Chitin May Be Responsible for Allergies to Shellfish, Dust, and Mold
Researchers at the University of California in San Francisco (U
CSF) have discovered a strong association between chitin and allergy, as well as asthma. The results of these studies have been published this week in an early online version of the journal Nature, with a print version due soon.
Chitin is a polysaccharide properly termed N-acetyl-B-D-glucosamine, and makes up the rigid exoskeleton of crabs, shrimp, and insects like dust mites. It is also found in various fungi and molds. While chitin is the most common biopolymer after cellulose, it is never found in organisms containing an internal skeleton, such as humans and other vertebrates. In fact, humans and other animals are genetically programmed to recognize the substance and eliminate it via an enzyme called acidic mammalian chitinase (AMCase). Unfortunately, a less active form of AMCase can also be activated, leading to inflammation and allergic response to chitin. In severe cases, asthma can result.
For this study, Richard Locksley and his colleagues at UCSF sprayed aerosolized chitin into the lungs of laboratory mice. The mice developed an immediate immune response to the chitin, producing the inflammatory cytokines interleukin (IL) 4 and 13. White blood cells, termed eosinophils and basophils, then entered the lung tissue and mounted an attack against the chitin. This kind of acquired immune response would be expected if the mice had been previously exposed to chitin, but they had not. Furthermore, the rapid involvement of the interleukins and white blood cells is characteristic of a classic allergic response, which relies upon previous exposure to the allergen.
Chitin is a polysaccharide properly termed N-acetyl-B-D-glucosamine, and makes up the rigid exoskeleton of crabs, shrimp, and insects like dust mites. It is also found in various fungi and molds. While chitin is the most common biopolymer after cellulose, it is never found in organisms containing an internal skeleton, such as humans and other vertebrates. In fact, humans and other animals are genetically programmed to recognize the substance and eliminate it via an enzyme called acidic mammalian chitinase (AMCase). Unfortunately, a less active form of AMCase can also be activated, leading to inflammation and allergic response to chitin. In severe cases, asthma can result.
For this study, Richard Locksley and his colleagues at UCSF sprayed aerosolized chitin into the lungs of laboratory mice. The mice developed an immediate immune response to the chitin, producing the inflammatory cytokines interleukin (IL) 4 and 13. White blood cells, termed eosinophils and basophils, then entered the lung tissue and mounted an attack against the chitin. This kind of acquired immune response would be expected if the mice had been previously exposed to chitin, but they had not. Furthermore, the rapid involvement of the interleukins and white blood cells is characteristic of a classic allergic response, which relies upon previous exposure to the allergen.
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