Innate immune and chronic heat stress responses in sturgeons: Advances and insights from studies on Russian sturgeons

Impact of chronic heat stress in broiler breeders on egg quality, hatchability, and day old chick quality.

This study aimed to investigate the effects of chronic heat stress on the immunophenotyping of lymphocytes in immune organs of growing pigs. A single-factor randomized block design was used, and 15 healthy growing large white barrows (5 litters, 3 pigs/litter) with similar body weight (40.8 kg) were assigned into 3 groups (5 pigs in each group). Groups were: control group (Con, in 23 °C environmental control chamber, fed ad libitum), heat stress group (HS, in 33 °C environmental control chamber, fed ad libitum), and pair-fed group (PF, in 23 °C environmental control chamber, fed diets according to the feed intake of HS group). After a 7-d adaption, the experiment lasted for 21 d. The results showed as follows: (1) activated T cells in the thymus of HS pigs were higher than those in PF pigs (P < 0.05). Monocytes and dendritic cells in the thymus of HS pigs were significantly higher than that in Con and PF pigs (P < 0.05), while the proportions of these 2 lymphocytes in the thymus of Con pigs did not differ from PF pigs (P > 0.05). Compared with Con pigs, the proportion of CD4+ (P < 0.05) and CD8+ T cells (P < 0.10) in the thymus was increased in HS pigs, while the proportion of CD4+ and CD8+ T cells in PF pigs did not differ from Con pigs (P > 0.05). (2) Compared with Con pigs, significantly decreased T cells, increased B cells and monocytes were found in the spleen of pigs exposed to heat stress (P < 0.05); the proportions of these 3 types of lymphocytes were not significantly different between Con and PF pigs (P > 0.05). The proportions of CD4+ T cells and Treg cells in the spleen of pigs exposed to heat stress tended to be lower than those in the Con pigs (P < 0.10). (3) The proportion of lymphocytes in the tonsils of pigs exposed to heat stress did not differ from Con pigs (P > 0.05); compared with PF pigs, the proportion of Treg cells was significantly decreased in HS pigs (P < 0.05). In conclusion, chronic heat stress stimulates the development and maturation of T cells in the pig thymus toward CD4+ and CD8+ T cells and increases the proportion of monocytes and dendritic cells; under the condition of chronic heat stress, the immune response process in the spleen of pigs is enhanced, but chronic heat stress impairs the survival of CD4+ T cells in the spleen.

Heat stress has received growing concerns regarding the impact on seafood quality. However, the effects of heat stress on the sensory properties of seafood remain unknown. In this study, the sensory properties of fresh oyster (Crassostrea ariakensis) treated with chronic heat stress (30 °C) for 8 weeks were characterized using electronic nose, electronic tongue, sensory evaluation, HS–SPME–GC–MS, LC–MS and transcriptomics. Overall, chronic heat stress reduced the overall sensory properties of oysters. The metabolic network constructed. based on enrichment results of 423 differential metabolites and 166 differentially expressed genes, showed that the negative effects of chronic heat stress on the sensory properties of oysters were related to oxidative stress, protein degradation, lipid oxidation, and nucleotide metabolism. The results of the study provide valuable insights into the effects of heat stress on the sensory properties of oysters, which are important for ensuring a sustainable supply of high-quality seafood and maintaining food safety.

Chronic heat stress caused by global warming can have serious implications for fish survival. The kidney plays a central role in many homeostatic functions, including water and electrolyte regulation. However, there is limited knowledge about the effect of heat stress on fish kidneys. In this study, water temperatures were increased from 20 °C to 24 °C and 28 °C in 8 days at a warming rate of 1 °C/d, and then maintained for 12 days. We investigated the effects of mild heat stress (24 °C) and high heat stress (28 °C) on Siberian Sturgeon (Acipenser baerii) kidneys using histological observation, flow cytometry detection, and RT-qPCR. Our histological observations revealed that heat stress caused significant infiltration of inflammatory cells in the kidney, especially at 28 °C. The flow cytometry assay demonstrated a significant increase in the number of apoptotic cells after heat stress at 28 °C compared to a control group at 20 °C (p = 0.033). The level of plasma creatinine was significantly increased in the 28 °C group compared to the control group (p = 0.001). In addition, the mRNA expression levels of heat shock protein GRP75 increased (p = 0.009). The results indicate that heat stress at 28 °C caused damage to the kidneys of A. baerii and triggered the protective response of heat shock proteins. In conclusion, this study contributes to the understanding of the coping strategies of the kidney of A. baerii for chronic heat stress.

