surfactant, pulmonary-associated protein A1 | |
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Identifiers | |
Symbol | SFTPA1 |
Alt. symbols | SFTP1 |
Entrez | 6435 |
HUGO | 10798 |
OMIM | 178630 |
RefSeq | NM_005411 |
UniProt | Q8IWL2 |
Other data | |
Locus | Chr. 10 q22.3 |
surfactant, pulmonary-associated protein A2B | |
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Identifiers | |
Symbol | SFTPA2B |
Entrez | 6436 |
HUGO | 10799 |
OMIM | 178642 |
RefSeq | NM_006926 |
UniProt | Q8IWL1 |
Other data | |
Locus | Chr. 10 q22.3 |
Surfactant protein A is an innate immune system collectin. It is water-soluble and has collagen-like domains similar to SP-D. It is part of the innate immune system and is used to opsonize bacterial cells in the alveoli marking them for phagocytosis by alveolar macrophages. SP-A may also play a role in negative feedback limiting the secretion of pulmonary surfactant. SP-A is not required for pulmonary surfactant to function but does confer immune effects to the organism.[1]
The role of Surfactant protein A (or SP-A) in childbirth is indicated in studies with mice.[2] Mice which gestate for 19 days typically show signs of SP-A in amniotic fluid at around 16 days. If SP-A is injected into the uterus at 15 days, mice typically deliver early. Inversely, an SP-A inhibitor injection causes notable delays in birth.
The presence of Surfactant Protein A seemed to trigger an inflammatory response in the uterus of the mice, but later studies found an anti-inflammatory response in humans.[3] In fact, the level of SP-A in a human uterus typically decreases during labor.
Research on SP-A has been done mainly in rodents including mice and rats. This research has shown that mice deficient in SP-A are more susceptible to infections from group B Streptoccoal organisms,[4] Pseudomonas aeruginosa,[5] and likely other organisms. The immune functions of SP-A are time, temperature, and concentration dependant.[6]
SP-A is found in the pulmonary surfactant in lungs. SP-A and SP-D are also present in extrapulmonary tissues.[7]
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