Surfactant protein A is defective in abrogating inflammation in asthma.

Abstract

Surfactant protein A (SP-A) regulates a variety of immune cell functions. We determined the ability of SP-A derived from normal and asthmatic subjects to modulate the inflammatory response elicited by Mycoplasma pneumoniae, a pathogen known to exacerbate asthma. Fourteen asthmatic and 10 normal control subjects underwent bronchoscopy with airway brushing and bronchoalveolar lavage (BAL). Total SP-A was extracted from BAL. The ratio of SP-A1 to total SP-A (SP-A1/SP-A) and the binding of total SP-A to M. pneumoniae membranes were determined. Airway epithelial cells from subjects were exposed to either normal or asthmatic SP-A before exposure to M. pneumoniae. IL-8 protein and MUC5AC mRNA were measured. Total BAL SP-A concentration did not differ between groups, but the percentage SP-A1 was significantly increased in BAL of asthmatic compared with normal subjects. SP-A1/SP-A significantly correlated with maximum binding of total SP-A to M. pneumoniae, but only in asthma. SP-A derived from asthmatic subjects did not significantly attenuate IL-8 and MUC5AC in the setting of M. pneumoniae infection compared with SP-A derived from normal subjects. We conclude that SP-A derived from asthmatic subjects does not abrogate inflammation effectively, and this dysfunction may be modulated by SP-A1/SP-A.

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Published Version (Please cite this version)

10.1152/ajplung.00381.2010

Publication Info

Wang, Ying, Dennis R Voelker, Njira L Lugogo, Guirong Wang, Joanna Floros, Jennifer L Ingram, Hong Wei Chu, Tony D Church, et al. (2011). Surfactant protein A is defective in abrogating inflammation in asthma. American journal of physiology. Lung cellular and molecular physiology, 301(4). pp. L598–L606. 10.1152/ajplung.00381.2010 Retrieved from https://hdl.handle.net/10161/25440.

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