1.
Inflammatory Bowel Diseases and Food Additives: To Add Fuel on the Flames!
Marion-Letellier, R, Amamou, A, Savoye, G, Ghosh, S
Nutrients. 2019;11(5)
-
-
-
Free full text
Plain language summary
Inflammatory Bowel Diseases (IBDs), such as Crohn’s disease (CD) and Ulcerative Colitis (UC) are becoming increasingly common. Diet is thought to play a role in the development of IBDs. The consumption of Ultra Processed Food (UPF) is increasing and has been associated with a higher risk of some chronic diseases. Food additives may be an aspect of UPF responsible for its harmful effects. This literature review examined the role of food additives in the development and severity of IBDs. The authors discuss how common food additives such as salt, emulsifiers, stabilisers, bulking agents, sweeteners, and food colouring may promote inflammation and disrupt gut bacteria. Metals and compounds found in food packaging such as aluminium and bisphenol A (BPA) may trigger intestinal permeability and increase inflammatory markers. Much of the evidence available is based on clinical trials on animals, whilst epidemiological studies on food additives and IBD risk are still limited. The authors concluded that the majority of food consumed by IBD patients should be home-cooked in order to reduce exposure to additives in the diet.
Abstract
Inflammatory bowel diseases (IBDs) develop in genetically predisposed individuals in response to environmental factors. IBDs are concomitant conditions of industrialized societies, and diet is a potential culprit. Consumption of ultra-processed food has increased over the last decade in industrialized countries, and epidemiological studies have found associations between ultra-processed food consumption and chronic diseases. Further studies are now required to identify the potential culprit in ultra-processed food, such as a poor nutritional composition or the presence of food additives. In our review, we will focus on food additives, i.e., substances from packaging in contact with food, and compounds formed during production, processing, and storage. A literature search using PubMed from inception to January 2019 was performed to identify relevant studies on diet and/or food additive and their role in IBDs. Manuscripts published in English from basic science, epidemiological studies, or clinical trials were selected and reviewed. We found numerous experimental studies highlighting the key role of food additives in IBD exacerbation but epidemiological studies on food additives on IBD risk are still limited. As diet is a modifiable environmental risk factor, this may offer a scientific rationale for providing dietary advice for IBD patients.
2.
Salmonella Infection in Chronic Inflammation and Gastrointestinal Cancer.
Zha, L, Garrett, S, Sun, J
Diseases (Basel, Switzerland). 2019;7(1)
-
-
-
Free full text
Plain language summary
Salmonella is a group of bacteria that is normally associated with food poisoning. In 2% to 5% of people with Salmonella food poisoning, the bacteria remain in the body, leading to long-term infection, which has been linked to various health problems. This literature review looked at the link between Salmonella infection and the development of diseases such as inflammatory bowel disease (IBD), gall bladder cancer and colon cancer. The authors describe how long-term Salmonella infection plays a role in several biological processes, such as stem cell maintenance, host cell transformation, and gut dysbiosis. Leaky gut, dysbiosis and inflammation are induced by the bacteria and contribute to the development of cancer. The authors conclude that more studies are needed to further understand the relationship between Salmonella infections and the risk of colon cancer.
Abstract
Salmonella not only causes acute infections, but can also cause patients to become chronic "asymptomatic" carriers. Salmonella has been verified as a pathogenic factor that contributes to chronic inflammation and carcinogenesis. This review summarizes the acute and chronic Salmonella infection and describes the current research progress of Salmonella infection contributing to inflammatory bowel disease and cancer. Furthermore, this review explores the underlying biological mechanism of the host signaling pathways manipulated by Salmonella effector molecules. Using experimental animal models, researchers have shown that Salmonella infection is related to host biological processes, such as host cell transformation, stem cell maintenance, and changes of the gut microbiota (dysbiosis). Finally, this review discusses the current challenges and future directions in studying Salmonella infection and its association with human diseases.
3.
Long-term outcome of patients with steroid-refractory acute severe UC treated with ciclosporin or infliximab.
