scholarly journals Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10644
Author(s):  
Hai Liang ◽  
Miao Yang ◽  
Cheng Zeng ◽  
Wei Wu ◽  
Liying Zhao ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Body Weight ◽  
Bowel Disease ◽  
Perfluorooctane Sulfonate ◽  
The Body ◽  
Crypt Depth ◽  
Proximal Duodenum ◽  
Amyloid A ◽  
Inflammatory Bowel ◽  
Pfos Exposure

Background Perfluorooctane sulfonate (PFOS), a type of perfluorinated compounds (PFCs), can induce various organ toxicity, including hepatomegaly, immunotoxicity, and gut microbiota disorder. PFCs have been associated with inflammatory bowel disease (IBD). Yet, whether PFOS exposure causes IBD-like disorder and the underlying mechanism remains undefined. Here, we investigated the influence of PFOS exposure on the development of IBD-like disorder in rats. Methods Sprague-Dawley rats were intraperitoneally injected with PFOS (1 or 10 mg/kg) or normal saline (NS) every other day for 15 days. Body weight, serum concentrations of serum amyloid A (SAA) and high sensitivity C reactive protein (hsCRP) were measured. Pathological assessments of villi height and crypt depth in the proximal duodenum and jejunum were performed using H&E staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to assay cell apoptosis in the jejunum. The infiltration of inflammatory cells and cytokines in the jejunum were detected by immunohistochemistry analysis. Results PFOS (10 mg/kg) significantly increased the body weight, SAA and hsCRP, whereas no significant differences were observed in PFOS 1 mg/kg group of rats. The villi height and crypt depth in the proximal duodenum and jejunum were significantly reduced upon PFOS exposure. PFOS induced higher histopathological score in intestinal tissues compared to NS. Notably, TUNEL-positive cells were significantly higher in the jejunum upon PFOS exposure. Further, neutrophil and macrophage accumulated, and inflammatory cytokines infiltration were also remarkably increased in rats exposed to PFOS. Conclusion PFOS induces IBD-like phenotypes in rats, with associated inflammatory infiltration to intestinal.

scholarly journals Fecal Lipocalin-2 as a Sensitive and Noninvasive Biomarker in the TNBS Crohn’s Inflammatory Bowel Disease Model

2016 ◽  
Vol 44 (8) ◽  
pp. 1084-1094 ◽  
Author(s):  
Heidi Hsieh ◽  
Jeffrey Morin ◽  
Cyndi Filliettaz ◽  
Rao Varada ◽  
Shelby LaBarre ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Body Weight ◽  
Bowel Disease ◽  
Saline Water ◽  
Disease Model ◽  
Recovery Phase ◽  
Lipocalin 2 ◽  
Trinitrobenzenesulfonic Acid ◽  
Noninvasive Biomarker ◽  
Inflammatory Bowel

Colitis induced by 2,4,6-Trinitrobenzenesulfonic acid (TNBS) has been used as a model for Crohn’s disease (CD) of inflammatory bowel disease (IBD). Lipocalin-2 (Lcn-2) is an emerging and clinically relevant biomarker of IBD. We investigated the performance of serum and fecal Lcn-2 in the TNBS model of colitis. Female, 7-week-old, BALB/c mice were administered intrarectally phosphate-buffered saline/water or 30% ethanol (vehicle control groups) for 5 days or TNBS for 5 days followed by a 28-day recovery phase. Serum and fecal levels of Lcn-2 were quantified, and effects on body weight, clinical scores, colon weight and length, gross pathology, and histopathology were investigated. Increased serum Lcn-2 levels correlated only with marked to severe inflammation. A clear differentiation in Lcn-2 fecal levels between TNBS-treated and vehicle-treated control mice was most noticeable on days 2 and 3. There was a strong correlation between body weight change, histopathologic scores of inflammation, and/or fecal Lcn-2 levels on days 2 and 5. Both serum and fecal Lcn-2 levels declined over time as the colonic mucosa recovered. Fecal Lcn-2 was found to be a more sensitive biomarker (vs. serum Lcn-2) and was able to discriminate mild, moderate, and severe colonic inflammation.

HEALING THROUGH CYTOKINE REGULATION IN DNBS INDUCED INFLAMMATORY BOWEL DISEASE IN RATS BY HOLARRHENA ANTIDYSENTERICA

INDIAN DRUGS ◽  
2016 ◽  
Vol 53 (08) ◽  
pp. 57-64
Author(s):  
S. Johari ◽  
◽  
C. Joshi ◽  
T. Gandhi
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Body Weight ◽  
Bowel Disease ◽  
Stool Consistency ◽  
Cytokine Gene ◽  
Group Iii ◽  
Group I ◽  
Holarrhena Antidysenterica ◽  
Inflammatory Bowel

