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International Journal of Clinical & Medical Microbiology Volume 1 (2016), Article ID 1:IJCMM-109, 6 pages
https://doi.org/10.15344/2456-4028/2016/109
Mini Review
Can Crohn's Disease Really be Caused by Mycobacterium avium Subspecies Paratuberculosis?-With My Alternative Theory that Reduction in Commensal Gut Bacteria and Resultant Impaired Inactivation of Digestive Proteases as the Primary Cause

Xiaofa Qin

GI Biopharma Inc, 918 Willow Grove Road, Westfield, NJ 07090, United States
Dr. Xiaofa Qin, GI Biopharma Inc, 918 Willow Grove Road, Westfield, NJ 07090, United States, Tel: +1-908-4637423; E-mail: xiaofa_qin@yahoo.com
06 June 2015; 08 August 2016; 10 August 2016
Qin X (2016) Can Crohn's Disease Really be Caused by Mycobacterium avium Subspecies Paratuberculosis?-With My Alternative Theory that Reduction in Commensal Gut Bacteria and Resultant Impaired Inactivation of Digestive Proteases as the Primary Cause. Int J Clin Med Microbiol 1: 109. doi: https://doi.org/10.15344/2456-4028/2016/109

Abstract

The role of Mycobacterium avium subspecies paratuberculosis (MAP) in Crohn's disease (CD) has been debated for more than a century. Up to date, it remains a highly controversy issue as there are a large amounts of “solid” scientific evidence on both sides. However, I feel many of these conflicts are superficial and the core issue is just the extreme scarcity of MAP in CD and thus the still unresolved conflict between sensitivity and specificity. Along with in-depth analyses of the likely intimate nature of CD, MAP, and the so-called cell-wall deficient spheroplasts, as well as weighted assessment of findings from treatment and epidemiology, here I suggested that the evidences against a critical role of MAP in CD greatly overweigh those support it. Here I also shared a unified hypothesis I developed during the last 15 years regarding the etiology of inflammatory bowel disease (IBD), including the cause and mechanism of IBD as well as the relationship between CD and ulcerative colitis (UC). I proposed that reduction in commensal microbiota in modern society and the resultant impairment in inactivation of pancreatic digestive protease in the lower gut rather than any specific pathogens may have played the primary causative role in both CD and UC.