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Serological investigation of IgG and IgE antibodies against food antigens in patients with inflammatory bowel disease.
Wang, HY, Li, Y, Li, JJ, Jiao, CH, Zhao, XJ, Li, XT, Lu, MJ, Mao, XQ, Zhang, HJ
World journal of clinical cases. 2019;7(16):2189-2203
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Crohn's disease and ulcerative colitis are relapsing gut inflammatory diseases that are usually referred to as Inflammatory Bowel Disease (IBD). It may be triggered by an imbalance in immune response in response to environmental factors such as diet. The aim of this retrospective study was to evaluate the presence of IgG and IgE mediated antibodies to food antigens in IBD patients. There were one hundred and thirty-seven IBD patients participating in this study, including forty Ulcerative colitis patients and ninety-seven Crohn's disease patients against fifty healthy controls to test serum IgG antibodies to fourteen specific food antigens and serum IgE antibodies to fourteen specific food antigens. There were significantly higher IgG antibodies in response to food antigens in Crohn's disease patients than in Ulcerative colitis patients and healthy controls. Food antigens such as tomato, corn, egg, rice, and soybean exhibited varying levels of IgG antibody responses in Crohn's disease patients and ulcerative colitis patients. Smokers were more likely to develop IgG reactions. Further robust research is needed to examine more IgG-specific food antigens to help manage IBD with an elimination rotation diet. The results of this study can help healthcare professionals understand the importance of diagnosing food intolerances when treating IBD.
Abstract
BACKGROUND Food antigens have been shown to participate in the etiopathogenesis of inflammatory bowel disease (IBD), but their clinical value in IBD is still unclear. AIM: To analyze the levels of specific immunoglobulin G (IgG) and E (IgE) antibodies against food antigens in IBD patients and to determine their clinical value in the pathogenesis of IBD. METHODS We performed a retrospective study based on patients who visited the First Affiliated Hospital of Nanjing Medical University between August 2016 and January 2018. A total of 137 IBD patients, including 40 patients with ulcerative colitis (UC) and 97 patients with Crohn's disease (CD), and 50 healthy controls (HCs), were recruited. Serum food-specific IgG antibodies were detected by semi-quantitative enzyme-linked immunosorbent assay, and serum food-specific IgE antibodies were measured by Western blot. The value of food-specific IgG antibodies was compared among different groups, and potent factors related to these antibodies were explored by binary logistic regression. RESULTS Food-specific IgG antibodies were detected in 57.5% of UC patients, in 90.72% of CD patients and in 42% of HCs. A significantly high prevalence and titer of food-specific IgG antibodies were observed in CD patients compared to UC patients and HCs. The number of IgG-positive foods was greater in CD and UC patients than in HCs (CD vs HCs, P = 0.000; UC vs HCs, P = 0.029). The top five food antigens that caused positive specific IgG antibodies in CD patients were tomato (80.68%), corn (69.32%), egg (63.64%), rice (61.36%), and soybean (46.59%). The foods that caused positive specific IgG antibodies in UC patients were egg (60.87%), corn (47.83%), tomato (47.83%), rice (26.09%), and soybean (21.74%). Significantly higher levels of total food-specific IgG were detected in IBD patients treated with anti-TNFα therapy compared to patients receiving steroids and immunosuppressants (anti-TNFα vs steroids, P = 0.000; anti-TNFα vs immunosuppressants, P = 0.000; anti-TNFα vs steroids + immunosuppressants, P = 0.003). A decrease in food-specific IgG levels was detected in IBD patients after receiving anti-TNFα therapy (P = 0.007). Patients who smoked and CD patients were prone to developing serum food-specific IgG antibodies [Smoke: OR (95%CI): 17.6 (1.91-162.26), P = 0.011; CD patients: OR (95%CI): 12.48 (3.45-45.09), P = 0.000]. There was no difference in the prevalence of food-specific IgE antibodies among CD patients (57.1%), UC patients (65.2%) and HCs (60%) (P = 0.831). CONCLUSION CD patients have a higher prevalence of food-specific IgG antibodies than UC patients and HCs. IBD patients are prone to rice, corn, tomato and soybean intolerance. Smoking may be a risk factor in the occurrence of food-specific IgG antibodies. Food-specific IgG antibodies may be a potential method in the diagnosis and management of food intolerance in IBD.
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Interplay of host genetics and gut microbiota underlying the onset and clinical presentation of inflammatory bowel disease.
Imhann, F, Vich Vila, A, Bonder, MJ, Fu, J, Gevers, D, Visschedijk, MC, Spekhorst, LM, Alberts, R, Franke, L, van Dullemen, HM, et al
Gut. 2018;67(1):108-119
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Patients with inflammatory bowel disease (IBD) present with a variety of clinical characteristics, making prevention, diagnosis and therapy very complex. Based on recent studies, it is hypothesised that the heterogeneity among patients with IBD is likely due to individual differences in the interaction between the host genome and gut microbiota. The aim of this case-control study was to analyse the gut microbiota, host genetics and clinical characteristics of 313 patients with IBD compared with 582 healthy controls. This extensive analysis has identified the gut microbiota as the key mediator in the development of IBD through new associations at the genetic and clinical level. Based on these findings, the authors conclude that a better understanding of gene-microbiota interactions can lead to new therapeutics and improved prevention strategies.
