期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 301, 期 4, 页码 L598-L606出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00381.2010
关键词
epithelial cell; mycoplasma; SP-A1
资金
- National Heart, Lung, and Blood Institute [HL P01-HL073907, P50-HL084917]
Wang Y, Voelker DR, Lugogo NL, Wang G, Floros J, Ingram JL, Chu HW, Church TD, Kandasamy P, Fertel D, Wright JR, Kraft M. Surfactant protein A is defective in abrogating inflammation in asthma. Am J Physiol Lung Cell Mol Physiol 301: L598-L606, 2011. First published July 22, 2011; doi: 10.1152/ajplung.00381.2010.-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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