The objective of the study was to ascertain antioxidant, anti-inflammatory and cytokine gene regulation activity of Holarrhena antidysenterica (HA) in dinitrobenzene sulfonic acid (DNBS) induced inflammatory bowel disease (IBD) in rats. Sprague Dawley rats were divided into 6 groups, Group I (normal), Group II (50% ethanol intracolonically on 11th day), Group III (Model). Group IV to VI were given standard drug 5-amino salicylic acid (5-ASA) (100mg/kg) and hydromethanolic extract of Holarrhena antidysenterica (MEHA) 450 mg/kg and MEHA 600 mg/kg respectively for 18 days once p.o. Colitis was induced with DNBS (180mg/kg in 50% ethanol) intracolonically in animals of Group III-VI on 11th day. Body weight, food & water intake and stool consistency of each group was noted. On 18th day, blood was collected for cortisol estimation. Colon length and weight was measured. Cytokine gene expression studies of colon in group I, II, III, IV and VI was done using Real Time RT-PCR. Colon histopathology, Disease Activity Index (DAI) and Colon Mucosal Disease index (CMDI) parameters were studied. Nitric oxide (NO), malondialdehyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) were estimated in colon homogenate. DNBS model control showed significant reduction in body weight, water and food intake, SOD, colon length and significant increase in stool consistency, colon weight, MDA, MPO, NO, CMDI, DAI, cortisol, IL-4, IL-6, IL-12 and IFN-gamma cytokines gene expression. Pretreatment with 5-ASA (100mg/kg) and MEHA (450 and 600 mg/kg) significantly reversed the above. MEHA reduced severity of IBD induced by DNBS through its anti-inflammatory, antioxidant and gene modulatory activity.

scholarly journals Going Beyond Bacteria: Uncovering the Role of Archaeome and Mycobiome in Inflammatory Bowel Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Yashar Houshyar ◽  
Luca Massimino ◽  
Luigi Antonio Lamparelli ◽  
Silvio Danese ◽  
Federica Ungaro
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
The Body ◽  
Inflammatory Conditions ◽  
Relapsing Remitting ◽  
Health And Disease ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Inflammatory Bowel Disease (IBD) is a multifaceted class of relapsing-remitting chronic inflammatory conditions where microbiota dysbiosis plays a key role during its onset and progression. The human microbiota is a rich community of bacteria, viruses, fungi, protists, and archaea, and is an integral part of the body influencing its overall homeostasis. Emerging evidence highlights dysbiosis of the archaeome and mycobiome to influence the overall intestinal microbiota composition in health and disease, including IBD, although they remain some of the least understood components of the gut microbiota. Nonetheless, their ability to directly impact the other commensals, or the host, reasonably makes them important contributors to either the maintenance of the mucosal tissue physiology or to chronic intestinal inflammation development. Therefore, the full understanding of the archaeome and mycobiome dysbiosis during IBD pathogenesis may pave the way to the discovery of novel mechanisms, finally providing innovative therapeutic targets that can soon implement the currently available treatments for IBD patients.

Dysbiosis in Microbiome Leading to Colitis-Associated Cancer

2021 ◽  
pp. 142-169
Author(s):  
Priyamvada Priyamvada
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Risk Factor ◽  
Bowel Disease ◽  
Gut Microbiome ◽  
The Body ◽  
Physiological Processes ◽  
Microbiome Diversity ◽  
The World ◽  
Inflammatory Bowel

Colitis-associated cancers are a metastatic form of inflammatory bowel disease considered a vital health associated risk factor causing the death of approximately five lacs people every year throughout the world. There are trillions of bacteria that are associated with our gut as a part of our healthy microbiome. The microbiota plays a plethora of important role in determining the normal physiological processes of the cells and, subsequently, the body. The imbalance in microbiome diversity (dysbiosis) due to abnormal dietary habitats, hectic lifestyle, and other factors thus alters the normal physiological processes of the body, thereby causing several chronic diseases. Therefore, it is essential to maintain the homeostasis between the host and their gut microbiome. So, based on the facts mentioned above, this chapter is entirely devoted to providing an overview of colitis-associated cancer and their relation with the dysbiosis of a healthy microbiome. Moreover, the mechanism involved in the development of colorectal cancer and its preventive insights has also been addressed.

scholarly journals Pathophysiological Roles of PPARγin Gastrointestinal Epithelial Cells

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Brian M. Necela ◽  
E. Aubrey Thompson
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Epithelial Cells ◽  
Bowel Disease ◽  
The Body ◽  
Published Data ◽  
Physiological Functions ◽  
Considerable Controversy ◽  
Inflammatory Bowel ◽  
Gastrointestinal Epithelium

Although the highest levels of PPARγexpression in the body have been reported in the gastrointestinal epithelium, little is known about the physiological functions of that receptor in the gut. Moreover, there is considerable controversy concerning the effects of thiazolidinedione PPARγagonists on the two major diseases of the gastrointestinal track: colorectal cancer and inflammatory bowel disease. We will undertake to review both historical and recently published data with a view toward summarizing what is presently known about the roles of PPARγin both physiological and pathological processes in the gastrointestinal epithelium.

