Heat as a stressor of poultry has been studied extensively for many decades; it affects poultry production on a worldwide basis and has significant impact on well-being and production. More recently, the involvement of heat stress in inducing oxidative stress has received much interest. Oxidative stress is defined as the presence of reactive species in excess of the available antioxidant capacity of animal cells. Reactive species can modify several biologically cellular macromolecules and can interfere with cell signaling pathways. Furthermore, during the last decade, there has been an ever-increasing interest in the use of a wide array of natural feed-delivered phytochemicals that have potential antioxidant properties for poultry. In light of this, the current review aims to (1) summarize the mechanisms through which heat stress triggers excessive superoxide radical production in the mitochondrion and progresses into oxidative stress, (2) illustrate that this pathophysiology is dependent on the intensity and duration of heat stress, (3) present different nutritional strategies for mitigation of mitochondrial dysfunction, with particular focus on antioxidant phytochemicals. Oxidative stress that occurs with heat exposure can be manifest in all parts of the body; however, mitochondrial dysfunction underlies oxidative stress. In the initial phase of acute heat stress, mitochondrial substrate oxidation and electron transport chain activity are increased resulting in excessive superoxide production. During the later stage of acute heat stress, down-regulation of avian uncoupling protein worsens the oxidative stress situation causing mitochondrial dysfunction and tissue damage. Typically, antioxidant enzyme activities are upregulated. Chronic heat stress, however, leads to downsizing of mitochondrial metabolic oxidative capacity, up-regulation of avian uncoupling protein, a clear alteration in the pattern of antioxidant enzyme activities, and depletion of antioxidant reserves. Some phytochemicals, such as various types of flavonoids and related compounds, were shown to be beneficial in chronic heat-stressed poultry, but were less or not effective in non-heat-stressed counterparts. This supports the contention that antioxidant phytochemicals have potential under challenging conditions. Though substantial progress has been made in our understanding of the association between heat stress and oxidative stress, the means by which phytochemicals can alleviate oxidative stress have been sparsely explored.

https://biblio.ugent.be/publication/8518014/file/8519404.pdf

Association between heat stress and oxidative stress in poultry; mitochondrial dysfunction and dietary interventions with phytochemicals.

/pdf/association-between-heat-stress-and-oxidative-stress-in-1u02je9s5g.pdf

Association between heat stress and oxidative stress in poultry; mitochondrial dysfunction and dietary interventions with

Use of polyphenol-rich grape by-products in monogastric nutrition. A review

Oxidative damage to poultry: from farm to fork

Resveratrol (3,4′,5-trihy- droxystilbene), a natural phytoalexin polyphenol, exhibits anti-oxidant, anti-inflammatory, and anti-carcinogenic properties. This phytoalexin is well-absorbed and rapidly and extensively metabolized in the body. Inflammation is an adaptive response, which could be triggered by various danger signals, such as invasion by microorganisms or tissue injury. In this review, the anti-inflammatory activity and the mechanism of resveratrol modulates the inflammatory response are examined. Multiple experimental studies that illustrate regulatory mechanisms and the immunomodulatory function of resveratrol both in vivo and in vitro. The data acquired from those studies are discussed.

https://www.mdpi.com/1420-3049/26/1/229/pdf

Anti-Inflammatory Action and Mechanisms of Resveratrol

Resveratrol induces antioxidant and heat shock protein mRNA expression in response to heat stress in black-boned chickens

The aim of this study was to investigate whether supplementation with resveratrol could alleviate intestinal injuries and to explore how resveratrol regulates heat shock protein (HSP)70, HSP90, nuclear factor kappa B (NF-κB) and epidermal growth factor (EGF) expression in the jejunal mucosa of black-boned chickens under circular heat stress. A total of 300 black-boned chicks of 42-d-old were randomly assigned to five treatment groups. The positive control chickens were kept in a normal-temperature (NT, 24 ± 2 °C) chamber and fed with a basal diet. The other four groups were kept in a circular high-temperature (HT, 37 ± 2 °C) chamber for 8 h and fed a basal diet supplemented with 0, 200, 400, or 600 mg per kg of resveratrol for 15 days. The results showed that the heat-stress responses damaged the villus structures of the jejunum and ileum, resulting in shortened intestinal villi, deepened crypts, and a reduced villus height to crypt depth (V/C) ratio and decreased the numbers of goblet cells and lymphocytes. Heat stress also caused increased mRNA and protein expression of HSP70, HSP90 and NF-κB, and reduced EGF in the jejunal mucosa. Dietary supplementation with 400 mg per kg of resveratrol improved the villus morphology, increased the numbers of goblet cells and lymphocytes, attenuated the mRNA overexpression of HSP70, HSP90 and NF-κB on the 6th, 10th and 15th day of heat stress (P < 0.05), and activated the expression of EGF (P < 0.05) in the jejunal mucosa. Resveratrol reduced protein expression of HSP70, HSP90 and NF-κB in the jejunal villi after 15 days of heat stress, and increased EGF expression from the lamina propria toward the epithelial cells of the villi. These results suggest that dietary resveratrol offers a potential nutritional strategy to improve the intestinal morphology and alleviate jejunum mucosa injuries by modulating the mRNA and protein expression of HSPs, and the epithelial growth factor and transcription factor in black-boned chickens subjected to circular heat stress.

