Purpose of review: The 'hygiene hypothesis' implies that infections in early childhood prevent the development of atopy. Atopy is caused by the interaction of the environment with genetic factors. Therefore, both contacts with microbial products such as endotoxin as well as CD14, a gene involved in the immunological response to endotoxin, are discussed in this review.
Recent findings: CD14 is a multifunctional receptor for endotoxin and other bacterial wall components. Membrane-bound CD14 is expressed on monocytes and macrophages. It forms a complex with Toll-like receptor 4. Genetic studies have shown an association of variants in the CD14 gene with the prevention of (and severity of) atopy. However, phenotype definitions and the allele that showed association differed between studies. In addition, the presence of endotoxin in house dust appears to be inversely related to atopy in different studies.
Summary: It can be hypothesized that different levels of endotoxin exposure could interact with specific CD14 variants in the prevention of atopy. If confirmed in prospective cohort studies, this might represent an important gene by environmental interaction in the development of atopy. This could possibly open ways for the primary prevention of atopy.