Production of alpha interferon in Cowdria ruminantium-infected cattle and its effect on infected endothelial cell cultures

• Published in: Infection and Immunity Vol. 62; no. 6; pp. 2600 - 2604
• Main Authors: Totté, P, Jongejan, F, de Gee, A L, Wérenne, J
• Format: Journal Article
• Language: English
• Published: United States American Society for Microbiology 01.06.1994
• Subjects: Animals; Antibodies, Bacterial - analysis; bovin; Cattle; cell culture; Cells, Cultured; cowdria; Cowdria ruminantium; crecimiento; croissance; cultivo de celulas; culture de cellule; disease resistance; Ehrlichia ruminantium - drug effects; Ehrlichia ruminantium - immunology; Endothelium, Vascular - microbiology; epitelio; epithelium; Female; ganado bovino; growth; Heartwater Disease - immunology; Heartwater Disease - metabolism; inhibicion; inhibition; interferon; Interferon Type I - pharmacology; Interferon-alpha - biosynthesis; interferonas; interferons; Recombinant Proteins; resistance aux maladies; resistencia a la enfermedad
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/iai.62.6.2600-2604.1994

Cattle that resisted experimental heartwater infection caused by the rickettsia Cowdria ruminantium produced significant levels of circulating alpha interferon (IFN-alpha), whereas animals that died from heartwater did not. In vitro, recombinant bovine IFN-alpha was found to significantly reduce the yield of Cowdria organisms in bovine endothelial cells, but even at a high concentration (1,000 U/ml), IFN-alpha did not completely prevent the growth of Cowdria organisms in these cells. This limited inhibitory effect of IFN-alpha is in agreement with the in vivo situation where an infectious process has to take place to induce a protective immune response. Our results suggest that IFN-alpha produced in vivo in response to Cowdria infection may represent an efficient way to slow down the infection and allow the animal to mount a protective immune response. IFN-alpha is the first endogenously produced factor shown to have anti-Cowdria activity.