The roughskin sculpin ( Trachidermus fasciatus ) belongs to the family Cottidae and is a small carnivorous catadromous fish distributed along the coasts of China, Korea, and Japan. The effects of heat stress on roughskin sculpin have yet to be systematically performed. This study aimed to explore the effects of chronic heat stress on the roughskin sculpin. The survival rate, gill histopathological changes, and heat stress protein gene expression patterns of roughskin sculpin were analyzed after different temperature stresses of 19 ℃, 22 ℃, 25 ℃, 28 ℃, and 31 ℃ for 0, 3, 6, 9, and 12 days. The results revealed that roughskin sculpin could not survive at 33 ℃. Chronic heat stress can cause severe damage to gill tissue, reducing the gills’ respiratory efficiency. Moreover, the expressions of hspb1, hspb7, and hspb11 changed significantly after heat stress. In the 31 ℃ treatment group, as stress time increased, hspb1, hspb7, and hspb11 expression initially increased and then decreased. This study’s results provide a reference for the study of heat stress physiology of roughskin sculpin as well as a new idea and method for evaluating and breeding heat stress traits of roughskin sculpin.

Chronic heat stress inhibits glycogen synthesis through gga-miR-212-5p/GYS1 axis in the breast muscle of broilers

BackgroundHeat stress in laying hens negatively affects egg production and shell quality by disrupting the homeostasis of plasma calcium and phosphorus levels. Although the kidney plays an important role in calcium and phosphorus homeostasis, evidence regarding the effect of heat stress on renal injury in laying hens is yet to be elucidated. Therefore, the aim of this study was to evaluate the effects of chronic heat stress on renal damage in hens during laying periods.MethodsA total of 16 white-leghorn laying hens (32 weeks old) were randomly assigned to two groups (n = 8). One group was exposed to chronic heat stress (33 °C for 4 weeks), whereas the other group was maintained at 24 °C.ResultsChronic heat exposure significantly increased plasma creatinine and decreased plasma albumin levels (P < 0.05). Heat exposure also increased renal fibrosis and the transcription levels of fibrosis-related genes (COLA1A1, αSMA, and TGF-β) in the kidney. These results suggest that renal failure and fibrosis were induced by chronic heat exposure in laying hens. In addition, chronic heat exposure decreased ATP levels and mitochondrial DNA copy number (mtDNA-CN) in renal tissue, suggesting that renal mitochondrial dysfunction occurs under conditions of heat stress. Damaged mitochondria leak mtDNAs into the cytosol and mtDNA leakage may activate the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) signaling pathway. Our results showed that chronic heat exposure activated the cGAS-STING pathway as indicated by increased expression of MDA5, STING, IRF7, MAVS, and NF-κB levels. Furthermore, the expression of pro-inflammatory cytokines (IL-12) and chemokines (CCL4 and CCL20) was upregulated in heat-stressed hens.ConclusionsThese results suggest that chronic heat exposure induces renal fibrosis and mitochondrial damage in laying hens. Mitochondrial damage by heat stress may activate the mtDNA-cGAS-STING signaling and cause subsequent inflammation, which contributes to the progression of renal fibrosis and dysfunction.

Effect of chronic heat stress on some physiological and immunological parameters in different breed of broilers.

