scholarly journals Dietary Red Meat Adversely Affects Disease Severity in a Pig Model of DSS-Induced Colitis Despite Reduction in Colonic Pro-Inflammatory Gene Expression

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1728
Author(s):  
Tina S. Nielsen ◽  
Marlene Fredborg ◽  
Peter K. Theil ◽  
Yuan Yue ◽  
Lærke V. Bruhn ◽  
...  
Keyword(s):  
Control Diet ◽  
Clinical Signs ◽  
Epidemiologic Studies ◽  
Red Meat ◽  
Mucosal Inflammation ◽  
Negative Effects ◽  
Increased Risk ◽  
Meat Diet ◽  
Inflammatory Bowel ◽  
Systemic Health

Diet plays a substantial role in the pathogenesis and management of ulcerative colitis (UC), and epidemiologic studies indicate an association between red meat intake and increased risk of UC development. Therefore, we evaluated the effect of a red meat diet on dextran sulfate sodium (DSS)-induced colitis in pigs. Weaned pigs (42 days old) were fed either a control diet or a diet substituted with 15% minced, cooked and dried beef from experimental day 0 to 14. From day 14 to 18, half of the pigs on each diet received a daily oral dose of DSS. Dietary red meat aggravated the severity of colitis based on clinical signs of disease (negative performance score) and histopathological parameters in the colon such as erosion/ulceration and the overall inflammation score but no negative effects were observed on systemic health or small intestinal permeability. Importantly, dietary meat also caused a potential beneficial reduction in the colonic expression of the pro-inflammatory cytokines IL-17A and IL-6, the pro-inflammatory enzyme PTGS2 and in the chemokine IL-8. The present study emphasizes the potential of diet to modulate mucosal inflammation and that a red meat diet might be a risk factor for the development of inflammatory bowel disease.

scholarly journals Colorectal Cancer in Inflammatory Bowel Disease

2020 ◽  
Vol 33 (05) ◽  
pp. 305-317
Author(s):  
Martina Nebbia ◽  
Nuha A. Yassin ◽  
Antonino Spinelli
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Severe Disease ◽  
Critical Role ◽  
Mucosal Inflammation ◽  
Surgical Approaches ◽  
Increased Risk ◽  
Significant Difference ◽  
Inflammatory Bowel

AbstractPatients with inflammatory bowel disease (IBD) are at an increased risk for developing colorectal cancer (CRC). However, the incidence has declined over the past 30 years, which is probably attributed to raise awareness, successful CRC surveillance programs and improved control of mucosal inflammation through chemoprevention. The risk factors for IBD-related CRC include more severe disease (as reflected by the extent of disease and the duration of poorly controlled disease), family history of CRC, pseudo polyps, primary sclerosing cholangitis, and male sex. The molecular pathogenesis of inflammatory epithelium might play a critical role in the development of CRC. IBD-related CRC is characterized by fewer rectal tumors, more synchronous and poorly differentiated tumors compared with sporadic cancers. There is no significant difference in sex distribution, stage at presentation, or survival. Surveillance is vital for the detection and subsequently management of dysplasia. Most guidelines recommend initiation of surveillance colonoscopy at 8 to 10 years after IBD diagnosis, followed by subsequent surveillance of 1 to 2 yearly intervals. Traditionally, surveillance colonoscopies with random colonic biopsies were used. However, recent data suggest that high definition and chromoendoscopy are better methods of surveillance by improving sensitivity to previously “invisible” flat dysplastic lesions. Management of dysplasia, timing of surveillance, chemoprevention, and the surgical approaches are all areas that stimulate various discussions. The aim of this review is to provide an up-to-date focus on CRC in IBD, from laboratory to bedside.

scholarly journals Calcium carbonate suppresses haem toxicity markers without calcium phosphate side effects on colon carcinogenesis