Resveratrol modulates intestinal morphology and HSP70/90, NF-κB and EGF expression in the jejunal mucosa of black-boned chickens on exposure to circular heat stress.

Xuefeng black-boned chicken is one of the famous native breeds in China. In this work, we reported the complete mitochondrial genome sequence of the Xuefeng black-boned chicken for the first time, which was determined through PCR-based method. The total length of the mitogenome was 16,783 bp, with the base composition of 30.24% for A, 23.72% for T, 32.52% for C, 13.53% for G, in the order C > A > T > G feature occurring in the Xuefeng black-boned chicken. It contained the typical structure, including 2 ribosomal RNA genes, 13 protein-coding genes, 22 transfer RNA genes and 1 non-coding control region (D-loop region). It was similar to the gene arrangement in Silky chicken. The complete mitochondrial genome sequence of the Xuefeng black-boned chicken provided an important data for further study on the genetic mechanism.

The complete mitochondrial genome of the Xuefeng black-boned chicken

Taoyuan chicken is excellent native breeds in China. This study firstly determined the complete mitochondrial genome sequence of Taoyuan chicken using PCR-based amplification and Sanger sequencing. The characteristic of the entire mitochondrial genome was analyzed in detail, with the base composition of 30.26% A, 23.79% T, 32.44% C, 13.50% G in the Taoyuan chicken (16,784 bp in length). It contained 2 ribosomal RNA genes, 13 protein-coding genes, 22 transfer RNA genes and a major non-coding control region (D-loop region). The complete mitochondrial genome sequence of Taoyuan chicken will be useful for the phylogenetics of poultry, and be available as basic data for the genetics and breeding.

Determination and analysis of the complete mitochondrial genome sequence of Taoyuan chicken

Primary infection of Toxoplasma gondii can cause serious abnormal pregnancy outcomes such as miscarriage and stillbirth. Inhibitory molecule B7-H4 is abundantly expressed in dendritic cells (DCs) and plays an important role in maintaining immune tolerance. However, the role of B7-H4 in decidual DCs (dDCs) in T. gondii-induced abnormal pregnancy outcomes is not clear.We established T. gondii-infected abnormal pregnancy model in wild-type (WT) and B7-H4 knockout (B7-H4-/-) pregnant mice in vivo and cultured primary human dDCs in vitro. The abnormal pregnancy outcomes were observed and the expression of B7-H4, functional molecules (CD80, CD86, and MHC-II or HLA-DR), indoleamine 2,3-dioxygenase (IDO), cytokines (IL-10 and IL-12), and signaling molecules JAK2/STAT3 in dDCs was detected by flow cytometry and Western blot.Our results showed that T. gondii infection significantly decreased B7-H4 expression in dDCs. In addition, B7-H4-/- infected pregnant mice showed much more severe abnormal pregnancy outcomes than their counterparts. Importantly, B7-H4-/- infection further regulated the expression of molecules (CD80, CD86, and MHC-II or HLA-DR), enzyme IDO, and cytokines (IL-10 and IL-12) in dDCs. We further discovered that B7-H4-/- infection impairs the JAK2/STAT3 pathway, contributing to dDC dysfunction.Taken together, the results show that reduction of B7-H4 by T. gondii infection significantly modulates the decrease in cytokine IL-10 and enzyme IDO and the increase in cytokine IL-12, contributing to dDC dysfunction. Moreover, the JAK2/STAT3 pathway is involved in the regulation of B7-H4 by T. gondii infection and in the subsequent IDO and cytokine production, which ultimately contributes to abnormal pregnancy outcomes. 

/pdf/b7-h4-reduction-induced-by-toxoplasma-gondii-infection-1hmuax78.pdf

Hong-Bing Xie

Papers

Resveratrol induces antioxidant and heat shock protein mRNA expression in response to heat stress in black-boned chickens

Resveratrol modulates intestinal morphology and HSP70/90, NF-κB and EGF expression in the jejunal mucosa of black-boned chickens on exposure to circular heat stress.

The complete mitochondrial genome of the Xuefeng black-boned chicken

Determination and analysis of the complete mitochondrial genome sequence of Taoyuan chicken

B7-H4 reduction induced by Toxoplasma gondii infection results in dysfunction of decidual dendritic cells by regulating the JAK2/STAT3 pathway