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.

Highlights

  • It has been more than a century since Dr Dalziel proposed a possible same etiology of Johne’s disease in cattle, known as being caused by Mycobacterium avium subspecies paratuberculosis (MAP), with the chronic interstitial enteritis in human, known as Crohn’s disease (CD) [1]

  • I would like to share my thoughts on this issue, along with a hypothesis I first proposed 15 years ago 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 propose that reduction in commensal microbiota along with improved hygiene condition and inhibition by antibiotics and dietary chemicals such as saccharin and sucralose 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 for both CD and UC

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Summary

Introduction

It has been more than a century since Dr Dalziel proposed a possible same etiology of Johne’s disease in cattle, known as being caused by Mycobacterium avium subspecies paratuberculosis (MAP), with the chronic interstitial enteritis in human, known as Crohn’s disease (CD) [1]. I propose that reduction in commensal microbiota along with improved hygiene condition and inhibition by antibiotics and dietary chemicals such as saccharin and sucralose 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 for both CD and UC.

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