scholarly journals Correlations between Psoriasis and Inflammatory Bowel Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Nevena Skroza ◽  
Ilaria Proietti ◽  
Riccardo Pampena ◽  
Giorgio La Viola ◽  
Nicoletta Bernardini ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Genetic Correlations ◽  
Epidemiological Studies ◽  
The Body ◽  
Th22 Cells ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Common Pathogenesis

For a long time the relationship between inflammatory bowel diseases (IBDs) and psoriasis has been investigated by epidemiological studies. It is only starting from the 1990s that genetic and immunological aspects have been focused on. Psoriasis and IBD are strictly related inflammatory diseases. Skin and bowel represent, at the same time, barrier and connection between the inner and the outer sides of the body. The most important genetic correlations involve the chromosomal loci 6p22, 16q, 1p31, and 5q33 which map several genes involved in innate and adaptive immunity. The genetic background represents the substrate to the common immune processes involved in psoriasis and IBD. In the past, psoriasis and IBD were considered Th1-related disorders. Nowadays the role of new T cells populations has been highlighted. A key role is played by Th17 and T-regs cells as by the balance between these two cells types. New cytokines and T cells populations, as IL-17A, IL-22, and Th22 cells, could play an important pathogenetic role in psoriasis and IBD. The therapeutic overlaps further support the hypothesis of a common pathogenesis.

scholarly journals The Role of Enterobacteriaceae in Gut Microbiota Dysbiosis in Inflammatory Bowel Diseases

2021 ◽  
Vol 9 (4) ◽  
pp. 697
Author(s):  
Valerio Baldelli ◽  
Franco Scaldaferri ◽  
Lorenza Putignani ◽  
Federica Del Chierico
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Species Level ◽  
Unknown Etiology ◽  
Gut Dysbiosis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Symbiotic Microbiota ◽  
Gut Microbiota Dysbiosis

Inflammatory bowel diseases (IBDs) are a group of chronic gastrointestinal inflammatory diseases with unknown etiology. There is a combination of well documented factors in their pathogenesis, including intestinal microbiota dysbiosis. The symbiotic microbiota plays important functions in the host, and the loss of beneficial microbes could favor the expansion of microbial pathobionts. In particular, the bloom of potentially harmful Proteobacteria, especially Enterobacteriaceae, has been described as enhancing the inflammatory response, as observed in IBDs. Herein, we seek to investigate the contribution of Enterobacteriaceae to IBD pathogenesis whilst considering the continuous expansion of the literature and data. Despite the mechanism of their expansion still remaining unclear, their expansion could be correlated with the increase in nitrate and oxygen levels in the inflamed gut and with the bile acid dysmetabolism described in IBD patients. Furthermore, in several Enterobacteriaceae studies conducted at a species level, it has been suggested that some adherent-invasive Escherichia coli (AIEC) play an important role in IBD pathogenesis. Overall, this review highlights the pivotal role played by Enterobacteriaceae in gut dysbiosis associated with IBD pathogenesis and progression.

Clinical Comparison of 99Tcm-Hmpao Labelled Leucocytes and 99Tcm-Nanocolloid in the Detection of Inflammation

1989 ◽  
Vol 30 (6) ◽  
pp. 633-637 ◽  
Author(s):  
M. Vorne ◽  
T. Lantto ◽  
S. Paakkinen ◽  
S. Salo ◽  
I. Soini
Keyword(s):  
Soft Tissue ◽  
Inflammatory Bowel Diseases ◽  
Vascular Graft ◽  
Inflammatory Diseases ◽  
Reliable Information ◽  
Imaging Method ◽  
Joint Diseases ◽  
Labelled Leucocytes ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Forty-five patients with various inflammatory diseases were imaged with 99Tcm-HMPAO labelled leucocytes and 99Tcm-nanocolloid within 7 days. The overall sensitivity of 99Tcm-leucocytes was 97% and that of 99Tcm-nanocolloid 59% and both agents had a 100% specificity. The 99Tcm-leucocyte method showed reliable results in various inflammatory and infectious conditions, and seems suitable as a primary imaging method. On the contrary, 99Tcm-nanocolloid cannot be recommended for use in inflammatory bowel diseases, soft tissue abscesses or prosthetic vascular graft infections. However, 99Tcm-nanocolloid gave reliable information in inflammatory and infectious bone and joint diseases in which it had a 90% sensitivity and 100% specificity. In those lesions the 99Tcm-nanocolloid method may be useful, because it is simple, fast and cheap. Yet, further evaluation is needed.

scholarly journals Innate Immunity Modulation by the IL-33/ST2 System in Intestinal Mucosa

