(Mp), a pathogen associated with asthma exacerbations, and functions to attenuate Mp pathogenicity and abrogate lung inflammation. In addition, SP-A has been shown to inhibit Mp-induced eosinophil peroxidase (EPO) release, a toxic product that can compromise the integrity of the delicate airway epithelia. We have determined that genetic variation in SP-A2 at position 223 that results in a glutamine (Q) to a lysine (K) substitution alters the ability of SP-A to inhibit EPO release and may offer a mechanistic explanation as to why some SP-A extracted from subjects with asthma is unable to carry out normal immune regulatory functions.
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Dy et al. (2018) studied this question.
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