scholarly journals Gastrointestinal: Mycobacterium avium paratuberculosis and Crohn's disease

2005 ◽  
Vol 20 (12) ◽  
pp. 1943-1943 ◽  
Author(s):  
RB Gearry ◽  
JM Aitken ◽  
RL Roberts ◽  
S Ismail ◽  
J Keenan ◽  
...  
2003 ◽  
Vol 124 (4) ◽  
pp. A321
Author(s):  
Dimitrios Polymeros ◽  
Dimitrios P. Bogdanos ◽  
Ajeya Shetty ◽  
Roser Vega ◽  
Cinzia Papadia ◽  
...  

2010 ◽  
Vol 24 (10) ◽  
pp. 619-624 ◽  
Author(s):  
Greg Rosenfeld ◽  
Brian Bressler

Mycobacterium avium paratuberculosis(MAP) is an obligate intracellular organism that has frequently been associated with Crohn’s disease (CD). Because CD is a chronic inflammatory condition, many researchers have speculated that an infectious agent must be the cause of CD. MAP has often been proposed to be one such agent; however, despite considerable research, the evidence remains inconclusive. Higher levels of MAP have been found in the tissues and blood of CD patients than in controls, forming the foundation for much of the research into the role of MAP in CD and the primary argument in support of a causative role for MAP in CD. MAP is a slow-growing and fastidious organism that is difficult to grow in culture and, therefore, challenging to detect in patients. As a result, there has been variability in the results of studies attempting to detect the presence of MAP in CD patients, and considerable controversy over whether this organism has a causative role in the etiology of CD. Two main hypotheses exist with respect to the role of MAP in CD. The first is that MAP is a principal cause of CD, while the second is that MAP is more prevalent because of the immune dysfunction seen in CD but does not play a causative role. Clinicians are often faced with questions regarding the role of this organism and the need to treat it. The present article attempts to provide an overview of the controversy including the nature of the mycobacterium, the difficulty in detecting it, the use of antimycobacterial agents to treat it and the effect of immunosuppressive agents – all from a clinician’s perspective. Although the role of MAP in CD remains controversial and an area of considerable research, it is currently only of academic interest because there is no clinically useful test to identify the presence of the organism, and no evidence to support the use of antibiotics to eradicate it for the treatment of CD.


2017 ◽  
Vol 4 (3) ◽  
Author(s):  
Harry A. Oken ◽  
Paul G. Saleeb ◽  
Robert R. Redfield ◽  
Stephen C. Schimpff

Abstract We present and discuss a 30-month investigation of a patient that presented with abdominal pain, postprandial diarrhea, bloating, and night sweats and was treated for Crohn’s disease without significant improvement. The patient underwent an ileocecetomy with removal of an atonic segment with resolution of functional gastrointestinal symptoms, but profound night sweats continued postoperatively. The patient was presumptively treated for a mixed mycobacterial infection, blood cultures later grew Mycobacterium avium paratuberculosis (MAP), and she improved over time. We discuss MAP and its possible relationship to Crohn’s disease.


2021 ◽  
Vol 9 (5) ◽  
pp. 1086
Author(s):  
Dania AlQasrawi ◽  
Ebraheem Naser ◽  
Saleh A. Naser

Recently, we reported that nicotine plays a role in the failure of the macrophage in the clearance of Mycobacterium avium subspecies paratuberculosis (MAP) during infection in Crohn’s disease smokers. We also demonstrated that nicotine enhances macrophages cellular survival during MAP infection. Blocking α7 nicotinic acetylcholine receptor (α7nAChR) with the pharmacological antagonist—mecamylamine—subverted the anti-inflammatory effect of nicotine in macrophages. Yet, it is still unknown how α7nAChR is involved in the modulation of the macrophage response during MAP infection. Here, we studied the mechanistic role of nicotine-α7nAChR interaction in modulating NF-ĸB survival pathway, autophagy, and effect on cathelicidin production in MAP-infected macrophages using THP-1 cell lines. Our results showed that nicotine upregulated α7nAChR expression by 5-folds during MAP infection compared to controls. Bcl-2 expression was also significantly increased after nicotine exposure. Moreover, Nicotine inhibited autophagosome formation whereas infection with MAP in absence of nicotine has significantly increased LC-3b in macrophages. Nicotine also further upregulated NF-ĸB subunits expression including Rel-B and p100, and increased nuclear translocation of p52 protein. We also discovered that cathelicidin production was significantly suppressed in MAP-infected macrophages, treatment with nicotine showed no effect. Overall, the study provides new insight toward understanding the cellular role of nicotine through α7nAChR/NF-ĸB p100/p52 signaling pathway in inducing anti-apoptosis and macrophage survival during MAP infection in Crohn’s disease smokers.


2006 ◽  
Vol 131 (1) ◽  
pp. 85-96 ◽  
Author(s):  
Dimitrios Polymeros ◽  
Dimitrios P. Bogdanos ◽  
Richard Day ◽  
Dimitryi Arioli ◽  
Diego Vergani ◽  
...  

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