The Hygiene Hypothesis and Hypersensitivity

 

The Hygiene Hypothesis

In most modern societies, good hygiene is associated with regular bathing, and good health with cleanliness. But some recent studies suggest that the association between health and clean living may be a faulty one. Some go so far as to suggest that children should be encouraged to play in the dirt—or even eat dirt[1]—for the benefit of their health. This recommendation is based on the so-called hygiene hypothesis, which proposes that childhood exposure to antigens from a diverse range of microbes leads to a better-functioning immune system later in life.

The hygiene hypothesis was first suggested in 1989 by David Strachan,[2] who observed an inverse relationship between the number of older children in a family and the incidence of hay fever. Although hay fever in children had increased dramatically during the mid-20th century, incidence was significantly lower in families with more children. Strachan proposed that the lower incidence of allergies in large families could be linked to infections acquired from older siblings, suggesting that these infections made children less susceptible to allergies. Strachan also argued that trends toward smaller families and a greater emphasis on cleanliness in the 20th century had decreased exposure to pathogens and thus led to higher overall rates of allergies, asthma, and other immune disorders.

Other researchers have observed an inverse relationship between the incidence of immune disorders and infectious diseases that are now rare in industrialized countries but still common in less industrialized countries.[3] In developed nations, children under the age of 5 years are not exposed to many of the microbes, molecules, and antigens they almost certainly would have encountered a century ago. The lack of early challenges to the immune system by organisms with which humans and their ancestors evolved may result in failures in immune system functioning later in life.

 

Table summarizing four types of hypersensitivities. Type I uses immune reactant IgE and a soluble antigen. The mechanism of activation is: Allergen-specific IgE antibodies bind to mast cells via their Fc receptor. When the specific allergen binds to the IgE, cross-linking of IgE induces degranulation of mast cells. Examples of hypersensitive reactions include: Local and systemic anaphylaxis, seasonal hay fever, food allergies, and drug allergies. Type II uses immune reactant IgG or IgM and a cell-bound antigen. The mechanism of activation is: IgG or IgM antibody binds to cellular antigen, leading to complement activation and cell lysis. IgG can also mediate ADCC with cytotoxic T cells, natural killer cells, macrophages, and neutrophils. Examples of hypersensitive reactions include: Red blood cell destruction after transfusion with mismatched blood types or during hemolytic disease of the newborn. Type III uses immune reactant IgG or IgM and a soluble antigen. The mechanism of activation is: Antigen-antibody complexes are deposited in tissues. Complement activation provides inflammatory mediators and recruits neutrophils. Enzymes released from neutrophils damage tissue. Examples of hypersensitive reactions include: Local and systemic Post-streptococcal glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus. Type IV uses immune reactant T cells and a soluble or cell-bound antigen. The mechanism of activation is: Th2 cells secreete cytokines, which activate macrophages and cytotoxic T cells.. Examples of hypersensitive reactions include: Contact dermatitis, type I diabetes mellitus, and multiple sclerosis.

Figure 10. Components of the immune system cause four types of hypersensitivities. Notice that types I–III are B-cell/antibody-mediated hypersensitivities, whereas type IV hypersensitivity is exclusively a T-cell phenomenon.


  1. S.T. Weiss. “Eat Dirt—The Hygiene Hypothesis and Allergic Diseases.” New England Journal of Medicine 347 no. 12 (2002):930–931.
  2. D.P. Strachan “Hay Fever, Hygiene, and Household Size.” British Medical Journal 299 no. 6710 (1989):1259.
  3. H. Okada et al. “The ‘Hygiene Hypothesis’ for Autoimmune and Allergic Diseases: An Update.” Clinical & Experimental Immunology 160 no. 1 (2010):1–9.