Mild Heat Stress Research Articles

Hormetic effects of mild heat stress on the primary culture of mouse prefrontal cerebrocortical neurons

BackgroundHormesis is an adaptive response of a biological system to low dose of stressors. It exerts beneficial effects to enable the cells and organisms to sustain the unfavourable conditions. Mild heat stress is one of the widely studied hormetic agents having antiageing and lifespan prolonging effects. In order to study the effect of mild heat stress on the primary culture of mouse prefrontal cerebrocortical neurons with reference to ageing-associated degenerative alterations the present investigations were carried out.Study designThe prefrontal cerebrocortical neurons of E17 day mouse embryo were cultured on poly-l-lysine coated coverslips and fed with neurobasal medium supplemented with B-27 at 37 °C and 5% CO2. The neurons were divided into two groups: control group and mild heat stress group. The neurons from the control group were incubated at 37 °C without any heat stress. The neurons from the mild heat stress group were subjected to hyperthermic stress of 38 °C for 30 min on 2nd, 4th and 6th day of seeding.MethodsOn the 3rd, 5th and 7th day of incubation, viability was studied by calcein-AM and propidium iodide assay and cell death assay was carried out by lactate dehydrogenase (LDH) assay. The surviving neurons were enumerated on 10th, 15th and 20th day of incubation by live cell imaging. All microscopic studies were carried out by observer blinding.ResultsIt was observed that there was higher percentage of viable neurons and lower percentage of degenerating neurons in the mild heat stress group than the control. The difference was highly significant (p < 0.001).ConclusionMild heat stress (38 °C for 30 min on every alternate day up to 6 days of incubation) exerts hormetic effects on the primary culture of mouse prefrontal cerebrocortical neurons by delaying the degenerative alterations.

Optical Feedback Loop Involving Dinoflagellate Symbiont and Scleractinian Host Drives Colorful Coral Bleaching

Coral bleaching, caused by the loss of brownish-colored dinoflagellate photosymbionts from the host tissue of reef-building corals, is a major threat to reef survival. Occasionally, bleached corals become exceptionally colorful rather than white. These colors derive from photoprotective green fluorescent protein (GFP)-like pigments produced by the coral host. There is currently no consensus regarding what causes colorful bleaching events and what the consequences for the corals are. Here, we document that colorful bleaching events are a recurring phenomenon in reef regions around the globe. Our analysis of temperature conditions associated with colorful bleaching events suggests that corals develop extreme coloration within 2 to 3weeks after exposure to mild or temporary heat stress. We demonstrate that the increase of light fluxes in symbiont-depleted tissue promoted by reflection of the incident light from the coral skeleton induces strong expression of the photoprotective coral host pigments. We describe an optical feedback loop involving both partners of the association, discussing that the mitigation of light stress offered by host pigments could facilitate recolonization of bleached tissue by symbionts. Our data indicate that colorful bleaching has the potential to identify local environmental factors, such as nutrient stress, that can exacerbate the impact of elevated temperatures on corals, to indicate the severity of heat stress experienced by corals and to gauge their post-stress recovery potential. VIDEO ABSTRACT.

Mild Stress Conditions during Laboratory Culture Promote the Proliferation of Mutations That Negatively Affect Sigma B Activity in Listeria monocytogenes.

In Listeria monocytogenes, the full details of how stress signals are integrated into the σB regulatory pathway are not yet available. To help shed light on this question, we investigated a collection of transposon mutants that were predicted to have compromised activity of the alternative sigma factor B (σB). These mutants were tested for acid tolerance, a trait that is known to be under σB regulation, and they were found to display increased acid sensitivity, similar to a mutant lacking σB (ΔsigB). The transposon insertions were confirmed by whole-genome sequencing, but in each case, the strains were also found to carry a frameshift mutation in the sigB operon. The changes were predicted to result in premature stop codons, with negative consequences for σB activation, independently of the transposon location. Reduced σB activation in these mutants was confirmed. Growth measurements under conditions similar to those used during the construction of the transposon library revealed that the frameshifted sigB operon alleles conferred a growth advantage at higher temperatures, during late exponential phase. Mixed-culture experiments at 42°C demonstrated that the loss of σB activity allowed mutants to take over a population of parental bacteria. Together, our results suggest that mutations affecting σB activity can arise during laboratory culture because of the growth advantage conferred by these mutations under mild stress conditions. The data highlight the significant cost of stress protection in this foodborne pathogen and emphasize the need for whole-genome sequence analysis of newly constructed strains to confirm the expected genotype.IMPORTANCE In the present study, we investigated a collection of Listeria monocytogenes strains that all carried sigB operon mutations. The mutants all had reduced σB activity and were found to have a growth advantage under conditions of mild heat stress (42°C). In mixed cultures, these mutants outcompeted the wild type when mild heat stress was present but not at an optimal growth temperature. An analysis of 22,340 published L. monocytogenes genome sequences found a high rate of premature stop codons present in genes positively regulating σB activity. Together, these findings suggest that the occurrence of mutations that attenuate σB activity can be favored under conditions of mild stress, probably highlighting the burden on cellular resources that stems from deploying the general stress response.

