# Impact of bovine respiratory disease on tissue-specific regulation of Zn and vitamin a metabolism and apparent absorption and retention of trace minerals

## TL;DR

This study shows how bovine respiratory disease affects the body's handling of zinc and vitamin A, moving these nutrients to specific tissues during infection.

## Contribution

The study reveals systemic redistribution of trace minerals and altered vitamin A metabolism in cattle during respiratory disease.

## Key findings

- Plasma zinc and retinol concentrations decreased in clinical disease despite no change in absorption or retention.
- Zinc concentrations increased in liver and kidney tissues during clinical disease, indicating redistribution.
- Vitamin A metabolism genes were upregulated in non-lesion lung tissue compared to diseased lung tissue.

## Abstract

Micronutrients are essential for the immune response; however, little is known about their metabolism during bovine respiratory disease infections. In this study, we characterize micronutrient metabolism during clinical and subclinical bovine respiratory disease challenges. This work provides a foundation for developing nutritional interventions to support cattle health during a disease of significant economic importance.

This study aimed to characterize trace mineral and vitamin A metabolism and redistribution during clinical and subclinical respiratory infection in beef on dairy crossbred steers (n = 29; BW = 230 ± 2.14 kg). Steers were assigned to one of four groups encompassing days −6 to −1, 0 to 5, 5 to 10, and 10 to 15 of an experimental viral-bacterial respiratory challenge. Steers were adapted to metabolism crates for 5 d prior to a 5-d total urine and fecal collection period and necropsied at the end of the period. On day 0, steers were inoculated with bovine respiratory syncytial virus strain 375 followed by an intratracheal inoculation with Mannheimia haemolytica strain D153 on day 7. A natural disease challenge occurred during the study, leading to all steers showing signs of disease at necropsy. Lung pathology scores, plasma Fe concentrations, and rectal temperatures for 5 d prior to necropsy were used to categorize animals into clinical (n = 9) and subclinical (n = 20) disease. These categories were confirmed by decreases in dry matter intake (P = 0.06) and nitrogen retention (P = 0.06) in animals with clinical disease compared to subclinical. Plasma concentrations of Zn and retinol were lesser in clinical disease (P ≤ 0.005). Conversely, liver (P = 0.02) and kidney (P = 0.06) concentrations of Zn were higher in clinical disease. This tissue sequestration occurred despite no difference in apparent Zn absorption or retention (P ≥ 0.69), providing evidence of systemic mineral redistribution. There was also no difference in the apparent absorption of Cu, Fe, and Mn (P ≥ 0.44), despite some differences in tissue concentrations. At the site of infection, expression of genes regulating vitamin A transport and metabolism (STRA6, RXRα, RBP4) increased (P ≤ 0.002) in non-lesion lung relative to diseased lung. In both lesion and non-lesion lung, clinical disease decreased RALDH2 expression relative to subclinical disease (P = 0.05). These findings demonstrate that BRD induces a coordinated redistribution of trace minerals from circulation to key tissues and alters local vitamin A metabolism in the lung. This highlights that plasma micronutrient concentrations during infection are not reflective of total body status, but rather an organized physiological response that prioritizes tissue-level demands.