scholarly journals Paratuberculosis: A Potential Zoonosis and a Neglected Disease in Africa

2020 ◽  
Vol 8 (7) ◽  
pp. 1007 ◽  
Author(s):  
Julius Boniface Okuni ◽  
Sören Hansen ◽  
Kamal H. Eltom ◽  
ElSagad Eltayeb ◽  
Ahmad Amanzada ◽  
...  

The Mycobacterium avium subspecies paratuberculosis (MAP) is the causative agent of paratuberculosis, which is an economically important disease of ruminants. The zoonotic role of MAP in Crohn’s disease and, to a lesser extent, in ulcerative colitis, the two major forms of idiopathic inflammatory bowel disease (IIBD), has been debated for decades and evidence continues to mount in support of that hypothesis. The aim of this paper is to present a review of the current information on paratuberculosis in animals and the two major forms of IIBD in Africa. The occurrence, epidemiology, economic significance and “control of MAP and its involvement IIBD in Africa” are discussed. Although the occurrence of MAP is worldwide and has been documented in several African countries, the epidemiology and socioeconomic impacts remain undetermined and limited research information is available from the continent. At present, there are still significant knowledge gaps in all these areas as far as Africa is concerned. Due to the limited research on paratuberculosis in Africa, in spite of growing global concerns, it may rightfully be considered a neglected tropical disease with a potentially zoonotic role.

2013 ◽  
Vol 33 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Feti Tulubas ◽  
Rafet Mete ◽  
Meltem Oznur ◽  
Birol Topcu

Summary Metabolic changes resulting from obesity, insulin insensitivity, and imbalances in hormones such as adiponectin, leptin, resistin, apelin and visfatin, which are derived from white adipose tissue-derived hormone, are directly linked to both colon cancer (CC) and inflammatory bowel diseases increasing tissue-derived risk. We conducted this study to evaluate the relationship between the circulating concentrations of adiponectin, leptin, resistin, apelin and visfatin and colon adenoma and CC. Our study included 90 participants aged >18 years who were divided into three groups: colon cancer, adenoma and control. The serum concentrations of the investigated adipohormones were measured with ELISA in 30 patients with colon adenoma, 30 with CC and 30 controls with no colon pathology. Demographic, anthropometric, metabolic and hormonal parameters were also recorded. The group means were compared by using one-way analysis of variance (ANOVA). Dual comparisons between groups were analyzed with the Tukey test. Pearson correlation coefficient was used to determine the relation between continuous variables. Adiponectin and leptin levels in patients with adenomas (p<0.000; p<0.000, respectively) and CC (p<0.000; p<0.000, respectively) were lower than in controls. Apelin level in patients with CC (p<0.000; p<0.000, respectively) was lower than in patients with adenomas and in controls. Resistin and visfatin levels in patients with CC (p<0.000; p<0.000, respectively) were higher than in patients with adenomas and in controls.


2020 ◽  
Vol 21 (16) ◽  
pp. 5801 ◽  
Author(s):  
Dania AlQasrawi ◽  
Ahmad Qasem ◽  
Saleh A. Naser

Cigarette smoke (CS) has adverse effects in patients with Crohn’s disease (CD), an inflammatory bowel disease (IBD) that has been associated with microbial infection, immuno-dysregulation, and mucosal dysfunction. However, CS seems to provide relief and protection to patients with another IBD known as ulcerative colitis (UC). These two subsets are featured as M1- and M2-mediated responses, respectively. Nicotine is the most active, addictive, and studied ingredient in CS. The mechanism of how nicotine and/or other CS ingredients induce pro-inflammatory or anti-inflammatory phenotypes in IBD patients remains under investigation. Our most recent in vitro nicotine study provided significant insights toward understanding the contradictory effects of nicotine on IBD patients, and it elucidated the mechanistic role of α7nAChR in modulation of macrophages in tobacco smokers. Shifting the beneficial effect of nicotine to a harmful outcome in CD patients was linked to a nicotine-microbe interaction that supports a microbial etiology in CD pathogenesis. Among the most debated pathogens in CD etiology is Mycobacterium avium subspecies paratuberculosis (MAP). Other studies associated nicotine with upregulation of miR-124 expression in macrophages, which led to anti-inflammatory response. This review discusses published work on the role of nicotine in modulation of the innate immune response and subsequent signaling in macrophages in IBD subsets.


Author(s):  
Kimberley W J van der Sloot ◽  
Michiel D Voskuil ◽  
Tjasso Blokzijl ◽  
Annemieke Dinkla ◽  
Lars Ravesloot ◽  
...  

Abstract Background The role of Mycobacterium avium subspecies paratuberculosis (MAP) in inflammatory bowel disease (IBD), especially Crohn’s disease (CD) is controversial due conflicting results, lack of reproducibility and standardized tests. The current study focuses on the role of MAP in disease progression and genetic susceptibility as MAP is likely one of many factors involved in the complex pathogenesis of IBD, potentially affecting a subgroup depending on genetic susceptibility. Methods Serum from 812 patients was evaluated with seven immunoglobulin (Ig) isotype-specific serology tests assessing humoral response to three different MAP antigens. For each of these in total 21 tests, the intra-assay and inter-assay coefficients were used to evaluate test accuracy. Reliable assays were subsequently analyzed in relation to disease characteristics and need for biological therapy/surgery. Genome wide genotyping was available for all participants. Genetic determinants of humoral response to MAP antigens were evaluated using genome-wide association analysis and polygenic risk scores (PRS). Results High IgA or IgM response to MAP2609 was associated with increased use of biological therapy in CD and UC (odds ratio 2.69; 95% confidence interval 1.44-5.01; 2.60, 1.46-4.64, respectively). No associations were seen for risk of surgery (p-values&gt;0.29). We could not identify genetic determinants nor polygenic risk scores for MAP response with genome-wide significance. Conclusions Extensive assays for serological response to MAP were evaluated using stringent criteria for reliability. Increased IgA and IgM response to MAP antigens was seen in patients exposed to biological therapy, while no genetic determinants underlying this humoral response were found.


