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Abstract Title:

Effects of 1, 25-dihydroxy vitamin D3 on clinical symptoms, pro-inflammatory and inflammatory cytokines in calves with experimental pneumonia.

Abstract Source:

Res Vet Sci. 2020 Oct ;132:186-193. Epub 2020 May 17. PMID: 32593863

Abstract Author(s):

Parisa Asgharpour, Mohammad Reza Mokhber Dezfouli, Mohammad Goli Nadealian, Zohre Eftekhari, Gholam Reza Nikbakht Borojeni

Article Affiliation:

Parisa Asgharpour

Abstract:

1, 25-dihydroxycholecalciferol is recognized as a potent immune-modulator which can fight against the pathogens via the activation of vitamin D3 receptors (VDRs), as well as stimulating various cytokines in infectious diseases. In the present study, because of the vitamin D3 has an appropriate immunomodulatory, the effects of this vitamin on the levels of pre-inflammatory and anti-inflammatory cytokines have been investigated in calves with experimental pasteurellosis. This study was experimentally carried out on 10 Holstein crossbred male calves (2-4 months) that were divided into two groups. Prepared Pasteurella multocida (3 × 10 CFU/mL) was inoculated in the trachea with a lavage catheter and then the treatment group was injected with 1, 25-dihydroxycholecalciferol after confirming pneumonia. Blood sampling, clinical symptoms scoring and radiological evaluation were recorded for both groups at different time intervals. The prescription of, vitamin Dto the treatment group caused a decline in clinical symptoms score and changed interstitial and alveolo-interstitial lung pattern to such a degree that it could recover in comparison with the control group. The concentrations of pro-inflammatory cytokines (i.e., IL-1β, IL-6, and TNF-α) and the chemokine (IL-8) showed a significant decrease in the treatment group while the concentration of IL-10 increased in the treatment groups following the vitamin Dinjection (P = .001). The evidence from the current study suggests that vitamin D3 exert the immunomodulatory effects in infectious diseases through the regulation of cytokines and activation of VDR pathways to produce antimicrobial peptides.

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