scholarly journals Elevated Serum Levels of IL-6 and TNF-α in Patients with Irritable Bowel Syndrome

2019 ◽  
Vol 27 (2) ◽  
pp. 21-29
Author(s):  
Marzieh Azizyan ◽  
Habibolah Turki ◽  
Asad Mirzaei ◽  
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...  
2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Elif Börekci ◽  
Mahmut Kılıç ◽  
Zeynep Ozan ◽  
Hasan Börekci ◽  
Tekin Yıldırım ◽  
...  

Abstract Objectives There is no reliable and valid biomarker to identify Irritable bowel syndrome (IBS) and its subtypes. The aim of this study is to explore potential serum biomarkers that may be associated with IBS subtypes, particularly in the vitamin D pathway. Methods The study population comprised 75 IBS patients and 79 controls. Patients divided into IBS subtypes. Routine biochemical parameters, 25-OH-vitamin D, vitamin D binding protein (VDBP) and vitamin D receptor (VDR) serum levels were compared between IBS subtypes and controls. Factors related to IBS subtypes were examined by multivariate logistic regression analysis. Results Vitamin D levels were lower; VDBP and VDR were higher in all IBS patients than in controls (p<0.001; 0.047 and 0.029, respectively). According to logistic regression analysis, VDBP was a disease-related parameter as much as vitamin D in all IBS subtypes. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were higher especially in diarrhea-dominant IBS (IBS-D) (p=0.041; 0.046) and vitamin B12 were significantly lower in constipation-dominant IBS (IBS-C) (p=0.001). Conclusions Increased VDBP levels were associated with all IBS subtypes. Patients, especially in IBS-D, had higher serum levels of VDBP, CRP and ESR. Vitamin B12 deficiency, which we consider as a result of the disease, was more common in IBS-C.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Changrong Zhang ◽  
Yongquan Huang ◽  
Peiwu Li ◽  
Xinlin Chen ◽  
Fengbin Liu ◽  
...  

Abstract Background Ginger or ginger extracts have been used in traditional medicine relieve pain caused by diarrhea predominant irritable bowel syndrome (IBS-D), but few data exists about its effectiveness. This present study was to validate the effect of ginger on visceral pain, and to further explore the possible underlying mechanism by which ginger is used to relieve IBS-D intestinal hypersensitivity. Methods First, the IBS-D rat model was established by chemical stimulation and acute and chronic pressure stimulation. Then, different dose of ginger were administrated to IBS-D rats and evaluate the defecation frequency, fecal water content (FWC) and abdominal withdrawal reflex (AWR) scores in IBS-D rats. Further, the IBS-D rats were sacrificed to collecte the colonic tissues to evaluate the effect of ginger administration on its pathology and changes of pro-inflammatory factors, and changes of NF-κB pathway. Second, the ginger was taken to HPLC analysis and 6-gingerol was choosen to further experiment. Then, IBS-D rats were treated with different dose of 6-gingerol, and the behavioral evaluation were to evaluate the effect of 6-gingerol on IBS-D rats. Further, colonic epithelial cells (CECs) were collectted and to evaluate the effect of 6-gingerol on the expression of inflammatory factors and changes of NF-κB pathway. Results The IBS-D rat model was successfully established by chemical stimulation and acute and chronic pressure stimulation. And ginger treatment significantly reduced the defecation frequency, fecal water content and AWR scores in IBS-D rats. Histopathological analysis showed that ginger treatment can significantly reduce colonic edema and promote the recovery of inflammation in IBS-D rats, and the effect is equivalent to rifaximin. Elisa and RT-qPCR showed that ginger inhibited the expression of proinflammatory factors (TNF-α, IL-6, iNOS) in IBS-D rats. Western blot showed IkBα was up-regulated while p-p65 was inhibited under ginger treatment. HPLC analysis showed that 6-gingerol was the main component of ginger, which could improve clinical symptoms in IBS-D rats. Western blot and RT-qPCR showed that 6-gingerol inhibited the expression of proinflammatory factors (TNF-α, IL-6, iNOS) in CECs, and inhibition of IκBα degradation and phosphorylation of p65 involved in NF-κB pathway. Conclusion Ginger and ginger extract could relieve intestinal hypersensitivity of IBS-D by inhibiting proinflammatory response.


2019 ◽  
Vol 10 (5) ◽  
pp. 2906-2913 ◽  
Author(s):  
Yanlong Li ◽  
Xudong Tian ◽  
Shengcai Li ◽  
Lijun Chang ◽  
Ping Sun ◽  
...  

Dysfunction of the intestinal epithelial barrier plays an important role in the pathogenesis of several intestinal diseases, including celiac disease, inflammatory bowel disease, and irritable bowel syndrome.


