Surfactant protein A is defective in abrogating inflammation in asthma

Ying Wang, Dennis R. Voelker, Njira L. Lugogo, Guirong Wang, Joanna Floros, Jennifer L. Ingram, Hong Wei Chu, Tony D. Church, Pitchaimani Kandasamy, Daniel Fertel, Jo Rae Wright, Monica Kraft

Research output: Contribution to journalArticle

31 Scopus citations


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. pneumonia 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 SPA1/ SP-A.

Original languageEnglish (US)
Pages (from-to)L598-L606
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number4
Publication statusPublished - Oct 2011
Externally publishedYes



  • Epithelial cell
  • Mycoplasma
  • SP-A1

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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