Anti-instinctive Learning Behavior Revealed by Locomotion-Triggered Mild Heat Stress in Drosophila.

Anti-instinctive learning, an ability to modify an animal's innate behaviors in ways that go against one's innate tendency, can confer great evolutionary advantages to animals and enable them to better adapt to the changing environment. Yet, our understanding of anti-instinctive learning and its underlying mechanisms is still limited. In this work, we describe a new anti-instinctive learning behavior of fruit flies. This learning paradigm requires the fruit fly to respond to a recurring, aversive, mild heat stress by modifying its innate locomotion behavior. We found that experiencing movement-triggered mild heat stress repeatedly significantly reduced walking activity in wild type fruit flies, indicating that fruit flies are capable of anti-instinctive learning. We also report that such learning ability is reduced in dopamine 1-like receptor 1 (Dop1R1) null mutant and dopamine 2-like receptor (Dop2R) null mutant flies, suggesting that these two dopamine receptors are involved in mediating anti-instinctive learning in flies.

Effects of heat stress on pullet cloacal and body temperature

One measure of the thermal status of poultry is cloacal temperature measured with a cloacal thermometer; however, this method requires handling the bird, is invasive, and can be stressful. Infrared thermography is an alternative means for assessing bird thermal status. The objective of this study was to investigate the body temperature response of pullets subjected to different environmental air temperatures during the growing phase and to evaluate the relationship between the cloacal temperature and the body parts surface temperature. A total of 648 chicks (Lohmann LSL Lite) were used in 2 different phases, phase I (day 1 through 6 wk of age) and phase II (week 7 through 17). During phase I, chicks were reared at 1 of 3 different thermal environments: thermal comfort (35°C–19°C), mild heat stress (38°C–22°C), or mild cold stress (28°C–17°C). In phase II, pullets were randomly redistributed to 1 of 4 daytime temperature treatments: 20°C; 25°C; 30°C; and 35°C, all with night time temperature of 20°C. Cloacal temperature and body surface temperature for 8 parts (head, eye, comb, chest, back, wing, leg, head area, and body area) were obtained weekly from 4 to 2 birds per treatment, respectively, during phase II. There were no effects for the interactions between the 2 experimental phases for cloacal and body parts surface temperature. There was a strong correlation (P < 0.001) between cloacal temperature and each body part temperature; cloacal temperature followed a quadratic response to environmental air temperature treatments. Pullets subjected to 35°C/20°C and 30°C/20°C had the highest body parts temperatures compared with the other 2 treatments (P < 0.05). The leg surface temperature was greatest in all treatments, and the chest the lowest. Regression between cloacal and body parts temperature had a 95% predictive accuracy of better than 0.4°C, suggesting a useful alternative to direct cloacal temperature measurement.

HSP70 Inhibition Leads to the Activation of Proteasomal System under Mild Hyperthermia Conditions in Young and Senescent Fibroblasts.

Aging has been characterized with the accumulation of oxidized proteins, as a consequence of progressive decline in proteostasis capacity. Among others, proteasomal system is an efficient protein turnover complex to avoid aggregation of oxidized proteins. Heat shock protein 70 (HSP70) is another critical player that is involved in some key processes including the correct folding of misfolded proteins and targeting aggregated proteins to the proteasome for rapid degradation. The aim of this study was to determine the role of proteasomal system and heat shock proteins to maintain proteome balance during replicative senescence in mild hyperthermia conditions. Our results demonstrated that HSP40/70 machinery is induced by mild hyperthermia conditions independent from senescence conditions. Since HSP70 is largely responsible for the rapidly inducible cell protection following hyperthermia, the activation of “heat shock response” resulted in the elevation of HSP40/70 expressions as well as the proteasome activity. Interestingly, when HSP70 expression was inhibited, increased proteasomal activation was shown to be responsive to mild hyperthermia. Since HSP70 is involved in various stress-related pathways such as oxidative and endoplasmic reticulum stress, depletion of HSP70 expression may induce proteasomal degradation to maintain proteome balance of the cell. Thus, our data suggests that in mild heat stress conditions, molecular chaperone HSP70 plays an important role to avoid protein oxidation and aggregation; however, activities of proteasomal system are induced when HSP70 expression is depleted.

