Hygiene hypothesis and the increasing incidence of allergic diseases in the children and adolescent population
Authors:
V. Bencko; P. Šíma
Authors‘ workplace:
Ředitel: RNDr. Martin Bilej, DrSc.
; Mikrobiologický ústav AV ČR v. v. i., Praha
; Přednosta: doc. MUDr. Milan Tuček, CSc.
; Ústav hygieny a epidemiologie
; 1. lékařská fakulta
; Univerzita Karlova v Praze
Published in:
Prakt. Lék. 2016; 96(6): 275-279
Category:
Of different specialties
Overview
Hygiene hypothesis was an important contribution to understanding the causes of the increasing incidence of allergic, atopic and other immunopathological conditions in the children population and, later increased incidence of non-communicable disease (e.g. Type 2 diabetes, cardiovascular and autoimmune diseases) in adulthood. Key risk factors relating to the "hygiene hypothesis" and the incidence immunopathological conditions in the children population were: lack of sufficient/adequate exposure to antigens in the environment, “cold chain hypothesis“, infectious agents in the context of antibiotics overuse, urban lifestyle/education possible proportion of excessively meticulous daily care for children and a high standard of hygiene and household, protective factors such as breastfeeding, family size and sibling relationships in a larger family.
The literature generally states that the reduced exposure to microbial antigens in children probably plays an important role in the growth of incidence of allergies, and immunopathological diseases in child and adolescent population.
The reliable supportive assistance data for each of these above mentioned factors vary considerably. The most promising factors that could be causally associated with the development of allergies include exposure to intestinal microbiome, breastfeeding and sibling factors. However, most studies in this area suffer from serious methodological flaws, particularly the reliance on retrospective recall the requested information, making it difficult to determine the validity of the "hygiene hypothesis". However, the "hygiene hypothesis" as well as follow-up "old friends hypothesis“, based on knowledge of the critical impact of the intestinal microbiome to the development of the immune system in children are an important area of research, which could provide clues to understanding the causes of the current adverse developments in the incidence of allergies, including atopy as such, chronic autoimmune, inflammatory bowel disease not only in children but also the population of adolescents and adults..
Keywords:
hygiene hypothesis – exposure to antigenic stimuli – cold chain hypothesis – overuse of antibiotics – old friends hypothesis – breast feeding
Sources
1. Askling J, Grahnquist L, Ekbom A, Finkel Y. Incidence of paediatric Crohn’s disease in Stockholm, Sweden. Lancet 1999; 354: 1179.
2. Yao T, Matsui T, Hiwatashi N. Crohn’s disease in Japan: diagnostic criteria and epidemiology. Dis Colon Rectum 2000; 43: S85–S93.
3. Feeney MA, Murphy F, Clegg AJ, et al. A case-control study of childhood environmental risk factors for the development of inflammatory bowel disease. Eur J Gastroenterol Hepatol 2002; 14: 529–534.
4. Mathers CD, Fat DM, Inoue M, et al. Counting the dead and what they died from: an assessment of the global status of cause of death data. Bull World Health Organ 2005; 83: 171–177.
5. Strachan DP. Hay fever, hygiene, and household size. BMJ 1989; 299: 1259–1260.
6. Bloomfield SF, Stanwell-Smith R, Crevel RW, Pickup J. Too clean, or not too clean: the hygiene hypothesis and home hygiene. Clin Exp Allergy 2006; 36: 402–425.
7. Amre DK, Lambrette P, Law L, et al. Investigating the hygiene hypothesis as a risk factor in pediatric onset Crohn's disease: a case-control study. Am J Gastroenterol 2006; 101: 1005–1011.
8. Koloski NA, Bret L, Radford-Smith G. Hygiene hypothesis in inflamatory bowel disease: A critical review of the literature. World J Gastroenterol 2008: 14(2): 165–173.
9. Mocková A. Ovlivnění vývoje imunity v prenatálním a perinatálním období. Pediatr. praxi 2014; 15(4): 197–200.
10. Weinstock JV, Summers RW, Elliott DE, et al. The possible link between de-worming and the emergence of immunological disease. J Lab Clin Med 2002; 139: 334–338.
11. Satoguina J, Mempel M, Larbi J, et al. Antigen-specific T regulatory-1 cells are associated with immunosuppression in a chronic helminth infection (onchocerciasis). Microbes Infect 2002; 4: 1291–1300.
12. Doetze A, Satoguina J, Burchard G, et al. Antigen-specific cellular hyporesponsiveness in a chronic human helminth infection is mediated by T(h)3/T(r)1-type cytokines IL-10 and transforming growth factor-beta but not by a T(h)1 to T(h)2 shift. Int Immunol 2000; 12: 623–630.
13. King CL, Medhat A, Malhotra I, et al. Cytokine control of parasite-specific anergy in human urinary schistosomiasis. IL-10 modulates lymphocyte reactivity. J Immunol 1996; 156: 4715–4721.
14. Else KJ, Finkelman FD. Intestinal nematode parasites, cytokines and effector mechanisms. Int J Parasitol 1998; 28: 1145–1158.
15. McKay DM, Fairweather I. A role for the enteric nervous system in the response to helminth infections. Parasitol Today 1997; 13: 63–69.
