Crohn's disease: the cold chain hypothesis

@article{Hugot2003CrohnsDT,
  title={Crohn's disease: the cold chain hypothesis},
  author={Jean-Pierre Hugot and Corinne Alberti and Dominique Berrebi and Edouard Bingen and Jean Pierre C{\'e}zard},
  journal={The Lancet},
  year={2003},
  volume={362},
  pages={2012-2015}
}
Crohn’s Disease: Is the Cold Chain Hypothesis Still Hot?
TLDR
According to the cold chain hypothesis, the development of industrial and domestic refrigeration has led to frequent exposure of human populations to bacteria capable of growing in the cold, which is believed to be capable of inducing exacerbated inflammation of the intestine in genetically predisposed subjects.
Environmental Factors Affecting Inflammatory Bowel Disease: Have We Made Progress?
TLDR
A meta-analysis partially confirms previous findings that smoking was found to be protective against ulcerative colitis and, after the onset of the disease, might improve its course, decreasing the need for colectomy.
Abnormalities in the handling of intracellular bacteria in Crohn’s disease: a link between infectious etiology and host genetic susceptibility
TLDR
One theoretical link between susceptibility genes NOD2/CARD15, ATG16L1, and IRGM is that CD is primarily induced by the presence of a dysfunctional immunological response to persistent infection by intracellular bacterial pathogens such as Mycobacterium avium subspecies paratuberculosis or adherent-invasive Escherichia coli.
Crohn's disease: the cold chain hypothesis
TLDR
Support for the hypothesis that Crohn's disease was provoked by infantile exposure to micro-organisms that can survive refrigerator temperature reached statistical significance for those with Crohn’s disease compared to the controls.
Evidence for the involvement of infectious agents in the pathogenesis of Crohn's disease.
TLDR
Three not necessarily mutually exclusive theories have been proposed: an unidentified persistent pathogen; an abnormally permeable mucosal barrier leading to excessive bacterial translocation; and a breakdown in the balance between putative "protective" versus "harmful" intestinal bacteria ("dysbiosis").
Crohn’s Disease: an Immune Deficiency State
TLDR
A substantial body of data has emerged in recent years to suggest that the primary defect in Crohn’s disease is actually one of relative immunodeficiency, and the evidence for such a phenomenon is considered in contrast to alternative prevailing hypotheses and some of the potential paradoxes that it generates.
Innate immunity in inflammatory bowel disease: a disease hypothesis
TLDR
Rather than Crohn's disease being caused by excessive inflammation, the primary mechanism is actually that of an immunodeficiency, which can be compensated in some circumstances by signalling through NOD2.
The role of the NOD2 gene in the pathogenesis of Crohn’s disease
TLDR
MDP priming significantly modulates responses of monocytes to LPS, which may explain in part the pro-inflammatory consequence of mutations in the NOD2 gene and could provide mechanistic understanding of how mutations in this gene may cause Crohn’s disease.
The Role of Environmental Factors in the Pathogenesis of Inflammatory Bowel Diseases: A Review
TLDR
The data is reviewed suggesting how different environmental factors may modulate the risk of developing IBD including diets, smoking, lifestyle choices, enteric infections, appendectomy, air pollution, and the use of medications, with an emphasis on antibiotics.
Crohn’s Disease: Evolution, Epigenetics, and the Emerging Role of Microbiome-Targeted Therapies
TLDR
This review will focus on CD’s natural history and therapies in the context of epigenetics, immunogenetics, and the microbiome to personalize microbiome-targeted therapies and molecular classifications of CD.
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