Abstract
Pulmonary surfactant proteins have many roles in surfactant- related functions and innate immunity. One of these proteins is the surfactant protein A (SP-A) that plays a role in both surfactant-related processes and host defense and is the focus in this review. SP-A interacts with the sentinel host defense cell in the alveolus, the alveolar macrophage (AM), to modulate its function and expression profile under various conditions, as well as other alveolar epithelial cells such as the Type II cell. Via these interactions, SP-A has an impact on the alveolar microenvironment. SP-A is also important for surfactant structure and function. Much of what is understood of the function of SP-A and its various roles in lung health has been learned from SP-A knockout (KO) mouse experiments, as reviewed here. A vast majority of this work has been done with infection models that are bacterial, viral, and fungal in nature. Other models have also been used, including those of bleomycin-induced lung injury and ozone-induced oxidative stress either alone or in combination with an infectious agent, bone marrow transplantation, and other. In addition, models investigating the effects of SP-A on surfactant components or surfactant structure have contributed important information. SP-A also appears to play a role in pathways involved in sex differences in response to infection and/or oxidative stress, as well as at baseline conditions. To date, this is the first review to provide a comprehensive report of the functions of SP-A as learned through KO mice.
Highlights
Pulmonary surfactant has many critical roles in respiratory function
Research involving SP-A continues to reveal an increasing level of evidence regarding its critical role in host defense, surfactant-related functions, and other
Much has been learned by the study of SP-A KO mice
Summary
Pulmonary surfactant has many critical roles in respiratory function. One is to decrease surface tension at the air-liquid interface, preventing alveolar lung collapse at low lung volumes. Pulmonary surfactant is a lipoprotein complex consisting of lipids, primarily phospholipids, and several proteins, SP-A, SP-B, SP-C and SP-D (the latter co-isolates with surfactant) These proteins collectively play various roles in surfactant-related functions and innate immunity/host defense [2]. Humans have two SFTPA genes and these have been identified with extensive genetic and epigenetic variability and human SP-A protein variants have been shown to differentially affect AM and alveolar epithelial type II cells, as well as the alveolar microenvironment. These differential effects have been observed both under baseline conditions and in response to various insults, as assessed by studies of bronchoalveolar lavage samples, alveolar cells, or other. The direct and indirect roles of SP-A in combating various bacterial and viral pathogens or other types of insults, as well as the various SP-A-mediated activities that may affect surfactant structure, or activities of various surfactant components are noted
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