Heat-Shock Proteins Gene Expression in Peripheral Blood Mononuclear Cells as an Indicator of Heat Stress in Beef Calves.

Sang-Gun Roh,Jalil Ghassemi Nejad,Hong-Gu Lee,Won-Seob Kim

doi:10.3390/ani10050895

Sang-Gun Roh, Jalil Ghassemi Nejad + Show 2 more

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https://doi.org/10.3390/ani10050895

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Abstract

Simple SummaryThis study explores the effects of heat stress on the expression of various heat-shock protein (HSP) genes in bovine peripheral blood mononuclear cells (PBMCs) and cell viability as an indicator of stress in beef calves. We found that heat stress inhibits cell proliferation and increases the expression of HSPs in an in vitro model. In addition, HSPs were found to regulate the physiological mechanisms of adaptation to heat stress in an in vivo model. The results showed that HSPs expression in PBMCs can be used as an indicator of heat stress (HS) in beef calves.This study was conducted to investigate the effect of HS on HSPs gene expression in bovine PBMCs of beef calves in in vitro and in vivo models. In the in vitro experiment, blood samples were collected from the jugular vein of five beef calves (age: 174.2 ± 5.20 days, BW: 145.2 ± 5.21 kg). In the in vivo experiment, sixteen Korean native male beef calves (age: 169.6 ± 4.60 days, BW: 136.9 ± 6.23 kg) were exposed to ambient temperature for seven days (22 to 24 °C, relative humidity 60%; temperature–humidity index (THI) = 68 to 70) and subsequently to the temperature and humidity corresponding to the target THI level for 21 days (HS). For PBMC isolation, blood samples were collected every three days. In the in vitro model, the cell viability was significantly decreased in HS groups compared with the control group (p = 0.015). The expression of HSP70 (p = 0.022), HSP90 (p = 0.003) and HSPB1 (p = 0.026) genes was increased in the HS group in in vitro model. In the in vivo experiment, the HSP70 gene expression was increased after sudden exposure to HS conditions (severe THI levels; THI = 88 to 90), whereas HSP90 and HSPB1 showed no differences among the THI groups (p > 0.05). However, in the severe THI group, the HSP70 gene expression returned to normal range after six days of continuous HS. In conclusion, the HSP70 gene plays a pivotal role in protecting cells from damage and is sensitive to HS in immune cells compared with other HSP genes in in vitro and in vivo models. In addition, the in vivo models suggest that calves exhibit active physiological mechanisms of adaptation to HS after six days of continuous exposure by regulating the HSP70 gene expression.

Highlights

Heat stress (HS) alters the body’s physiological mechanisms, resulting in metabolic disorders and decreased immune function in animals [1]
For isolation of Peripheral blood mononuclear cells (PBMCs), the blood samples were processed within 8 h of the sample collection
All the PBMC isolation steps were performed at room temperature as per manufacturer’s instructions

Summary

Introduction

Heat stress (HS) alters the body’s physiological mechanisms, resulting in metabolic disorders and decreased immune function in animals [1]. Severe HS often occurs at the expense of Animals 2020, 10, 895; doi:10.3390/ani10050895 www.mdpi.com/journal/animals. Animals 2020, 10, 895 productivity because it interferes with the maintenance of body condition [2]. Heat-stressed animals reduce their dry matter intake (DMI), activity, rumination and metabolic rate to decrease metabolic heat production [3]. HS affects growth performance and energy metabolism by reducing. DMI in beef calves [4]. HS triggers changes in blood hormones and metabolic indicators by interfering with energy metabolism [5]. Different cellular mechanisms have been proposed to relieve thermal stress in animals [6]

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