Surfactant Protein A Stimulates Release of Neutrophil Chemotactic Factors by Alveolar Type II Pneumocytes

Abstract

Mucosal immunity is an important mechanism in the response to injury. Our hypothesis is that surfactant protein A (SP-A) is an autocrine factor that stimulates alveolar type II epithelial cell release of neutrophil chemotactic factors by binding to the SP-A receptor expressed by these cells. We examined (1) the effect of SP-A (20 μg/ml) or IL-1β (10 ng/ml) on release of neutrophil chemotactic factors by primary cultures of type II cells or alveolar macrophages, and (2) the effect of intratracheal instillation of the blocking antibody to the SP-A receptor on the response to oleic acid-induced lung injury in vivo. All media and cell culture supernates were assayed for neutrophil chemotactic activity, and bronchoalveolar lavage fluid from the in vivo experiments was analyzed for inflammatory cell counts. While SP-A and media used for the cell cultures has no intrinsic neutrophil chemotactic activity, supernates from primary cultures of type II cells incubated in either SP-A or IL-1β had twofold higher neutrophil chemotactic factor activity compared to supernates from controls. SP-A had no effect on release of neutrophil chemotactic factor by alveolar macrophages. Oleic acid-induced lung injury resulted in a marked influx of neutrophils into BAL, and this influx was reduced by 70% by pretreatment with the antibody to SP-A receptor. We conclude that SP-A stimulates the release of neutrophil chemotactic factor by alveolar type II cells, and this effect is mediated by the receptor for SP-A specifically expressed by these cells.

Tracheal colonization in preterm infants supported with nasal continuous positive airway pressure

“…However, the mechanism through which trachea gets colonized with bacteria in CPAP‐supported infants is unclear and has never been investigated, simply because of the lack of knowledge about its existence. Surfactant plays a function in the immune system of the respiratory system 19,20 . The exposure of lower respiratory tract and alveoli to oxygen may induce a bio‐trauma that ameliorates the integrity of the endothelial and epithelial cell‐lining, making them incompetent in preventing bacterial residence 21 .…”

“…Surfactant plays a function in the immune system of the respiratory system. 19,20 The exposure of lower respiratory tract and alveoli to oxygen may induce a bio-trauma that ameliorates the integrity of the endothelial and epithelial cell-lining, making them incompetent in preventing bacterial residence. 21 Another factor could be related to some limitation in the motility of premature infants while attached to the CPAP device.…”

Surfactant protein A is decreased in the lung of rats with hepatopulmonary syndrome

“…Additionally, previous studies have shown that SP-A stimulates the chemotactic activity of alveolar neutrophils 11 and myeloperoxidase activity is increased in hepatopulmonary syndrome in rats 26 .…”

“…Pulmonary surfactant, which is secreted by alveolar type II pneumocytes, reduces surface tension at the air/liquid interface of the alveoli and stabilizes alveoli at low lung volumes [9][10][11] .…”

The Role of Surfactant in Respiratory Distress Syndrome

“…SLPI prevents degradation of matrix metalloproteinase, a molecule involved in antigen apoptosis through the proteolytic breakdown of extracellular matrix components. Release of neutrophil chemotactic factors by alveolar type II pneumocytes is also regulated by SP-A [21]. Studies on animal models with SP-A and -D deficiencies have sought to confirm these findings.…”