2002 ◽  
Vol 47 (8) ◽  
pp. 742-749 ◽  
Author(s):  
Trino Baptista ◽  
Serge Beaulieu

Objective: To critically review published literature on the causal association between leptin, cytokines, and excessive body weight gain (BWG) induced by antipsychotic drugs (APs). Methods: We completed a Medline search using the words leptin, cytokines, antipsychotic drugs, neuroleptics, psychotropic drugs, weight gain, and obesity. We also included our empirical research on this topic in the discussion. We examined the relation between leptin, cytokines (mainly tumour necrosis factor alpha [TNF-α] and its soluble receptors), and AP-induced BWG, using the biological sciences' current theories of causality. Results: In the general field of weight regulation, there is scarce experimental evidence that leptin or TNF-α by themselves can induce obesity. Serum levels of leptin and TNF-α rather increase simultaneously as BWG occurs. This has also been reported during AP-induced BWG, with the equivocal exception of a study with clozapine. Some researchers have suggested that the absence of the expected correlation between leptin and body mass index (BMI) or serum insulin levels, and the lack of sex-related differences in leptin levels in AP-treated patients, may point to a causal relation. This contention requires more experimental support. In addition, future clinical studies must carefully control for sex and BMI. Conclusions: No conclusive evidence has been provided that leptin or TNF-α may induce obesity either in drug-free subjects or in AP-treated patients. In most cases, the elevated serum levels of these hormones appear to be a consequence rather than a cause of obesity. That does not mean that such an elevation is innocuous, since it may impair blood pressure and also carbohydrate and lipid metabolism regulation. Hence, all efforts should be made to prevent or attenuate BWG during treatment with APs.


2007 ◽  
Vol 292 (3) ◽  
pp. G779-G784 ◽  
Author(s):  
Kevin F. Foley ◽  
Cristen Pantano ◽  
Allison Ciolino ◽  
Gary M. Mawe

Recent studies have shown that mucosal serotonin (5-HT) transporter (SERT) expression is decreased in animal models of colitis, as well as in the colonic mucosa of humans with ulcerative colitis and irritable bowel syndrome. Altered SERT function or expression may underlie the altered motility, secretion, and sensation seen in these inflammatory gut disorders. In an effort to elucidate possible mediators of SERT downregulation, we treated cultured colonic epithelial cells (Caco2) with conditioned medium from activated human lymphocytes. Application of the conditioned medium caused a decrease in fluoxetine-sensitive [3H]5-HT uptake. Individual proinflammatory agents were then tested for their ability to affect uptake. Cells were treated for 48 or 72 h with PGE2 (10 μM), IFN-γ (500 ng/ml), TNF-α (50 ng/ml), IL-12 (50 ng/ml), or the nitric oxide-releasing agent S-nitrosoglutathione (GSNO; 100 μM). [3H]5-HT uptake was then measured. Neither PGE nor IL-12 had any effect on [3H]5-HT uptake, and GSNO increased uptake. However, after 3-day incubation, both TNF-α and IFN-γ elicited significant decreases in SERT function. Neither TNF-α nor IFN-γ were cytotoxic when used for this period of time and at these concentrations. These two cytokines also induced decreases in SERT mRNA and protein levels. By altering SERT expression, TNF-α and IFN-γ could contribute to the altered motility and expression seen in vivo in ulcerative colitis or irritable bowel syndrome.


2020 ◽  
Author(s):  
Huimin Huang ◽  
Mingxing Li ◽  
Yi Wang ◽  
Xiaoxiao Wu ◽  
Jing Shen ◽  
...  

Abstract BackgroundLongan is the fruit of Dimocarpus longan Lour. and the longan arillus has been used in traditional Chinese medicine for thousands of years possessing various health benefits. However, the excessive intake of longan is found in daily life to cause “shanghuo” syndrome. Shanghuo has been linked to increased disease susceptibility. The present study thus aimed to investigate the toxicological outcomes after excess longan treatment.MethodsLongan extract at a normal dosage of 4 g/kg and two excess dosages of 8 and 16 g/kg was orally administered to normal C57BL/6J mice for 2 weeks. Another set of study used C57BL/6J mice with dextran sulfate sodium (DSS)-induced colitis by giving mice drinking water containing 3.5% DSS for 5 consecutive days. Mouse feces were collected at the end of experiments for microbial analysis by 16S rRNA sequencing. After mice were sacrificed, colonic contents were collected for measurement of short-chain fatty acid (SCFA) contents. Colon tissue was used for histopathological observation after H&E staining, detection of ZO-1 protein expression by western blot, analysis of TNF-α and IL-6 gene expression, and detection of apoptotic cells by TUNEL assay. Serum was collected for analysis of LPS, TNF-α and IL-6 by ELISA method.ResultsIn normal mice, repeated longan intake at excess doses, but not the normal dose, increased infiltration of inflammatory cells, elevated serum levels of TNF-α and IL-6 and reduced production of SCFAs. In DSS-induced colitic mice, longan intake at 4 g/kg did not promoted colitis in mice, while excess longan (8 or 16 g/kg) enhanced colitis in mice, showing increased inflammation (shorter colon length, upregulated IL-1β and TNF-α), more serious histological abnormalities, increased gut permeability (decreased ZO-1 protein expression), and increased epithelia injury (increased TUNEL-positive cells) when compared to DSS alone. Excess longan induced a significant reduction of microbial diversity in colitic mice, accompanied with aggravated alterations of DSS-associated bacteria including the increase of Proteobacteria phylum and genera of Bacteroides, Akkermansia, Turicibacter and Escherchia-Shigella, and the decrease of norank_f__Muribaculaceae. The changed microbial compositions were accompanied with decreased SCFAs when longan was supplemented with DSS. The altered microbial communities and SCFAs were tightly correlated with aggravated colon injury in mice.ConclusionsExcess longan intake disturbs gut homeostasis and aggravates colitis via promoting inflammation and altering gut microbe compositions and associated metabolism in mice. Our findings warrant rational longan arillus consumption as a dietary supplement among general population and suggest contraindications such as inflammatory bowel disease of using longan as an herbal medicine.


Author(s):  
Anna-Karin Norlin ◽  
Susanna Walter ◽  
Adriane Icenhour ◽  
Åsa V. Keita ◽  
Sigrid Elsenbruch ◽  
...  

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