The main purpose of this study was to assess the effects of chronic heat stress (CHS) on humoral and cellular responses of DNA vaccination. Mice with the CHS were exposed to a temperature set at 38 +/- 1 degrees C, 2h per day, for 35 days, and mice with thermoneutral (TN) temperature were maintained at 24 +/- 1 degrees C for the same period of time. Both groups of mice were immunized with a DNA vaccine-expressed viruscapsid protein 1 (VP1) of foot-and-mouth disease virus (FMDV), and we tested their antigen-specific humoral and cellular responses during the treatments. Compared with the TN group, titers of total Imunoglobulin G (IgG) and IgG1 and expression of interleukin 4 (IL-4) in CD4(+) cells of CHS group were not affected significantly. In contrast, the levels of IgG2a, T cell proliferations, and expression of interferon-gama (IFN-gamma) in both CD4(+) and CD8(+) cells were suppressed significantly, and cytotoxic T-lymphocyte (CTL) responses in vivo were also weakened by the CHS condition. These results indicate that the CHS treatment has negatively affected the immune responses of DNA vaccination and particularly impaired to the cell-mediated responses. It suggests that vaccination in animals is affected by the changes of ambient temperature.

Expression of digestive enzyme and intestinal transporter genes during chronic heat stress in the thermally manipulated broiler chicken

BackgroundThis study investigated the effects of chronic heat stress on liver inflammatory injury and its potential mechanisms in broilers. Chickens were randomly assigned to the 1-week control group (Control 1), 1-week heat stress group (HS1), 2-week control group (Control 2), and a 2-week heat stress group (HS2) with 15 replicates per group. Broilers in the heat stress groups were exposed to heat stress (35 ± 2 °C) for 8 h/d for 7 or 14 consecutive days, and the rest of 26 hours/day were kept at 23 ± 2 °C like control group broilers. Growth performance and liver inflammatory injury were examined for the analysis of liver injury.ResultsThe results showed that heat stress for 2 weeks decreased the growth performance, reduced the liver weight (P < 0.05) and liver index (P < 0.05), induced obvious bleeding and necrosis points. Liver histological changes found that the heat stress induced the liver infiltration of neutrophils and lymphocytes in broilers. Serum levels of AST and SOD were enhanced in HS1 (P < 0.01, P < 0.05) and HS2 (P < 0.01, P < 0.05) group, compared with control 1 and 2 group broilers. The MDA content in HS1 group was higher than that of in control 1 group broilers (P < 0.05). Both the gene and protein expression levels of HSP70, TLR4 and NF-κB in the liver were significantly enhanced by heat stress. Furthermore, heat stress obviously enhanced the expression of IL-6, TNF-α, NF-κB P65, IκB and their phosphorylated proteins in the livers of broilers. In addition, heat stress promoted the activation of NLRP3 with increased NLRP3, caspase-1 and IL-1β levels.ConclusionsThese results suggested that heat stress can cause liver inflammation via activation of the TLR4-NF-κB and NLRP3 signaling pathways in broilers. With the extension of heat stress time, the effect of heat stress on the increase of NF-κB and NLRP3 signaling pathways tended to slow down.

Robustness to chronic heat stress in laying hens: a meta-analysis

This study investigated the effects of chronic heat stress (HS) on brain injury in broilers and the associated molecular changes. A chronic HS model was established by exposing broilers to 35 °C from 08:00 to 20:00 daily from 21 to 42 days of age, and samples were collected at 28, 35, and 42 days of age. Chronic HS significantly impaired growth performance and was associated with histopathological and ultrastructural alterations in brain tissue. Serum antioxidant enzyme activities and the total antioxidant capacity were significantly reduced, whereas malondialdehyde levels were significantly increased, indicating sustained oxidative stress (OS). Blood-brain barrier (BBB) permeability, assessed by Evans blue extravasation, was significantly higher in HS birds and was accompanied by reduced mRNA expression of the tight junction-related genes ZO-1 and Claudin-5. In addition, chronic HS was associated with increased mRNA expression in genes related to cellular stress, oxidative stress, and inflammation, including key components of the TLR4/MyD88/NF-κB/NLRP3 pathway, as well as decreased expression of IL-4. These findings suggest that chronic HS is associated with enhanced OS, altered neuroinflammatory gene expression, and BBB impairment in the broiler brain. Overall, this study provides evidence that chronic HS is associated with brain injury in broilers and highlights a potential link among OS, inflammation-related transcriptional changes, and BBB dysfunction, thereby offering a basis for further mechanistic and interventional studies.

