Open Access
Review
Genetic variant associations of human SP-A and SP-D with acute and chronic lung injury
Patricia Silveyra1,Joanna Floros1,2,*
1
Center for Host Defense, Inflammation, and Lung Disease (CHILD) Research, Department of Pediatrics, Pennsylvania State University College of Medicine, Pennsylvania
2
Department of Obstetrics and Gynecology, Pennsylvania State University College of Medicine, Pennsylvania
DOI: 10.2741/3935 Volume 17 Issue 2, pp.407-429
Published: 01 January 2012
(This article belongs to the Special Issue Pulmonary surfactant in human health and disease)
*Corresponding Author(s):  
Joanna Floros
E-mail:  
jfloros@psu.edu
Abstract

Pulmonary surfactant, a lipoprotein complex, maintains alveolar integrity and plays an important role in lung host defense, and control of inflammation. Altered inflammatory processes and surfactant dysfunction are well described events that occur in patients with acute or chronic lung disease that can develop secondary to a variety of insults. Genetic variants of surfactant proteins, including single nucleotide polymorphisms, haplotypes, and other genetic variations have been associated with acute and chronic lung disease throughout life in several populations and study groups. The hydrophilic surfactant proteins SP-A and SP-D, also known as collectins, in addition to their surfactant-related functions, are important innate immunity molecules as these, among others, exhibit the ability to bind and enhance clearance of a wide range of pathogens and allergens. This review focuses on published association studies of human surfactant proteins A and D genetic polymorphisms with respiratory, and non-respiratory diseases in adults, children, and newborns. The potential role of genetic variations in pulmonary disease or pathogenesis is discussed following an evaluation, and comparison of the available literature.

Key words

SFTPA1, SFTPA2, SP-D, Polymorphism, Single Nucleotide, collectins, lung disease, review

Share and Cite
Patricia Silveyra, Joanna Floros. Genetic variant associations of human SP-A and SP-D with acute and chronic lung injury. Frontiers in Bioscience-Landmark. 2012. 17(2); 407-429.