Surfactant protein-A (SP-A) plays a critical role in the innate immune system and has well
characterized effects in the lung where it attenuates inflammatory responses and controls
invasion of bacteria. Extra-pulmonary sources of SP-A have also been indentified : SP-A
mRNA has been detected in the murine neonatal and adult gastrointestinal (GI) tract, while
significant levels of SP-A protein have been detected in amniotic fluid.
A novel finding by the George research lab showed that SP-A knockout (-/-) newborn mice
raised in a bacterial laden corn dust environment exhibited intestinal inflammation-- instead
of pulmonary inflammation--and higher rates of death. Further studies have shown that
SP-A -/- mice exhibit abnormal bacterial colonization patterns in the GI tract compared to
their wild-type counterparts, indicating a role for SP-A in the newborn intestinal tract.
To date it is not clear if newborn intestinal exposure to SP-A comes from ingested amniotic
fluid or from production in the newborn intestinal tract. RT-qPCR showed low levels of SP-A
gene expression in the newborn murine GI tract; yet, we and others have had mixed results
regarding the detection of SP-A protein via immunohistochemistry.
To address the question of intestinal exposure of SP-A in the newborn, I will perform RNA in
situ hybridization to identify gene expression in specific cells of the GI tract. I have designed
a 438 bp digoxigenin-labeled antisense RNA probe specific for the SP-A gene. This probe
will be used on flash-frozen GI and lung tissue sections of mice at post-natal days of life 5
and 6 with an in situ hybridization protocol designed by the Panoskaltsis-Mortari laboratory.
Additional contributor: Caroline George (faculty mentor)
Expression of Surfactant Protein-A (SP-A) in the Developing MurineIntestinal Tract.
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