The CaChiVI2 Gene of Capsicum annuum L. Confers Resistance Against Heat Stress and Infection of Phytophthora capsici.

Extreme environmental conditions seriously affect crop growth and development, resulting in substantial reduction in yield and quality. However, chitin-binding proteins (CBP) family member CaChiVI2 plays a crucial role in eliminating the impact of adverse environmental conditions, such as cold and salt stress. Here, for the first time it was discovered that CaChiVI2 (Capana08g001237) gene of pepper (Capsicum annuum L.) had a role in resistance to heat stress and physiological processes. The full-length open-reading frame (ORF) of CaChiVI2 (606-bp, encoding 201-amino acids), was cloned into TRV2:CaChiVI2 vector for silencing. The CaChiVI2 gene carries heat shock elements (HSE, AAAAAATTTC) in the upstream region, and thereby shows sensitivity to heat stress at the transcriptional level. The silencing effect of CaChiVI2 in pepper resulted in increased susceptibility to heat and Phytophthora capsici infection. This was evident from the severe symptoms on leaves, the increase in superoxide (O2–) and hydrogen peroxide (H2O2) accumulation, higher malondialdehyde (MDA), relative electrolyte leakage (REL) and lower proline contents compared with control plants. Furthermore, the transcript level of other resistance responsive genes was also altered. In addition, the CaChiIV2-overexpression in Arabidopsis thaliana showed mild heat and drought stress symptoms and increased transcript level of a defense-related gene (AtHSA32), indicating its role in the co-regulation network of the plant. The CaChiVI2-overexpressed plants also showed a decrease in MDA contents and an increase in antioxidant enzyme activity and proline accumulation. In conclusion, the results suggest that CaChiVI2 gene plays a decisive role in heat and drought stress tolerance, as well as, provides resistance against P. capsici by reducing the accumulation of reactive oxygen species (ROS) and modulating the expression of defense-related genes. The outcomes obtained here suggest that further studies should be conducted on plants adaptation mechanisms in variable environments.

Dynamics of the Transcriptome Response to Heat in the Moss, Physcomitrella patens.

Thermal stress negatively impacts crop yields, and as the overall temperature of the earth’s atmosphere is gradually increasing, the identification of the temperature transduction pathway of the heat signal is essential in developing new strategies in order to adapt plant breeding to warmer climates. Heat stress damages the molecular structures and physiological processes in plants in proportion to the level and duration of the stress, which leads to different types of responses. In general, plants respond more efficiently when they are first subjected to a moderate temperature increase before being subjected to a higher temperature stress. This adaptive response is called the acclimation period and has been investigated in several plant species. However, there is a lack of information on the dynamic of the Heat Shock Response (HSR) over a continuous period of temperature rise without an acclimation period. In this paper, we investigated the effects of mild (30 °C) and high (37 °C) continuous heat stress over a 24-h period. Through RNA-Seq analysis, we assessed the remodeling of the transcriptome in the moss Physcomitrella patens. Our results showed that the 30 °C treatment particularly affected the expression of a few genes at 1 and 24 h, suggesting a biphasic response. Up-regulated genes at 1 h encode mainly HSR proteins (protein folding and endoplasmic reticulum stress), indicating an early heat response; while the up-regulated genes at 24 h belong to the thiamine biosynthesis pathway. In contrast, the genes involved in photosynthesis and carbon partitioning were repressed by this treatment. Under a higher temperature stress (37 °C), the induction of the HSR occurred rapidly (1 h) and was then attenuated throughout the time points investigated. A network approach (Weighted Gene Correlation Network Analysis, WGCNA) was used to identify the groups of genes expressing similar profiles, highlighting a HsfA1E binding motif within the promoters of some unrelated genes which displayed rapid and transient heat-activation. Therefore, it could be suggested that these genes could be direct targets of activation by a HsfA1E transcription factors.

