Submitted to: American Association of Immunologists Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: February 1, 2007
Publication Date: May 14, 2007
Citation: Lillehoj, H.S., Park, S.S. 2007. Characterization of chicken TNFSF15 and it's role in coccidiosis. American Association of Immunologists Proceedings. May 18-22. Miami Beach, Florida.
Interpretive Summary: Understanding basic immunobiology of host response to pathogens is important in the development of effective vaccines against many infectious diseases. There is in general limited information concerning the various immune molecules involved in controlling host immune response to microbial pathogens and this hinders rapid progress in the development of new vaccines. In this paper, ARS scientists describe a new effector molecule which is secreted by lymphocytes in response to coccidiosis, an economically important parasite infection affecting the gut. This factor called tumor necrosis factor super family 15 (TNFSF15) is produced locally by intestinal lymphocytes when coccidia parasites infect the gut and plays a role in local inflammatory response to coccidia parasites. The completion of DNA sequences of TNFSF15 and successful production of biologically active recombinant TNFSF15 as described in this paper now provides a solid basic knowledge for future studies on the role of this effector molecule in disease process. This paper enhances basic understanding of disease mechanisms and will help industry to design a better control strategy against avian coccidiosis.
A full-length cDNA encoding chicken tumor necrosis factor superfamily 15 (TNFSF15) was isolated and its functional role was investigated. TNFSF15 transcripts were primarily expressed in spleen, liver, intestinal intraepithelial lymphocytes (IEL), peripheral blood lymphocytes and bursa. In vitro infection of HTC macrophages with three species of Eimeria sporozoites induced TNFSF15 gene expression. In vivo experiments revealed that TNFSF15 gene was highly increased following primary infections with E. acervulina or E. maxima. In contrast, no consistent changes in transcript levels were seen following primary infection with E. tenella, or following secondary infection with any of the three Eimeria species. Following infection with E. acervulina and E. maxima, TNFSF15 transcripts were primarily expressed in intestinal CD4+ and TCR2+ IEL, respectively. A dose-dependent cytotoxic effect of recombinant TNFSF15 protein was observed on HTC and LSCC-RP9 tumor cells. These results indicate that TNFSF15 plays an important role in the local inflammatory response to Eimeria.