| surfactant, pulmonary-associated protein A1 | |
| Hgncid: | 10798 |
| Symbol: | SFTPA1 |
| Altsymbols: | SFTP1 |
| Entrezgene: | 6435 |
| Omim: | 178630 |
| Refseq: | NM_005411 |
| Uniprot: | Q8IWL2 |
| Chromosome: | 10 |
| Arm: | q |
| Band: | 22.3 |
| surfactant, pulmonary-associated protein A2B | |
| Hgncid: | 10799 |
| Symbol: | SFTPA2B |
| Entrezgene: | 6436 |
| Omim: | 178642 |
| Refseq: | NM_006926 |
| Uniprot: | Q8IWL1 |
| Chromosome: | 10 |
| Arm: | q |
| Band: | 22.3 |
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 (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]