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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Infectious Bacterial Diseases Research » Research » Publications at this Location » Publication #351807

Research Project: Characterization of Antigens, Virulence Markers, and Host Immunity in the Pathogenesis of Johne’s Disease

Location: Infectious Bacterial Diseases Research

Title: Vitamin D status and responses in dairy cows naturally infected with Mycobacterium avium subsp. paratuberculosis

item Stabel, Judith
item Reinhardt, Timothy
item Hempel, Randy

Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/26/2018
Publication Date: 12/26/2018
Citation: Stabel, J.R., Reinhardt, T.A., Hempel, R.J. 2018. Vitamin D status and responses in dairy cows naturally infected with Mycobacterium avium subsp. paratuberculosis. Journal of Dairy Science. 102(2):1594-1600.

Interpretive Summary: Johne's disease is a chronic, debilitating intestinal disorder in cattle characterized by diarrhea, reduced feed intake, weight loss and death. Cattle usually become infected as young calves by ingesting feces containing the causative bacteria. However, symptoms of disease do not usually present themselves until the animals reach 3 to 5 years of age or even older. During this time the animal is infected and may be shedding the organism in its feces without showing any clinical signs of disease. In addition to reduced milk production by these animals, they also present a potential infective threat to the rest of the herd. Johne’s disease is difficult to diagnose and therefore to control. Understanding nutrition is a critical factor in improving overall health of the herd and reducing incidence of morbidity. Vitamin D is an important nutrient that is known for its role in calcium homeostasis. In addition, it has demonstrated roles in host immunity to bacterial pathogens. In the present study, the impact of infection with Mycobacterium avium subsp. paratuberculosis on vitamin D metabolism was investigated. This study demonstrated that cows in the clinical stage of disease associated with chronic intestinal inflammation have reduced levels of serum 25OHD3 and changes in expression of genes associated with the vitamin D pathway. These data suggest that despite feeding high levels of vitamin D3 in the diet, efficient use of this nutrient/hormone may be retarded by chronic inflammatory reactions in the cow. Further work to elucidate the mechanism of vitamin D on immune cell function will help to determine its utility as a potential therapeutic during infectious disease.

Technical Abstract: Serum samples were obtained from Holstein dairy control cows and cows naturally infected with Mycobacterium avium subsp. paratuberculosis (MAP) to evaluate the effects of disease status on serum 25-hydroxyvitamin D3 (25OHD3) levels. Disease status was stratified for infected cows into asymptomatic, subclinical infection (n = 25) and cows demonstrating clinical signs (n = 20), along with noninfected control (n = 12) cows for comparison. In addition, portions of ileo-cecal valve were taken from a subsample of cows (n = 5 per treatment group) at necropsy and processed for gene transcription studies. Genes associated with vitamin D metabolism were queried to determine if there was an association between infection and gene expression. Serum 25OHD3 levels were significantly lower in cows in the clinical stage of disease compared to either cows in the subclinical stage and noninfected control cows. Differential expression for genes associated with the vitamin D pathway such as CYP27A1, CYP27B1, vitamin D binding protein and interferon-gamma was dependent upon infection status. An upregulation of CYP27A1 was noted for cows in subclinical status, whereas CYP27B1 expression was enhanced for clinical cows. Increased expression of vitamin D binding protein was observed for infected cattle, regardless of infection status. In summary, decreases in circulating 25OHD3 for animals in clinical disease may suggest that these cows have reduced innate immune responses, thereby influencing the ability of animals to fight infection.