Submitted to: American Association of Veterinary Parasitologists Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: March 5, 2002
Publication Date: September 3, 2002
Citation: Zarlenga, D.S., Morimoto, M., Urban Jr, J.F., Mccarter, J.P. 2002. A tgf-beta homologue within populations of ascaris suum 4th stage larvae (l4): evidence for multiple spliting and regulated transcription between l4 in the jejunum and ileum following spontaneously cure [abstract]. American Association of Veterinary Parasitologists Proceedings. Technical Abstract: Ascaris species represent the most prevalent parasitic worm infecting humans and swine worldwide. Ascaris suum larvae derived from infective eggs migrate from the caecum to the liver and lungs of pigs before L4 establish in the jejunum and develop into adults. However, a large percentage of L4 in the jejunum spontaneously cure between 14 and 21 days after inoculation as they are forced to the ileum and are eventually expelled from the intestine. Increases in intestinal mucosal mast cells reactive to L4 antigens and local changes in Th2-derived cytokines are coincidental with spontaneous cure. Increased expression of L4 genes for structural proteins related to parasite vigor were detected by cDNA microarray analysis, but gene products that alter host responses to parasitism have not been detected. To this end, a jejunum L4-derived EST library was generated and a putative TGF- homologue was identified and characterized by sequence similarity to the Brugia malayi Tgh-1gene and the TGF- -like growth factor from Caenorhabditis elegans. Partial sequence information from enzymatically-amplified cDNA revealed at least 2 differentially spliced transcripts. PCR analysis of transcript levels revealed similar quantities of the TGF- homologue in all larval stages analyzed except the L4 from the ileum where levels were remarkably lower. Given that mammalian TGF- is anti-inflammatory and down regulates the intensity of immune and inflammatory responses, these data support a relationship between L4 avoidance of spontaneous cure and the ability to modify local immunity. Characterization of these genes and their products may provide useful information on the infection process and in designing new control strategies.