Title: NITRIC OXIDE PRODUCTION BY MACROPHAGES STIMULATED WITH SPOROZOITES, LIPOPOLYSACCHARIDE, OR IFN-GAMMA AND ITS DYNAMIC CHANGES IN SC AND TK STRAINS OF CHICKENS INFECTED WITH EIMERIA TENELLA
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 30, 2003
Publication Date: July 14, 2003
Citation: Lillehoj, H.S., Li, G. 2003. Nitric oxide production by macrophages stimulated with sporozoites, lipopolysaccharide, or ifn-gamma and its dynamic changes in sc and tk strains of chickens infected with eimeria tenella. Avian Diseases. 48:244-253.
Interpretive Summary: Avian coccidiosis is an intestinal disease caused by several species of Eimeria protozoa. Economic loss due to avian coccidiosis is estimated to be > $700 million. Medication has been the primary method for coccidiosis control but this method will be phased out due to increasing concerns over drug resistance. Long-term goal of ARS research is to develop novel method to control coccidiosis. In order to do that, we need to understand basic immunobiology of host-parasite interactions which lead to protection. In this paper, ARS scientists examined the role of macrophages in coccidiosis. The results indicate that chicken macrophages produce high level of effector molecules, e.g., nitric oxide (NO) when stimulated with interferon-gamma, LPS or sporozoites of Eimeria. Since NO is a multifunctional signaling molecule involved in a diverse array of biological processes including regulation of host innate immunity, further studies on NO function in coccidiosis will lead to better understanding of host immunity against this pathogen. Information obtained from this study will help poultry scientists to devise a novel control method for avian coccidiosis.
Nitric oxide (NO) is an important mediator of innate and acquired immunities. In the studies reported here, we quantified NO produced in vitro by chicken leukocytes and macrophages and in vivo during the course of experimental infection with Eimeria, the causative agent of avian coccidiosis, and identified macrophages as the primary source of inducible NO. Chicken recombinant interferon- chrIFN-gamma) induced high levels of NO in normal spleen macrophages. E. tenella sporozoites, bacterial lipopolysaccharides LPS) and IFN-gamma induced NO in established chicken macrophage cell lines. E. tenella-infected chickens produced higher levels of NO compared with noninfected controls. In infected animals, NO levels were generally higher in serum and the intestinal duodenum and cecum of SC chickens compared with TK strain. These findings are discussed in the context of the genetic differences in SC and TK chickens that may contribute to their divergent disease phenotypes.