scholarly journals Use of Wild Type or Recombinant Lactic Acid Bacteria as an Alternative Treatment for Gastrointestinal Inflammatory Diseases: A Focus on Inflammatory Bowel Diseases and Mucositis

2017 ◽  
Vol 8 ◽  
Author(s):  
Rodrigo D. De Oliveira Carvalho ◽  
Fillipe L. R. do Carmo ◽  
Alberto de Oliveira Junior ◽  
Philippe Langella ◽  
Jean-Marc Chatel ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Alternative Treatment ◽  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Wild Type ◽  
Bowel Diseases ◽  
Inflammatory Bowel

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.

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.

scholarly journals IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore

2021 ◽  
Author(s):  
James Byrne ◽  
Kevin Baker ◽  
Aileen Houston ◽  
Elizabeth Brint
Keyword(s):  
Wound Healing ◽  
Sequence Homology ◽  
Inflammatory Bowel Diseases ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Malignant Diseases ◽  
Bowel Diseases ◽  
Health And Disease ◽  
Inflammatory Bowel

AbstractThe IL-36 family of cytokines were first identified in 2000 based on their sequence homology to IL-1 cytokines. Over subsequent years, the ability of these cytokines to either agonise or antagonise an IL-1R homologue, now known as the IL-36 Receptor (IL-36R), was identified and these cytokines went through several cycles of renaming with the current nomenclature being proposed in 2010. Despite being identified over 20 years ago, it is only during the last decade that the function of these cytokines in health and disease has really begun to be appreciated, with both homeostatic functions in wound healing and response to infection, as well as pathological functions now ascribed. In the disease context, over activation of IL-36 has now been associated with many inflammatory diseases including Psoriasis and inflammatory bowel diseases, with roles in cancer also now being investigated. This review summarises the current knowledge of IL-36 biology, its role in inflammatory diseases and focuses on an emerging role for IL-36 in cancer.

scholarly journals P795 Risk of incident paradoxical immune-mediated inflammatory diseases in patients with inflammatory bowel diseases treated with anti-TNF therapies: a nationwide Danish cohort study

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S625-S625
Author(s):  
D WARD ◽  
S Gørtz ◽  
N Nyboe Andersen ◽  
J Kirchgesner ◽  
T Jess
Keyword(s):  
Rheumatoid Arthritis ◽  
Cohort Study ◽  
Inflammatory Bowel Diseases ◽  
Hidradenitis Suppurativa ◽  
Inflammatory Diseases ◽  
Hazard Ratios ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Lag Period ◽  
Inflammatory Bowel

Abstract Background Tumour necrosis factor (TNF) has a central role in the pathophysiology of immune-mediated inflammatory diseases (IMIDs) including rheumatoid arthritis, psoriasis, hidradenitis suppurativa, and inflammatory bowel diseases (IBD). However, there have been case reports of patients receiving an anti-TNF therapy for one IMID subsequently developing a second IMID. We conducted a nationwide cohort study investigating the risk of incident IMID following anti-TNF exposure in patients with IBD in Denmark. Methods We followed patients with IBD from 1 January 2005 or date of IBD diagnosis (whichever occurred last) to an outcome event including incident diagnosis of hidradenitis suppurativa, arthropathic psoriasis, other forms of psoriasis, or rheumatoid arthritis; or emigration, death or 31 December 2018 (whichever occurred first). Patients were defined as exposed after a 3-month lag period from first anti-TNF infusion throughout follow-up, analogous to an intention-to-treat design. The lag period was censored from analyses to avoid including incipient IMIDs, unlikely to be caused by newly initiated anti-TNF treatment. We excluded patients initiating anti-TNF or with an outcome diagnosis before either 1 January 2005 or IBD diagnosis. We used Cox regression models with age as the underlying timescale, and sex, type of IBD (Crohn’s disease or ulcerative colitis), and calendar period of IBD diagnosis (in 5 year groups) as strata to estimate hazard ratios for each outcome, comparing anti-TNF users and non-users. Results Incidence rates (and 95% confidence intervals [CI]) as events per 100 000 person-years among anti-TNF users and non-users were, respectively, 138 (109–173) and 25.6 (22.0–29.7) for hidradenitis suppurativa, 26.3 (15.6–44.4) and 7.81 (5.95–10.2) for arthropathic psoriasis, 1177 (1085–1277) and 204 (121–189) for other forms of psoriasis, and 152 (121–189) and 95.6 (88.5–103) for rheumatoid arthritis. Hazard ratios (and 95% C.I.) were increased for hidradenitis suppurativa 2.91 (2.15–3.94), arthropathic psoriasis 2.62 (1.40–4.93), other forms of psoriasis 4.76 (4.27–5.31), and rheumatoid arthritis 2.35 (1.83–3.01). Conclusion The results indicate that patients with IBD receiving anti-TNF have an increased risk of IMIDs. An almost 5-fold increase in the risk of psoriasis is consistent with previous reports of psoriasiform skin lesions related to anti-TNF use. However, as more severe IBD is likely to be associated with both initiating anti-TNF and the incidence of other inflammatory diseases, the results are subject to confounding by indication. Thus, these results should be considered preliminary, and we plan to further address confounding by using propensity score methods.

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 Chitinases and Chitinase-Like Proteins as Therapeutic Targets in Inflammatory Diseases, with a Special Focus on Inflammatory Bowel Diseases

2021 ◽  
Vol 22 (13) ◽  
pp. 6966
Author(s):  
Marzena Mazur ◽  
Anna Zielińska ◽  
Marcin M. Grzybowski ◽  
Jacek Olczak ◽  
Jakub Fichna
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Glycosyl Hydrolase ◽  
Chitinase Activity ◽  
Chronic Obstructive ◽  
Special Focus ◽  
Interacting Protein ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Chitinases belong to the evolutionarily conserved glycosyl hydrolase family 18 (GH18). They catalyze degradation of chitin to N-acetylglucosamine by hydrolysis of the β-(1-4)-glycosidic bonds. Although mammals do not synthesize chitin, they possess two enzymatically active chitinases, i.e., chitotriosidase (CHIT1) and acidic mammalian chitinase (AMCase), as well as several chitinase-like proteins (YKL-40, YKL-39, oviductin, and stabilin-interacting protein). The latter lack enzymatic activity but still display oligosaccharides-binding ability. The physiologic functions of chitinases are still unclear, but they have been shown to be involved in the pathogenesis of various human fibrotic and inflammatory disorders, particularly those of the lung (idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, sarcoidosis, and asthma) and the gastrointestinal tract (inflammatory bowel diseases (IBDs) and colon cancer). In this review, we summarize the current knowledge about chitinases, particularly in IBDs, and demonstrate that chitinases can serve as prognostic biomarkers of disease progression. Moreover, we suggest that the inhibition of chitinase activity may be considered as a novel therapeutic strategy for the treatment of IBDs.

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