|Zhao, Chengquan - UCLA, LOS ANGELES, CA|
|Nguyen, Tung - UCLA, LOS ANGELES, CA|
|Liu, Lide - UCLA, LOS ANGELES, CA|
|Lehrer, Robert - UCLA, LOS ANGELES, CA|
Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 8, 2001
Publication Date: N/A
Interpretive Summary: Intensive production contributes to the productivity and efficiency of the poultry industry. However, as a consequence of intensive production, there is increased risk and spread of infectious diseases. Producers and poultry health specialists continually rate respiratory disease as the most economically significant group of diseases. Innate or non-specific immunity is critical in the early response to respiratory diseases. Cells lining the airway can produce substances that kill or inhibit the growth of microbes. One group of these substances is known as defensins. In the present study, defensins produced by cells of the airway in poultry were isolated and characterized. Two new defensins were identified, one from chickens and one from turkeys. These defensins are similar to those isolated from other animals. In chickens infected with a respiratory microbe, the expression of the defensin was increased. The results of this sstudy will increase our basic knowledge of the avian immune response to respiratory diseases and will provide information necessary to develop strategies for disease resolution.
Technical Abstract: Gallinacin-3 and gallopavin-1 are newly characterized, epithelial beta- defensins of the chicken (Gallus gallus) and turkey (Meleagris gallopavo), respectively. In normal chickens, the expression of gallinacin-3 was especially prominent in the tongue, bursa of Fabricius and trachea. It also occurred in other organs, including the skin, esophagus, air sacs, large intestine and kidney. Tracheal expression of gallinacin-3 increased significantly after experimental infection of chickens with Hemophilus paragallinarium, whereas its expression in the tongue, esophagus and bursa of Fabricius was unaffected. The precursor of gallinacin-3 contained a 21-residue C-terminal extension not present in the gallopavin (GPV)-1 prepropeptide. By comparing the cDNA sequences of gallinacin-3 and GPV-1, we concluded that a 2 nt insertion into the gallinacin-3 gene had induced a frame shift that read through the original stop condon and allowed the chicken propeptide to lengthen. The strikin g structural resemblance of the precursors of beta-defensins to those of crotamines (highly toxic peptides found in rattlesnake venom) supports their homology, even though defensins are specialized to kill micro-organisms and crotamines to kill much larger prey.