User:LiZhang1312/sandbox
Evolutionary
[edit]The low incidence of pathogens within modern societies are thought to have contributed to Inflammatory Bowel Disease vulnerability[1][2] . This has been known as the Hygiene Hypothesis[1] . Humanity has been exposed to a wide range of bacteria and viruses with the advent of agriculture[1] . The increase of the rates in IBD has been coincided with the increase in hygiene [1] . Infectious vectors that have co-evolved with humans are thought to had conferred protection against auto-immune disorders [1] . In the modern society, improved sanitation and medicine has lowered pathogen exposure[1] [3][2] . This leads to an evolutionary mismatch between adaptation and environment where the low pathogen exposure increases susceptibility to Inflammatory Bowel Disease[1] . This is a result of an inappropriate response from the immune system that has not been exposed to many pathogens[1] .
A mechanism of the hygiene hypothesis that has been suggested is the T-helper type 1 (Th1)/Th2 imbalance[3] . Th1 is associated with the inflammatory response while Th2 is associated with the allergic response[3] . It is suggested that the low microbial exposure early in life has predisposed hosts to allergy[3]. For example, helminthic infection is shown to modulate a strong Th2 response[1]. The increase in Th2 decreases the Th1 response which is associated with auto-immune and Crohn's Disease[1] . Newer perspectives have lessened the impact of this mechanism as autoimmune diseases have also shown to protect the Th1 response[3].
Another mechanism that has been proposed is the dysregulation of the immune system. Problems in the inability to terminate inappropriate inflammatory cytokines has been implicated in IBD etiology[2] . Regulatory T-cells (Treg) are made in response to "pseudo-commensal" microbial agents such as helminths and have been suggested to reduce the inflammatory response [2] [3]. Taken together, these suggest that the active immune system is mismatched in the modern, low pathogen setting and may be a reason for vulnerability to IBD.[1]
References
[edit]- ^ a b c d e f g h i j k Koloski, Natasha A.; Bret, Laurel; Radford-Smith, Graham (1/14/08). "Hygiene Hypothesis in Inflammatory Bowel Disease: A Critical Review of the Literature". World Journal of Gastroenterology. 14 (2): 185–173. doi:10.3748/wjg.14.165. PMC 2675108. PMID 18186549.
{{cite journal}}: Check date values in:|date=and|year=/|date=mismatch (help); Unknown parameter|month=ignored (help)CS1 maint: unflagged free DOI (link) - ^ a b c d Rook, Graham (January 2009). "Review series on helminths, immune modulation and the hygiene hypothesis: The broader implications of the hygiene hypothesis". British Society for Immunology. 126: 3–11. doi:10.1111/j.1365-2567.2008.03007.x. PMC 2632706. PMID PMC2632706.
{{cite journal}}: Check|pmid=value (help)CS1 maint: date and year (link) - ^ a b c d e f Okada, H.; Kuhn, C.; Feillet, H.; Bach, J. F. (4/10). "The 'hygiene hypothesis' for autoimmune and allergic diseases: an update". Clinical and Experimental Immunology. 160 (1): 1–9. doi:10.1111/j.1365-2249.2010.04139.x. PMC 2841828. PMID 20415844.
{{cite journal}}: Check date values in:|date=and|year=/|date=mismatch (help); Unknown parameter|month=ignored (help)