Surfactant protein A

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surfactant, pulmonary-associated protein A1
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
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]

During Parturition

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.

Immune Functions

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]

Location

SP-A is found in the pulmonary surfactant in lungs. SP-A and SP-D are also present in extrapulmonary tissues.[7]

See also

External links

References

  1. Boron W, Boulpaep E. Medical Physiology. 2nd ed. Philadelphia: Elsevier; 2012.
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  4. http://www.jimmunol.org/content/158/9/4336.short
  5. http://europepmc.org/abstract/MED/9761768
  6. http://europepmc.org/abstract/MED/2306370/
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