The Golgi Glycoprotein MGAT4D is an Intrinsic Protector of Testicular Germ Cells From Mild Heat Stress

Male germ cells are sensitive to heat stress and testes must be maintained outside the body for optimal fertility. However, no germ cell intrinsic mechanism that protects from heat has been reported. Here, we identify the germ cell specific Golgi glycoprotein MGAT4D as a protector of male germ cells from heat stress. Mgat4d is highly expressed in spermatocytes and spermatids. Unexpectedly, when the Mgat4d gene was inactivated globally or conditionally in spermatogonia, or mis-expressed in spermatogonia, spermatocytes or spermatids, neither spermatogenesis nor fertility were affected. On the other hand, when males were subjected to mild heat stress of the testis (43 °C for 25 min), germ cells with inactivated Mgat4d were markedly more sensitive to the effects of heat stress, and transgenic mice expressing Mgat4d were partially protected from heat stress. Germ cells lacking Mgat4d generally mounted a similar heat shock response to control germ cells, but could not maintain that response. Several pathways activated by heat stress in wild type were induced to a lesser extent in Mgat4d[−/−] heat-stressed germ cells (NFκB response, TNF and TGFβ signaling, Hif1α and Myc genes). Thus, the Golgi glycoprotein MGAT4D is a novel, intrinsic protector of male germ cells from heat stress.

Frequent and mild scrotal heat stress impairs embryo development, implantation and offspring sex ratio in mice.

Frequent and mild scrotal heat stress (fmSHS) often occurs in humans. The aim of this study was to determine the impact of fmSHS on natural fertility, the IVF-embryo transfer (IVF-ET) process and the offspring sex ratio. Male mice were randomly divided into four groups: no scrotal heat stress (SHS) (controls) and those subjected to SHS at 37°C, 39°C or 41°C for 30min once a week for 5 consecutive weeks. The testis, epididymis and sperm quality were assessed to evaluate the effects of different degrees of SHS, to establish an fmSHS model. Then, natural fertility, IVF-embryo transfer (IVF-ET) results, embryo development, offspring sex ratio and the X/Y chromosome-bearing sperm ratio were examined. SHS at 39°C and 41°C caused mild impairment to spermatozoa, leading to a phenotype similar to oligoasthenozoospermia in humans. Given that most SHS conditions in humans are close to body temperature, SHS of 39°C was adopted to build the fmSHS model. fmSHS reduced the fertilization rate, impaired on-time development and reduced the implantation rate of the embryos in the IVF-ET process, but it did not affect the development or function of blastocysts. The fmSHS mice produced more Y chromosome-bearing spermatozoa and propagated more male offspring. fmSHS not only reduced the fertilization ability of spermatozoa but also influenced their function beyond fertilization, in addition to changing the offspring sex ratio. These results may help to shed new light on the infertility treatment of males with scrotal heat risk and the health concerns of offspring propagated from these fathers.

Effects of developmental plasticity on heat tolerance may be mediated by changes in cell size in Drosophila melanogaster.

There is a growing interest in the physiology underpinning heat tolerance of ectotherms and their responses to the ongoing rise in temperature. However, there is no consensus about the underlying physiological mechanisms. According to “the maintain aerobic scope and regulate oxygen supply” hypothesis, responses to warming at different organizational levels contribute to the ability to safeguard energy metabolism via aerobic pathways. At the cellular level, a decrease in cell size increases the capacity for the uptake of resources (e.g., food and oxygen), but the maintenance of electrochemical gradients across cellular membranes implies greater energetic costs in small cells. In this study, we investigated how different rearing temperatures affected cell size and heat tolerance in the fruit fly Drosophila melanogaster. We tested the hypothesis that smaller‐celled flies are more tolerant to acute, intense heat stress whereas larger‐celled flies are more tolerant to chronic, mild heat stress. We used the thermal tolerance landscape framework, which incorporates the intensity and duration of thermal challenge. Rearing temperatures strongly affected both cell size and survival times. We found different effects of developmental plasticity on tolerance to either chronic or acute heat stress. Warm‐reared flies had both smaller cells and exhibited higher survival times under acute, intense heat stress when compared to cold‐reared flies. However, under chronic, mild heat stress, the situation was reversed and cold‐reared flies, consisting of larger cells, showed better survival. These differences in heat tolerance could have resulted from direct effects of rearing temperature or they may be mediated by the correlated changes in cell size. Notably, our results are consistent with the idea that a smaller cell size may confer tolerance to acute temperatures via enhanced oxygen supply, while a larger cell may confer greater tolerance to chronic and less intense heat stress via more efficient use of resources.