scholarly journals Tryptophan-kynurenine metabolism: a link between the gut and brain for depression in inflammatory bowel disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Li-Ming Chen ◽  
Chun-Hui Bao ◽  
Yu Wu ◽  
Shi-Hua Liang ◽  
Di Wang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Metabolic Pathway ◽  
Bowel Disease ◽  
The Body ◽  
Metabolic Enzyme ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Bloody Stools ◽  
The Relationship

AbstractInflammatory bowel disease (IBD), which mainly includes ulcerative colitis (UC) and Crohn's disease (CD), is a group of chronic bowel diseases that are characterized by abdominal pain, diarrhea, and bloody stools. IBD is strongly associated with depression, and its patients have a higher incidence of depression than the general population. Depression also adversely affects the quality of life and disease prognosis of patients with IBD. The tryptophan-kynurenine metabolic pathway degrades more than 90% of tryptophan (TRP) throughout the body, with indoleamine 2,3-dioxygenase (IDO), the key metabolic enzyme, being activated in the inflammatory environment. A series of metabolites of the pathway are neurologically active, among which kynerunic acid (KYNA) and quinolinic acid (QUIN) are molecules of great interest in recent studies on the mechanisms of inflammation-induced depression. In this review, the relationship between depression in IBD and the tryptophan-kynurenine metabolic pathway is overviewed in the light of recent publications.

scholarly journals Ostomy creation with fewer sutures using tissue adhesives (cyanoacrylates) in inflammatory bowel disease: a pilot study

2018 ◽  
Vol 100 (3) ◽  
pp. 190-193
Author(s):  
M Uchino ◽  
H Ikeuchi ◽  
T Bando ◽  
H Sasaki ◽  
T Chohno ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Inflammatory Bowel Disease ◽  
Pilot Study ◽  
Adverse Events ◽  
Body Mass ◽  
Bowel Disease ◽  
The Body ◽  
Fistula Formation ◽  
Tissue Adhesives ◽  
Inflammatory Bowel

Introduction Fistula formation around the ostomy site is a stoma-related complication often requiring surgical intervention. This complication may be caused by sutures or may develop as a complication of inflammatory bowel disease. Before conducting a clinical trial, we set out to investigate the safety of ostomy creation with fewer sutures using tissue adhesives in this pilot study. Methods Patients with inflammatory bowel disease who required surgery with ostomy creation at the Hyogo College of Medicine between January 2014 and December 2015 were enrolled. Safety was assessed by evaluating the incidence of stoma-related complications. Ostomy was restricted to loop ileostomy and was created with two sutures and tissue adhesives. Results A total of 14 patients were enrolled. Mean body mass index was 18.9 ± 2.0 kg/m2. There were no cases of ostomy retraction and no severe adverse events were observed. Conclusions This pilot study demonstrates that ostomy creation using tissue adhesives is safe. Although retraction and adverse events were not observed, even in patients with inflammatory bowel disease who generally exhibit delayed wound healing, the body mass index was extremely low in this series. This study does not strongly recommend ostomy creation with tissue adhesives; further studies are needed to clarify the efficacy and safety of the procedure.

scholarly journals The Impact of MicroRNAs during Inflammatory Bowel Disease: Effects on the Mucus Layer and Intercellular Junctions for Gut Permeability

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3358
Author(s):  
Sarah Stiegeler ◽  
Kevin Mercurio ◽  
Miruna Alexandra Iancu ◽  
Sinéad C. Corr
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
The Body ◽  
Proper Function ◽  
Epithelial Barrier ◽  
Mucus Layer ◽  
Gut Permeability ◽  
Epithelial Junctions ◽  
Inflammatory Bowel ◽  
The Impact

Research on inflammatory bowel disease (IBD) has produced mounting evidence for the modulation of microRNAs (miRNAs) during pathogenesis. MiRNAs are small, non-coding RNAs that interfere with the translation of mRNAs. Their high stability in free circulation at various regions of the body allows researchers to utilise miRNAs as biomarkers and as a focus for potential treatments of IBD. Yet, their distinct regulatory roles at the gut epithelial barrier remain elusive due to the fact that there are several external and cellular factors contributing to gut permeability. This review focuses on how miRNAs may compromise two components of the gut epithelium that together form the initial physical barrier: the mucus layer and the intercellular epithelial junctions. Here, we summarise the impact of miRNAs on goblet cell secretion and mucin structure, along with the proper function of various junctional proteins involved in paracellular transport, cell adhesion and communication. Knowledge of how this elaborate network of cells at the gut epithelial barrier becomes compromised as a result of dysregulated miRNA expression, thereby contributing to the development of IBD, will support the generation of miRNA-associated biomarker panels and therapeutic strategies that detect and ameliorate gut permeability.

Sign in / Sign up

Export Citation Format

Share Document