16. Hugot JP, Alberti C, Berrebi D, et al. Crohn’s disease: the cold chain hypothesis. Lancet 2003; 362: 2012–2015.
17. Liu Y, van Kruiningen HJ, West AB, et al. Immunocytochemical evidence of Listeria, Escherichia coli, and Streptococcus antigens in Crohn's disease. Gastroenterology 1995; 108: 1396–1404.
18. Walmsley RS, Anthony A, Sim R, et al. Absence of Escherichia coli, Listeria monocytogenes, and Klebsiella pneumoniae antigens within inflammatory bowel disease tissues. J Clin Pathol 1998; 51: 657–661.
19. Forbes A, Kalantzis T. Crohn’s disease: the cold chain hypothesis. Int J Colorectal Dis 2006; 21: 399–401.
20. Garcia Rodriguez LA, Ruigomez A, Panes J. Acute gastroenteritis is followed by an increased risk of inflammatory bowel disease. Gastroenterology 2006; 130: 1588–1594.
21. Stallmach A, Carstens O. Role of infections in the manifestation or reactivation of inflammatory bowel diseases. Inflamm Bowel Dis 2002; 8: 213–218.
22. Montgomery SM, Morris DL, Pounder RE, Wakefield AJ. Paramyxovirus infections in childhood and subsequent inflammatory bowel disease. Gastroenterology 1999; 116: 796–803.
23. Hermon-Taylor J, Bull TJ, Sheridan JM, et al. Causation of Crohn’s disease by Mycobacterium avium subspecies paratuberculosis. Can J Gastroenterol 2000; 14: 521–539.
24. Haga Y, Funakoshi O, Kuroe K, et al. Absence of measles viral genomic sequence in intestinal tissues from Crohn’s disease by nested polymerase chain reaction. Gut 1996; 38: 211–215.
25. Iizuka M, Nakagomi O, Chiba M, et al. Absence of measles virus in Crohn’s disease. Lancet 1995; 345: 199.
26. Nielsen LL, Nielsen NM, Melbye M, et al. Exposure to measles in utero and Crohn’s disease: Danish register study. BMJ 1998; 316: 196–197.
27. Jones P, Fine P, Piracha S. Crohn’s disease and measles. Lancet 1997; 349: 473.
28. Haslam N, Mayberry JF, Hawthorne AB, et al. Measles, month of birth, and Crohn’s disease. Gut 2000; 47: 801–803.
29. Card T, Logan RF, Rodrigues LC, Wheeler JG. Antibiotic use and the development of Crohn’s disease. Gut 2004; 53: 246–250.
30. Ekbom A, Montgomery SM. Environmental risk factors (excluding tobacco and microorganisms): critical analysis of old and new hypotheses. Best Pract Res Clin Gastroenterol 2004; 18: 497–508.
31. Mulligan P, White NR, Monteleone G, et al. Breast milk lactoferrin regulates gene expression by binding bacterial DNA CpG motifs but not genomic DNA promoters in model intestinal cells. Pediatr Res 2006; 59: 656–661.
32. Baron S, Turck D, Leplat C, et al. Environmental risk factors in paediatric inflammatory bowel diseases: a population based case control study. Gut 2005; 54: 357–363.
33. Klement E, Cohen RV, Boxman J, et al. Breastfeeding and risk of inflammatory bowel disease: a systematic review with meta-analysis. Am J Clin Nutr 2004; 80: 1342–1352.
34. Corrao G, Tragnone A, Caprilli R, et al. Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC). Int J Epidemiol 1998; 27: 397–404.
35. Chalubinski M, Kowalski ML. Endocrine disrupters-potential modulators of the immune system and allergic response. Allergy 2006; 61: 1326–1335.
36. Danese S, Sans M, Fiocchi C. Inflammatory bowel disease: the role of environmental factors. Autoimmun Rev 2004; 3: 394–400.
37. Sicilia B, Lopez Miguel C, Arribas F, et al. Environmental risk factors and Crohn’s disease: a population-based, case-control study in Spain. Dig Liver Dis 2001; 33: 762–767.
38. Montgomery SM, Lambe M, Wakefield AJ, et al. Siblings and the risk of inflammatory bowel disease. Scand J Gastroenterol 2002; 37: 1301–1308.
39. Hampe J, Heymann K, Krawczak M, Schreiber S. Association of inflammatory bowel disease with indicators for childhood antigen and infection exposure. Int J Colorectal Dis 2003; 18: 413–417.
40. Blanchard JF, Bernstein CN, Wajda A, Rawsthorne P. Small area variations and sociodemographic correlates for the incidence of Crohn’s disease and ulcerative colitis. Am J Epidemiol 2001; 154: 328–335.
41. Ekbom A, Helmick C, Zack M, Adami HO. The epidemiology of inflammatory bowel disease: a large, population-based study in Sweden. Gastroenterology 1991; 100: 350–358.
42. Bernstein CN, Kraut A, Blanchard JF, et al. The relationship between inflammatory bowel disease and socioeconomic variables. Am J Gastroenterol 2001; 96: 2117–2125.
Labels
General practitioner for children and adolescents General practitioner for adultsArticle was published in
General Practitioner
2016 Issue 6
Most read in this issue
- Hospitalism in pediatric patients
- Complex rehabilitation of patients after stroke – project of Stroke centre in Thomayer’s hospital
- Cholesterol myths
- Hygiene hypothesis and the increasing incidence of allergic diseases in the children and adolescent population