Abstract
OBJECTIVE Patients with IBD display substantial heterogeneity in clinical characteristics. We hypothesise that individual differences in the complex interaction of the host genome and the gut microbiota can explain the onset and the heterogeneous presentation of IBD. Therefore, we performed a case-control analysis of the gut microbiota, the host genome and the clinical phenotypes of IBD. DESIGN Stool samples, peripheral blood and extensive phenotype data were collected from 313 patients with IBD and 582 truly healthy controls, selected from a population cohort. The gut microbiota composition was assessed by tag-sequencing the 16S rRNA gene. All participants were genotyped. We composed genetic risk scores from 11 functional genetic variants proven to be associated with IBD in genes that are directly involved in the bacterial handling in the gut: NOD2, CARD9, ATG16L1, IRGM and FUT2. RESULTS Strikingly, we observed significant alterations of the gut microbiota of healthy individuals with a high genetic risk for IBD: the IBD genetic risk score was significantly associated with a decrease in the genus Roseburia in healthy controls (false discovery rate 0.017). Moreover, disease location was a major determinant of the gut microbiota: the gut microbiota of patients with colonic Crohn's disease (CD) is different from that of patients with ileal CD, with a decrease in alpha diversity associated to ileal disease (p=3.28×10-13). CONCLUSIONS We show for the first time that genetic risk variants associated with IBD influence the gut microbiota in healthy individuals. Roseburia spp are acetate-to-butyrate converters, and a decrease has already been observed in patients with IBD.
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Oral versus intravenous iron replacement therapy distinctly alters the gut microbiota and metabolome in patients with IBD.
Lee, T, Clavel, T, Smirnov, K, Schmidt, A, Lagkouvardos, I, Walker, A, Lucio, M, Michalke, B, Schmitt-Kopplin, P, Fedorak, R, et al
Gut. 2017;66(5):863-871
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Iron deficiency is common in patients with Inflammatory Bowel Disease (IBD) and the standard management is with oral iron replacement therapy. However, this is thought to worsen IBD symptoms, as free iron in the gut can alter the composition of the resident gut bacteria and may contribute to inflammation. This open-labelled clinical trial compared oral iron replacement to intravenous iron replacement in subjects with Crohn’s disease (CD), Ulcerative Colitis and iron-deficient, non-inflamed subjects. The data collected included microbiome sequencing, metabolic profiling, serum iron and inflammation markers. Whilst both interventions alleviated deficiency, the intravenous iron replacement was slightly more effective at raising ferritin levels. The results showed that iron replacement therapy shifted the microbiome diversity and composition depending on free iron availability in the gut. A reduced microbiome diversity already distinguishes IBD from healthy subjects and a further decline in abundance following iron replacement therapy was particularly noticeable with oral iron supplementation and in Crohn's Disease subjects. However, over the short course of three months, this was not linked to disease severity in this study. This study affirms the importance of assessing for iron deficiency in IBD clients whilst supporting IV iron replacement being a favourable alternative to oral supplementation for individuals with unstable microbiota.
Abstract
OBJECTIVE Iron deficiency is a common complication in patients with IBD and oral iron therapy is suggested to exacerbate IBD symptoms. We performed an open-labelled clinical trial to compare the effects of per oral (PO) versus intravenous (IV) iron replacement therapy (IRT). DESIGN The study population included patients with Crohn's disease (CD; N=31), UC (N=22) and control subjects with iron deficiency (non-inflamed, NI=19). After randomisation, participants received iron sulfate (PO) or iron sucrose (IV) over 3 months. Clinical parameters, faecal bacterial communities and metabolomes were assessed before and after intervention. RESULTS Both PO and IV treatments ameliorated iron deficiency, but higher ferritin levels were observed with IV. Changes in disease activity were independent of iron treatment types. Faecal samples in IBD were characterised by marked interindividual differences, lower phylotype richness and proportions of Clostridiales. Metabolite analysis also showed separation of both UC and CD from control anaemic participants. Major shifts in bacterial diversity occurred in approximately half of all participants after IRT, but patients with CD were most susceptible. Despite individual-specific changes in phylotypes due to IRT, PO treatment was associated with decreased abundances of operational taxonomic units assigned to the species Faecalibacterium prausnitzii, Ruminococcus bromii, Dorea sp. and Collinsella aerofaciens. Clear IV-specific and PO-specific fingerprints were evident at the level of metabolomes, with changes affecting cholesterol-derived host substrates. CONCLUSIONS Shifts in gut bacterial diversity and composition associated with iron treatment are pronounced in IBD participants. Despite similar clinical outcome, oral administration differentially affects bacterial phylotypes and faecal metabolites compared with IV therapy. TRIAL REGISTRATION NUMBER clinicaltrial.gov (NCT01067547).