2010 ◽  
Vol 105 (3) ◽  
pp. 384-392 ◽  
Author(s):  
Ossama Allam ◽  
Diane Bahuaud ◽  
Sylviane Taché ◽  
Nathalie Naud ◽  
Denis E. Corpet ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Calcium Carbonate ◽  
Calcium Phosphate ◽  
Metal Ion ◽  
Control Diet ◽  
Red Meat ◽  
Preneoplastic Lesions ◽  
Increased Risk ◽  
High Calcium

Red meat intake is associated with an increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions, aberrant crypt foci (ACF), in the colon of rats. We have also shown that dietary calcium phosphate inhibits haemin-induced promotion and normalises faecal lipoperoxides and cytotoxicity. Unexpectedly, high-calcium phosphate control diet-fed rats had more preneoplastic lesions in the colon than low-Ca control diet-fed rats. The present study was designed to find a Ca supplementation with no adverse effect, by testing several doses and types of Ca salts. Onein vitrostudy and two short-term studies in rats identified calcium carbonate as the most effective Ca salt to bind haemin vitroand to decrease faecal biomarkers previously associated with increased carcinogenesis: faecal water cytotoxicity and thiobarbituric acid-reactive substances. A long-term carcinogenesis study in dimethylhydrazine-injected rats demonstrated that a diet containing 100 μmol/g calcium carbonate did not promote ACF, in contrast with a previously tested calcium phosphate diet. The results suggest that calcium carbonate, and not calcium phosphate, should be used to reduce haem-associated colorectal cancer risk in meat eaters. They support the concept that the nature of the associated anion to a protective metal ion is important for chemoprevention.

scholarly journals Dichotomous roles of neutrophils in modulating pathogenic and repair processes of inflammatory bowel diseases

2021 ◽  
Author(s):  
Huimin Chen ◽  
Xiaohan Wu ◽  
Chunjin Xu ◽  
Jian Lin ◽  
Zhanju Liu
Keyword(s):  
Immune Cells ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Mucosal Inflammation ◽  
Repair Processes ◽  
Microbial Invasion ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Abstract Neutrophils are considered as complex innate immune cells and play a critical role in maintaining intestinal mucosal homeostasis. They exert robust pro-inflammatory effects and recruit other immune cells in the acute phase of pathogen infection and intestinal inflammation, but paradoxically, they also limit exogenous microbial invasion and facilitate mucosal restoration. Hyperactivation or dysfunction of neutrophils results in abnormal immune responses, leading to multiple autoimmune and inflammatory diseases including systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel diseases (IBD). As a refractory intestinal inflammatory disease, the pathogenesis and progression of IBD are associated with complicated immune response processes in which neutrophils are profoundly involved. However, the consensus on potential roles of neutrophils in modulating pathogenic and repair processes of IBD remains not fully understood. Accumulated infiltrating neutrophils cross the epithelial barrier and contribute to microbial dysbiosis, aggravated intestinal architectural damage, compromised resolution of intestinal inflammation and increased risk of thrombosis during IBD. Paradoxically, activated neutrophils are also associated with effective elimination of invaded microbiota, promoted angiogenesis and tissue restoration of gut mucosa in IBD. Here, we discuss the beneficial and detrimental roles of neutrophils in the onset and resolution of intestinal mucosal inflammation and provide a precise overview of neutrophil functions in the pathogenesis of IBD.

scholarly journals Beef meat promotion of dimethylhydrazine-induced colorectal carcinogenesis biomarkers is suppressed by dietary calcium

2008 ◽  
Vol 99 (5) ◽  
pp. 1000-1006 ◽  
Author(s):  
Fabrice Pierre ◽  
Raphaëlle Santarelli ◽  
Sylviane Taché ◽  
Françoise Guéraud ◽  
Denis E. Corpet
Keyword(s):  
Colorectal Cancer ◽  
Olive Oil ◽  
Control Diet ◽  
Red Meat ◽  
Aberrant Crypt Foci ◽  
Colorectal Carcinogenesis ◽  
Beef Meat ◽  
Antioxidant Agents ◽  
Increased Risk ◽  
High Calcium