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Marina García-Miguel ◽  
M. Julieta González ◽  
Rodrigo Quera ◽  
Marcela A. Hermoso
Keyword(s):  
Ulcerative Colitis ◽  
Innate Immunity ◽  
Intestinal Mucosa ◽  
Inflammatory Bowel Diseases ◽  
The Body ◽  
Unknown Etiology ◽  
Adequate Food ◽  
Bowel Diseases ◽  
Surface Contact Area ◽  
Inflammatory Bowel

Innate immunity prevents pathogens from entering and spreading within the body. This function is especially important in the gastrointestinal tract and skin, as these organs have a large surface contact area with the outside environment. In the intestine, luminal commensal bacteria are necessary for adequate food digestion and play a crucial role in tolerance to benign antigens. Immune system damage can create an intestinal inflammatory response, leading to chronic disease including inflammatory bowel diseases (IBD). Ulcerative colitis (UC) is an IBD of unknown etiology with increasing worldwide prevalence. In the intestinal mucosa of UC patients, there is an imbalance in the IL-33/ST2 axis, an important modulator of the innate immune response. This paper reviews the role of the IL-33/ST2 system in innate immunity of the intestinal mucosa and its importance in inflammatory bowel diseases, especially ulcerative colitis.

Increased serum nesfatin-1 levels in patients with inflammatory bowel diseases

2021 ◽  
pp. postgradmedj-2020-139227
Author(s):  
Şengül Beyaz ◽  
Erdem Akbal
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Inflammatory Marker ◽  
White Cell Count ◽  
Characteristic Curve ◽  
Diagnostic Value ◽  
Healthy Individuals ◽  
Altered Expression ◽  
Bowel Diseases ◽  
Inflammatory Bowel

BackgroundAdipokines are adipose tissue–derived secreted molecules that can exert anti-inflammatory or proinflammatory activities. Altered expression of adipokines has been described in various inflammatory diseases, including inflammatory bowel diseases (IBDs) such as Crohn’s disease (CD) and ulcerative colitis (UC). Little is known about nesfatin-1, a recently identified adipokine, in IBD. The aim of this study was to investigate serum nesfatin-1 levels in patients with IBD.MethodsThis study included a total of 52 adult individuals (17 patients with CD, 18 patients with UC and 17 healthy volunteers) with similar age and body mass index. Serum nesfatin-1 levels were measured by ELISA in healthy individuals and patients with IBD in their active and remission periods. Blood inflammation markers including C reactive protein (CRP), erythrocyte sedimentation (ESR) and white cell count (WCC) were also measured in patients.ResultsWe found significantly elevated levels of serum nesfatin-1 in the active disease period in both patients with CD (p=0.00003) and patients with UC (p=0.00001), compared with healthy individuals. Serum nesfatin-1 levels moderately decreased in the remission period; however, they were still significantly higher than that of healthy individuals. Receiver operating characteristic curve analyses indicated serum nesfatin-1 with an excellent diagnostic value for IBD. Finally, patients had significantly high CRP, ESR and WCC in the active IBD; however, we found the nesfatin-1 strongly correlated only with ESR in the active CD.ConclusionThis is the first study investigating the circulating levels of nesfatin-1 in patients with IBD. Serum nesfatin-1 may serve as an additional inflammatory marker for diagnosis of IBD in affected individuals.

IRF5 Acts as a Potential Therapeutic Marker in Inflammatory Bowel Diseases

2020 ◽  
Author(s):  
Yonghong Yang ◽  
Cui Zhang ◽  
Dehuai Jing ◽  
Heng He ◽  
Xiaoyu Li ◽  
...  
Keyword(s):  
T Cells ◽  
Disease Activity ◽  
Inflammatory Bowel Diseases ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Mononuclear Cells ◽  
Orphan Receptor ◽  
Peripheral Blood Mononuclear ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Abstract Background Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic inflammatory disorders. As is well known, interferon regulatory factor (IRF) 5 is closely associated with the pathogenesis of various inflammatory diseases. But the exact role of IRF5 in IBD remains unclear. Methods In this study, we detected IRF5 expression in peripheral blood mononuclear cells (PBMCs) and inflamed mucosa from IBD patients by immunohistochemistry, western blot, and quantitative real-time polymerase chain reaction. Peripheral blood CD4+ T cells were stimulated with inflammatory cytokines and transfected by lentivirus. Results In active IBD patients, the expression of IRF5 in PBMCs and inflamed colonic tissues was obviously increased and significantly associated with disease activity. Ectopic overexpression of IRF5 could promote the differentiation of IBD CD4+ T cells into Th1 and Th17 cells by regulating T-bet and RAR related orphan receptor C, whereas knockdown of IRF5 had the opposite effects. Tumor necrosis factor (TNF)-α upregulated expression of IRF5 in CD4+ T cells, but anti-TNF treatment with infliximab could markedly reduce IRF5 expression in CD4+ T cells and intestinal mucosa of CD patients. Conclusion Our study reveals a novel mechanism that IRF5 levels are correlated with disease activity in IBD and might function as a possible marker for the management of IBD via regulating Th1 and Th17 immune responses and cytokine production.