Laharie, D, Bourreille, A, Branche, J, Allez, M, Bouhnik, Y, Filippi, J, Zerbib, F, Savoye, G, Vuitton, L, Moreau, J, et al
Gut. 2018;67(2):237-243
-
-
-
Free full text
-
Plain language summary
Intravenous steroids are the first-line therapy for ulcerative colitis (UC) patients who are hospitalised during a severe UC flare-up. In the 40% of patients who don’t respond to steroids, the drugs ciclosporin and infliximab have been found to be efficient in preventing surgery to remove part or all of the colon, but there is a lack of data on the long-term outcomes of using these medications in UC patients. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. Between 2007 and 2010, 115 patients with UC that did not respond to steroids were randomised to receive ciclosporin or infliximab in association with azathioprine. Patients were followed to January 2015 or death. After a median follow-up of 5.4 years, colectomy-free survival rates at 1 and 5 years were, respectively, 70.9% and 61.5% in patients who received ciclosporin and 69.1% and 65.1% in those who received infliximab. Long-term colectomy-free survival was independent from initial treatment. However, a higher proportion of patients initially treated with ciclosporin needed a new treatment compared with those who received infliximab first. The researchers concluded that these results further confirm a similar efficacy and good safety profiles of both drugs.
Abstract
OBJECTIVE Ciclosporin and infliximab have demonstrated short-term similar efficacy as second-line therapies in patients with acute severe UC (ASUC) refractory to intravenous steroids. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. DESIGN Between 2007 and 2010, 115 patients with steroid-refractory ASUC were randomised in 29 European centres to receive ciclosporin or infliximab in association with azathioprine. Patients were followed until death or last news up to January 2015. Colectomy-free survival rates at 1 and 5 years and changes in therapy were estimated through Kaplan-Meier method and compared between initial treatment groups through log-rank test. RESULTS After a median follow-up of 5.4 years, colectomy-free survival rates (95% CI) at 1 and 5 years were, respectively, 70.9% (59.2% to 82.6%) and 61.5% (48.7% to 74.2%) in patients who received ciclosporin and 69.1% (56.9% to 81.3%) and 65.1% (52.4% to 77.8%) in those who received infliximab (p=0.97). Cumulative incidence of first infliximab use at 1 and 5 years in patients initially treated with ciclosporin was, respectively, 45.7% (32.6% to 57.9%) and 57.1% (43.0% to 69.0%). Only four patients from the infliximab group were subsequently switched to ciclosporin. Three patients died during the follow-up, none directly related to UC or its treatment. CONCLUSIONS In this cohort of patients with steroid-refractory ASUC initially treated by ciclosporin or infliximab, long-term colectomy-free survival was independent from initial treatment. These long-term results further confirm a similar efficacy and good safety profiles of both drugs and do not favour one drug over the other. TRIAL REGISTRATION NUMBER EudraCT: 2006-005299-42; ClinicalTrials.gouv number: NCT00542152; post-results.
4.
Disruption of the Gut Ecosystem by Antibiotics.
Yoon, MY, Yoon, SS
Yonsei medical journal. 2018;59(1):4-12
-
-
-
Free full text
Plain language summary
The gut microbiome is a complex ecosystem of different micro-organisms, such as bacteria, viruses and fungi, living in the human intestines. It’s involved in numerous functions, such as extracting energy and nutrition from food, protecting against disease-causing microorganisms, and supporting the immune system of the host, and therefore affecting human health and disease. This paper is a review of studies on the effects of antibiotics on the gut microbiota. It outlines how different types of antibiotics can alter the intestinal environment and the composition of the microbes, resulting in various physiological changes that can trigger disease. Relevant mechanisms, such as inflammatory response and the use of intestinal nutrients by infectious bacteria are discussed. Finally, it discusses faecal microbiota transplantation (FMT) and probiotics as treatment approaches, aimed at restoring a disturbed intestinal environment.
Abstract
The intestinal microbiota is a complex ecosystem consisting of various microorganisms that expands human genetic repertoire and therefore affects human health and disease. The metabolic processes and signal transduction pathways of the host and intestinal microorganisms are intimately linked, and abnormal progression of each process leads to changes in the intestinal environment. Alterations in microbial communities lead to changes in functional structures based on the metabolites produced in the gut, and these environmental changes result in various bacterial infections and chronic enteric inflammatory diseases. Here, we illustrate how antibiotics are associated with an increased risk of antibiotic-associated diseases by driving intestinal environment changes that favor the proliferation and virulence of pathogens. Understanding the pathogenesis caused by antibiotics would be a crucial key to the treatment of antibiotic-associated diseases by mitigating changes in the intestinal environment and restoring it to its original state.