BackgroundChronic heat stress has a negative impact on poultry meat quality. Although this has been extensively investigated, previous studies have primarily focused on metabolic alterations and oxidative stress in the pectoralis major (PM) muscle under chronic heat stress, and not all of the underlying molecular mechanisms are completely understood.MethodsA total of 144 male Arbor Acres broilers (28 d old) were randomly allocated into 3 treatment groups: (1) the normal control (NC) group, with broilers raised at 22 °C and fed a basal diet; (2) the heat stress (HS) group, with birds raised at 32 °C and fed a basal diet; and (3) the pair-fed (PF) group, with birds raised at 22 °C and fed the amount of feed equal to the feed consumed on the previous day by the HS group. The experiment lasted for 14 d.ResultsChronic heat stress decreased the average daily feed intake and average daily gain, increased feed:gain ratio (P < 0.05); and increased drip loss, cooking loss, shear force, hardness, and decreased pH, redness (a*); and springiness of PM muscle (P < 0.05). Furthermore, chronic heat stress decreased muscle fiber density, increased connective tissue, and led to intracellular vacuolation. The transcriptome analyses indicated that the effect of chronic heat stress on meat quality was not only related to metabolism and oxidative stress, but also to signal transduction, immune system, transport and catabolism, cell growth and death, and muscle structure.ConclusionsChronic heat stress has a negative impact on the growth performance, meat quality, and the PM muscle structure of broilers. Transcriptome analysis revealed a comprehensive understanding of the mechanism of the chronic heat stress-induced deterioration of broiler meat quality at the transcriptional level.

BackgroundAs a result of climate change, dairy cows even in confinement systems are exposed to high ambient temperatures and environmental factors inducing heat stress. However, there are indications that chronic heat stress with reduced feed intake initially stimulates a systemic inflammatory response and progressively reduces the immunocompetence. This finally increases the disease susceptibility. This study aimed to elucidate the effects of chronic heat stress or equivalent reduced feed intake via pair-feeding at thermoneutrality on the daily hematological profile, leukocyte NF-κB p65 signaling pathway, immune function, and metabolism in peripheral blood mononuclear cells (PBMC) of dairy cows. MethodsPrimiparous, mid-lactating Holstein cows (n = 30) were assigned to heat-stressed (HS; temperature-humidity index (THI) 76, 28°C, relative humidity (RH) 50%), control (CON; THI 60, 16°C, RH 69%), or pair-fed (PF; THI 60, 16°C, RH 69%) group for 7 days. ResultsHS cows showed a lower number of erythrocytes, platelets, lymphocytes, hemoglobin, hematocrit, and iron concentration and increased endotoxin concentration compared to PF cows. The presence of NF-κB p65 in the nucleus of leukocytes was lower in HS than in the two other groups on day 5, while it was higher in HS cows on day 6. Furthermore, on day 6, RNA sequencing of PBMC showed an enrichment of higher expressed genes in pathways of platelet activation, coagulation cascade, leukocyte transendothelial migration, and focal adhesion in HS cows compared to both non-heat-stressed groups. However, T cell receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation, and metabolic processes were expressed lower in HS compared to CON cows. ConclusionThe results suggest that heat stress induces dynamic changes of the red blood cell and lymphocyte profiles but only transiently activating the leukocytic NF-κB p65 signaling pathway while suppressing T cell signaling, both likely in response to the increased circulating endotoxin concentration. The activation of platelets and the coagulation cascade were likely due to heat-stress-induced microvascular injuries, altered hematocrit, or vasodilatation. Altered blood coagulation and immune responses need to be considered in the management of heat-stressed dairy cows.