scholarly journals Fine tuning of the DNAM-1/TIGIT/ligand axis in mucosal T cells and its dysregulation in pediatric inflammatory bowel diseases (IBD)

2019 ◽  
Vol 12 (6) ◽  
pp. 1358-1369
Author(s):  
S. Battella ◽  
S. Oliva ◽  
L. Franchitti ◽  
R. La Scaleia ◽  
A. Soriani ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Bowel Diseases ◽  
Fine Tuning ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Mucosal T Cells

scholarly journals Vedolizumab: Potential Mechanisms of Action for Reducing Pathological Inflammation in Inflammatory Bowel Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Matthew Luzentales-Simpson ◽  
Yvonne C. F. Pang ◽  
Ada Zhang ◽  
James A. Sousa ◽  
Laura M. Sly
Keyword(s):  
T Cells ◽  
T Cell ◽  
Inflammatory Bowel Diseases ◽  
Necrosis Factor Alpha ◽  
Cell Recruitment ◽  
Inflammatory Monocytes ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Cytokine Tumor Necrosis Factor ◽  
Inflammatory Bowel

Inflammatory bowel diseases (IBD), encompassing ulcerative colitis (UC), and Crohn’s disease (CD), are a group of disorders characterized by chronic, relapsing, and remitting, or progressive inflammation along the gastrointestinal tract. IBD is accompanied by massive infiltration of circulating leukocytes into the intestinal mucosa. Leukocytes such as neutrophils, monocytes, and T-cells are recruited to the affected site, exacerbating inflammation and causing tissue damage. Current treatments used to block inflammation in IBD include aminosalicylates, corticosteroids, immunosuppressants, and biologics. The first successful biologic, which revolutionized IBD treatment, targeted the pro-inflammatory cytokine, tumor necrosis factor alpha (TNFα). Infliximab, adalimumab, and other anti-TNF antibodies neutralize TNFα, preventing interactions with its receptors and reducing the inflammatory response. However, up to 40% of people with IBD become unresponsive to anti-TNFα therapy. Thus, more recent biologics have been designed to block leukocyte trafficking to the inflamed intestine by targeting integrins and adhesins. For example, natalizumab targets the α4 chain of integrin heterodimers, α4β1 and α4β7, on leukocytes. However, binding of α4β1 is associated with increased risk for developing progressive multifocal leukoencephalopathy, an often-fatal disease, and thus, it is not used to treat IBD. To target leukocyte infiltration without this life-threatening complication, vedolizumab was developed. Vedolizumab specifically targets the α4β7 integrin and was approved to treat IBD based on the presumption that it would block T-cell recruitment to the intestine. Though vedolizumab is an effective treatment for IBD, some studies suggest that it may not block T-cell recruitment to the intestine and its mechanism(s) of action remain unclear. Vedolizumab may reduce inflammation by blocking recruitment of T-cells, or pro-inflammatory monocytes and dendritic cells to the intestine, and/or vedolizumab may lead to changes in the programming of innate and acquired immune cells dampening down inflammation.

scholarly journals P089 Extensive characterisation of cellular sources of IL-22BP in inflammatory bowel diseases indicates that T cells do not express IL-22BP

2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S130-S130
Author(s):  
A Fantou ◽  
A Abidi ◽  
L Delbos ◽  
J Podevin ◽  
A Jarry ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Bowel Diseases ◽  
Bowel Diseases ◽  
Inflammatory Bowel

T-cell-directed therapies in inflammatory bowel diseases

2010 ◽  
Vol 118 (12) ◽  
pp. 707-715 ◽  
Author(s):  
Giovanni Monteleone ◽  
Flavio Caprioli
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Inflammatory Bowel Diseases ◽  
Clinical Success ◽  
Mucosal Inflammation ◽  
Activated T Cells ◽  
Cell Accumulation ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Gut inflammation occurring in patients with IBDs (inflammatory bowel diseases) is associated with exaggerated and poorly controlled T-cell-mediated immune responses, which are directed against normal components of the gut flora. T-cells accumulate in the inflamed gut of IBD patients as a result of multiple mechanisms, including enhanced recruitment of cells from the bloodstream, sustained cell cycling and diminished susceptibility of cells to undergo apoptosis. Activated T-cells produce huge amounts of cytokines, which contribute to amplify and sustain the ongoing mucosal inflammation. Strategies aimed at interfering with T-cell accumulation and/or function in the gut have been employed with clinical success in patients with IBDs. In the present article, we review the available results showing that T-cell-directed therapies are useful to dampen the tissue-damaging immune response in IBDs.

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