Surfactant protein A is defective in abrogating inflammation in asthma.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Wang, Y; Voelker, DR; Lugogo, NL; Wang, G; Floros, J; Ingram, JL; Chu, HW; Church, TD; Kandasamy, P; Fertel, D; Wright, JR; Kraft, M

Published Date

  • October 2011

Published In

Volume / Issue

  • 301 / 4

Start / End Page

  • L598 - L606

PubMed ID

  • 21784968

Pubmed Central ID

  • 21784968

Electronic International Standard Serial Number (EISSN)

  • 1522-1504

Digital Object Identifier (DOI)

  • 10.1152/ajplung.00381.2010

Language

  • eng

Conference Location

  • United States