Red meat consumption is associated with increased risk of colorectal cancer. We have previously shown that haemin, Hb and red meat promote carcinogen-induced preneoplastic lesions: aberrant crypt foci (ACF) and mucin-depleted foci (MDF) in rats. We have also shown that dietary Ca, antioxidant mix and olive oil inhibit haemin-induced ACF promotion, and normalize faecal lipoperoxides and cytotoxicity. Here we tested if these strategies are effective also against red meat promotion in dimethylhydrazine-induced rats. Three diets with 60 % beef meat were supplemented with calcium phosphate (31 g/kg), antioxidant agents (rutin and butylated hydroxyanisole, 0·05 % each) and olive oil (5 %). ACF, MDF, faecal water cytotoxicity, thiobarbituric acid reactive substances (TBARS) and urinary 1,4-dihydroxynonane mercapturic acid (DHN-MA) were measured. Beef meat diet increased the number of ACF (+30 %) and MDF (+100 %) (P < 0·001), which confirms our previous findings. Promotion was associated with increased faecal water TBARs ( × 4) and cytotoxicity ( × 2), and urinary DHN-MA excretion ( × 15). Ca fully inhibited beef meat-induced ACF and MDF promotion, and normalized faecal TBARS and cytotoxicity, but did not reduce urinary DHN-MA. Unexpectedly, high-calcium control diet-fed rats had more MDF and ACF in the colon than low-Ca control diet-fed rats. Antioxidant mix and olive oil did not normalize beef meat promotion nor biochemical factors. The results confirm that haem causes promotion of colon carcinogenesis by red meat. They suggest that Ca can reduce colorectal cancer risk in meat-eaters. The results support the concept that toxicity associated with the excess of a useful nutrient may be prevented by another nutrient.

A rapid method for the direct identification of paramyxovirus in canine CSF by ultracentrifugation and negative staining as a rule out for distemper

1990 ◽  
Vol 48 (3) ◽  
pp. 594-595
Author(s):  
W.L. Steffens ◽  
M.B. Ard ◽  
C.E. Greene ◽  
A. Jaggy
Keyword(s):  
Subacute Sclerosing Panencephalitis ◽  
Clinical Signs ◽  
Viral Disease ◽  
Etiologic Agent ◽  
Mucosal Inflammation ◽  
Worldwide Distribution ◽  
Negative Stain ◽  
Viral Particles ◽  
Systemic Manifestations ◽  
Rule Out

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.

Thrombosis in IBD in the Era of JAK Inhibition

2020 ◽  
Vol 22 (1) ◽  
pp. 126-136
Author(s):  
Virginia Solitano ◽  
Gionata Fiorino ◽  
Ferdinando D’Amico ◽  
Laurent Peyrin-Biroulet ◽  
Silvio Danese
Keyword(s):  
Small Molecules ◽  
Arterial Thrombosis ◽  
Protective Role ◽  
Jak Inhibitors ◽  
Thrombotic Risk ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Thrombotic Complications ◽  
Inflammatory Bowel ◽  
Inflammatory Effect

: Patients with inflammatory bowel diseases (IBD) have an increased risk of thrombosis. The interaction between inflammation and coagulation has been extensively studied. It is well-known that some drugs can influence the haemostatic system, but several concerns on the association between therapies and increased risk of thrombosis remain open. While biologics seem to have a protective role against thrombosis via their anti-inflammatory effect, some concerns about an increased risk of thrombosis with JAK inhibitors have been raised. We conducted a literature review to assess the association between biologics/small molecules and venous/arterial thrombotic complications. An increased risk of venous and arterial thrombosis was found in patients treated with corticosteroids, whereas anti-TNF were considered protective agents. No thromboembolic adverse event was reported with vedolizumab and ustekinumab. In addition, thromboembolic events rarely occurred in patients with ulcerative colitis (UC) after therapy with tofacitinib. The overall risk of both venous and arterial thrombosis was not increased based on the available evidence. Finally, in the era of JAK inhibitors, treatment should be individualized by evaluating the pre-existing potential thrombotic risk balanced with the intrinsic risk of the medication used.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

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