Th2 and regulatory responses. Since ES L1 products represent a complex mixture of proteins and extracellular vesicles (TsEVs) the aim of this study was to investigate the impact of TsEVs, isolated from ES L1 products, on phenotypic and functional characteristics of DCs and to elucidate whether TsEVs could reproduce the immunomodulatory effects of the complete ES L1 product.

View Article and Find Full Text PDF

Introduction: Indoleamine-2,3-dioxygenase (IDO) converts L-tryptophan (T) to L-kynurenine (K) resulting in an immunosuppressive microenvironment. Aim of the current study is to evaluate in patients with neuroendocrine tumor (NET): 1) T and K concentrations; 2) correlation with clinical outcome; 3) relationship between IDO activity and inflammatory cytokines.

Methods: A cross-sectional study was performed to investigate the IDO pathway in patients in follow-up for NET.

View Article and Find Full Text PDF

Background: Accurate assessment of oxygen delivery relative to oxygen demand is crucial in the care of a critically ill patient. The central venous oxygen saturation (Svo) enables an estimate of cardiac output yet obtaining these clinical data requires invasive procedures and repeated blood sampling. Interpretation remains subjective and vulnerable to error.

View Article and Find Full Text PDF

Background: The immunologic factors are the chief reason for recurrent pregnancy loss (RPL) and induction of maternal-fetal tolerance is the main treatment for this cause of RPL, but the effect of this method is uncertainly and needs multiple doses and/or interventions. The aim of this study was to investigate whether a single administration of transforming growth factor-β1 (TGF-β1) can improve the pregnancy outcomes of RPL mice and whether the improvement is cause by TGF-β1 driving the expression of immune tolerance molecule indoleamine 2,3-dioxygenase (IDO).

Materials And Methods: In this experimental study, 40 RPL model mice were equally divided into a control group, that received 0.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!