Author(s):  
Christopher J. Tyler ◽  
Mauricio Guzman ◽  
Luke R. Lundborg ◽  
Shaila Yeasmin ◽  
Nadia Zgajnar ◽  
...  

AbstractT and B cells employ integrin α4β7 to migrate to intestine under homeostatic conditions. Whether those cells differentially rely on α4β7 for homing during inflammatory conditions has not been fully examined. This may have implications for our understanding of the mode of action of anti-integrin therapies in inflammatory bowel disease (IBD). Here, we examined the role of α4β7 integrin during chronic colitis using IL-10−/− mice, β7-deficient IL-10−/−, IgA-deficient IL-10−/− mice, and antibody blockade of MAdCAM-1. We found that α4β7 was predominantly expressed by B cells. β7 deficiency and MAdCAM-1 blockade specifically depleted antibody secreting cells (ASC) (not T cells) from the colonic LP, leading to a fecal pan-immunoglobulin deficit, severe colitis, and alterations of microbiota composition. Colitis was not due to defective regulation, as dendritic cells (DC), regulatory T cells, retinaldehyde dehydrogenase (RALDH) expression, activity, and regulatory T/B-cell cytokines were all comparable between the strains/treatment. Finally, an IgA deficit closely recapitulated the clinical phenotype and altered microbiota composition of β7-deficient IL-10−/− mice. Thus, a luminal IgA deficit contributes to accelerated colitis in the β7-deficient state. Given the critical/nonredundant dependence of IgA ASC on α4β7:MAdCAM-1 for intestinal homing, B cells may represent unappreciated targets of anti-integrin therapies.


2016 ◽  
Vol 140 (5) ◽  
pp. 413-428 ◽  
Author(s):  
Hwajeong Lee ◽  
Maria Westerhoff ◽  
Bo Shen ◽  
Xiuli Liu

Context.—Idiopathic inflammatory bowel disease manifests with different clinical phenotypes showing varying behavior and risk for neoplasia. The clinical questions that are posed to pathologists differ depending on phase of the disease and the clinical circumstances. Understanding the clinical aspects of the dynamic disease process will enhance the role of pathology in optimizing the care of patients with inflammatory bowel disease. Objective.—To review clinical and surgical aspects of inflammatory bowel disease that are relevant to practicing pathologists. Data Sources.—The literature was reviewed. Conclusions.—Diagnosis and management of inflammatory bowel disease require an integrated evaluation of clinical, endoscopic, radiologic, and pathologic features. Therefore, close interaction between clinicians and pathologists is crucial. Having this team approach improves understanding of the pertinent clinical and surgical aspects of the disease and assists in the recognition of unusual presentation of variants, as well as mimics of idiopathic inflammatory bowel disease, by pathologists.


2021 ◽  
Vol 10 (9) ◽  
pp. 1935
Author(s):  
Esther Bankole ◽  
Emily Read ◽  
Michael A. Curtis ◽  
Joana F. Neves ◽  
James A. Garnett

Mucins are a family of glycosylated proteins which are the primary constituents of mucus and play a dynamic role in the regulation of the protective mucosal barriers throughout the human body. Ulcerative colitis (UC) is an Inflammatory Bowel Disease (IBD) characterised by continuous inflammation of the inner layer of the large intestine, and in this systematic review we analyse currently available data to determine whether alterations exist in mucin activity in the colonic mucosa of UC patients. Database searches were conducted to identify studies published between 1990 and 2020 that assess the role of mucins in cohorts of UC patients, where biopsy specimens were resected for analysis and control groups were included for comparison. 5497 articles were initially identified and of these 14 studies were systematically selected for analysis, a further 2 articles were identified through citation chaining. Therefore, 16 studies were critically reviewed. 13 of these studies assessed the role of MUC2 in UC and the majority of articles indicated that alterations in MUC2 structure or synthesis had an impact on the colonic mucosa, although conflicting results were presented regarding MUC2 expression. This review highlights the importance of further research to enhance our understanding of mucin regulation in UC and summarises data that may inform future studies.


Author(s):  
R. F. Zeigel ◽  
W. Munyon

In continuing studies on the role of viruses in biochemical transformation, Dr. Munyon has succeeded in isolating a highly infectious human herpes virus. Fluids of buccal pustular lesions from Sasha Munyon (10 mo. old) uiere introduced into monolayer sheets of human embryonic lung (HEL) cell cultures propagated in Eagles’ medium containing 5% calf serum. After 18 hours the cells exhibited a dramatic C.P.E. (intranuclear vacuoles, peripheral patching of chromatin, intracytoplasmic inclusions). Control HEL cells failed to reflect similar changes. Infected and control HEL cells were scraped from plastic flasks at 18 hrs. of incubation and centrifuged at 1200 × g for 15 min. Resultant cell packs uiere fixed in Dalton's chrome osmium, and post-fixed in aqueous uranyl acetate. Figure 1 illustrates typical hexagonal herpes-type nucleocapsids within the intranuclear virogenic regions. The nucleocapsids are approximately 100 nm in diameter. Nuclear membrane “translocation” (budding) uias observed.


Sign in / Sign up

Export Citation Format

Share Document