Hygiene hypothesis and allergic disease
The hygiene hypothesis proposes that too little microbial exposure in early life alters immune development and raises the risk of allergy.
Remember
Too little early microbial exposure tilts the immune system towards Th2 cells (T cells that coordinate allergic responses) and IgE (the antibody class involved in allergy), which raises the risk of allergic disease. It is a hypothesis, not proof that cleanliness causes allergy.
The hygiene hypothesis is a proposed explanation for why type 1 hypersensitivity (immediate allergic reactions driven by IgE antibodies and mast cells) is generally more common in developed countries. Mast cells are tissue cells packed with inflammatory chemicals, and they carry IgE on their surface. The Western lifestyle is often associated with low infectious exposure.
David Strachan first described the idea in 1989. He noticed that children from larger families, who were exposed to more microbes early in life, seemed to have fewer cases of hay fever and eczema, which are allergic responses to harmless environmental substances.
Early contact with microbes is thought to shape the immune system. The idea is that, with too little of it, regulatory T-cells (cells that dampen other immune cells and help the body tolerate harmless things such as pollen or food) develop less well, so tolerance is weaker. The balance then tips towards Th2 responses, and Th2 cells prompt the body to make IgE. That IgE sits on mast cells and drives type 1 reactions.
Th1 responses (the protective, anti-infective arm of immunity) are not the pattern linked with low early microbial exposure. Low early microbial exposure is linked with Th2 responses and IgE.
Newer versions of the idea point to a loss of microbial diversity rather than cleanliness itself. The Western lifestyle is associated with lower microbial diversity, which upsets the symbiotic (mutually beneficial) relationships between microbes and the gut surface. Dysbiosis is the name for this loss of balance (an unhealthy shift in the community of microbes).
It is a proposed explanation for a pattern, not a proven single cause. Handwashing and vaccination, which prevent serious infections, remain part of normal hygiene, and the hypothesis is not a reason to stop them.
Key facts
- Main idea
- Too little microbial exposure early in life may alter immune development and raise the risk of allergy.
- Setting
- Type 1 hypersensitivity is generally more common in developed countries, where the Western lifestyle is often associated with low infectious exposure.
- Origin
- David Strachan first described the idea in 1989.
- Immune pattern
- Low early microbial exposure is linked with Th2 responses and IgE, not with a Th1 pattern.
- Tolerance
- The hypothesis proposes that regulatory T-cells develop less well with fewer early microbes, so tolerance is weaker.
- Dysbiosis
- A loss of microbial diversity that disrupts the healthy relationships between microbes and the gut lining.
- Limit
- It remains a hypothesis, not proof that cleanliness causes allergy.
Exam traps
- More Th1 activity from frequent early infections would not explain allergy, because Th1 responses form the protective, anti-infective arm of immunity, and frequent early infections are proposed to protect against allergy.
- A shortage of IgA is a different antibody problem from allergy. IgA is the main antibody of mucosal surfaces (mainly the gut), and allergy is driven by too much IgE rather than too little IgA.
- The hypothesis does not say that improved hygiene increases microbial diversity and immune tolerance. It proposes that a Western lifestyle is linked with lower microbial diversity, a less supportive immune environment and more allergy.
Read the full notes
Tested in 6 SimpleMed+ questions
Practice it in Immunology, with the answer and a full explanation after every question.
Practice these questions