An Insight into the Diverse Roles of Surfactant Proteins, SP-A and SP-D in Innate and Adaptive Immunity

Abstract

Surfactant proteins SP-A and SP-D are hydrophilic, collagen-containing calcium-dependent lectins, which appear to have a range of innate immune functions at pulmonary as well as extrapulmonary sites. These proteins bind to target ligands on pathogens, allergens, and apoptotic cells, via C-terminal homotrimeric carbohydrate recognition domains, while the collagen region brings about the effector functions via its interaction with cell surface receptors. SP-A and SP-D deal with various pathogens, using a range of innate immune mechanisms such as agglutination/aggregation, enhancement of phagocytosis, and killing mechanisms by phagocytic cells and direct growth inhibition. SP-A and SP-D have also been shown to be involved in the control of pulmonary inflammation including allergy and asthma. Emerging evidence suggest that SP-A and SP-D are capable of linking innate immunity with adaptive immunity that includes modulation of dendritic cell function and helper T cell polarization. This review enumerates immunological properties of SP-A and SP-D inside and outside lungs and discusses their importance in human health and disease.

Surfactant Protein-A Concentration in Sera from Dogs with Pulmonary Parenchymal Diseases

“…The mechanism by which SP-A leaks from the alveoli into blood circulation is poorly understood. However, the cause of serum SP-A concentration elevation in patients with interstitial lung disease is thought to be, because of not only SP-A overproduction in the lungs but also leakage into the circulation by the injured basement membranes of the alveoli and vessels [18,26].…”

“…SP-A acts similar to opsonin by binding directly and agglutinating with various pathogenic microbes, such as bacteria, viruses and certain fungi [1,14,29]. Furthermore, SP-A promotes bacterial phagocytosis by increasing cell surface expression of phagocytosis receptors (mannose receptor and scavenger receptor A) in macrophages and controls the inflammatory reaction of the pathogenic microbe component through interaction with Toll-like receptors and CD14 [10,18].…”

Maternal surfactant protein A influences the immunoprotective properties of milk in a murine model

“…KLH has previously been used to assess milk immunoglobulin production in rodent models, yet the impact of SP-A with this stimulus has not been studied (20). The nonhygienic environment has been characterized as a complex microbial and endotoxin-rich inhalational exposure, components to which SP-A can bind directly to and enhance phagocytosis (5,13). Total milk and lung IgA content is not affected by the SP-A null genotype or exposure to DNP-KLH, yet maternal SP-A allows for optimal DNP-KLH-specific milk sIgA production.…”

“…When purified SP-A is added to in vitro alveolar macrophages following lipopolysaccharide stimulation, cytokine production is downregulated (4). Recently, it has been demonstrated that SP-A can also impact the adaptive immune system by altering T-cell function (5). The ability of SP-A to promote or attenuate a proinflammatory response may be due to its ability to activate different cell surface signaling molecules and to differentially activate T-cells (6,7).…”

The Biomarker Salivary SP-D May Indicate Small Airway Inflammation and Asthma Exacerbation

“…[19,20]. Of note, glandular tissues in the minor salivary glands of asthmatics exhibit airway-like inflammation [21].…”