Access to shade reduces DNA damage of Holstein cows under mild heat stress

Context The effect of heat stress on the production and physiology of lactating dairy cows is well documented in literature. However, little is known about the effect of the provision of shade on DNA damage. Aims The present study aimed to evaluate the effects of shade provision on physiological, oxidative-stress, and DNA-strand damage in dairy cows exposed to mild heat stress. Methods The study was conducted at Lages, SC, Brazil, during 15 days in a southern hemisphere summer (January and February), with 14 lactating Holstein (n = 10) and Holstein × Jersey crossbreed (n = 4) dairy cows. Animals were randomly allocated to two groups of seven animals each (named as shaded and unshaded). These two groups were evaluated in the following three different periods: pre-stress period (5-day duration), stress period (4-day duration) and post-stress period (6-day duration). Shaded cows had free access to shade throughout the study; unshaded cows were prevented from accessing shade only in the stress period. Physiological (rectal temperature, heart and respiratory frequencies and panting score) and DNA-damage parameters (through Comet assay), as well as oxidative stress (in blood: carbonyl content, nitrite:nitrate ratio, thiobarbituric acid-reactive substances, TBARS) were evaluated. Key results In the stress period, shade deprivation resulted in higher values of respiratory rate, indicating that cows were under heat stress. In addition, DNA-damage levels were higher in this circumstance, probably due to inhibition of the DNA-repair systems by the thermal stress as well as thermal stress acting as a DNA-damage agent. Conclusions In a high-altitude subtropical region, during the hot season, shade provision decreases solar radiation heating effects and, thus, reduces DNA damage and the negative effects on cow metabolism and cell structure. Implications Shade effects on cow metabolism and cell structure must be taken into consideration in the planning of dairy farms and our results suggest that shade availability must not be disregarded, even in situations of mild heat stress.

A Role for Both V1a and V2 Receptors in Renal Heat Stress Injury Amplified by Rehydration with Fructose.

Chronic vasopressin secretion induced by recurrent mild heat stress exposure is significantly enhanced by limited rehydration with a fructose-containing beverage both in rodents and in humans. Moreover, this effect has been associated with upregulation of the polyol–fructokinase pathway and increased renal oxidative stress. Previously, we have shown that pharmacological inhibition of both V1a and V2 vasopressin receptors with conivaptan improved such renal alterations. The aim of this study was to evaluate the independent contributions of V1a and V2 receptors to the renal damage caused by mild heat stress and limited rehydration with a fructose-containing beverage. Osmotic minipumps were used to deliver either relcovaptan (0.64 mg/day) or tolvaptan (0.25 mg/day) in male Wistar rats for two weeks. Corresponding dilution vehicles were used as controls. To induce dehydration, rats were exposed to mild heat stress (37 °C for 1 h, Monday to Friday). All groups received a 10% fructose solution as a rehydration fluid for 2 h after mild heat stress. For the remainder of the day and on weekends, rats received tap water. The independent blockade of either the V1a or the V2 receptor prevented renal damage, reduced oxidative stress, and decreased plasma cortisol and systemic inflammation. However, the beneficial effects were regulated by different mechanisms. Tolvaptan inhibited polyol–fructokinase pathway overactivation, while relcovaptan prevented upregulation of the renin–angiotensin system and SGK1 expression. These data suggest that both V1a and V2 receptors participate in renal damage caused by heat stress-induced dehydration when fructose-containing beverages are used as rehydration fluids.

Impact of Rumen-Protected Niacin on Milk Production Performance and Blood Biochemical Indexes of Dairy Cows Under Mild Heat Stress

To study the influence of rumen-protected niacin on mild heat-stressed dairy cow, 30 healthy high-yielding dairy cows with similar parity were selected and randomly divided into three groups and were fed the rations with 0g/d, 6g/d and 12g/d rumen-protected niacin respectively. The results showed that the dairy cows were in mild heat stress during the experiment and the time of test day significantly affected the milk yield, FCM and respiration rate of cows. Rumen-protected niacin supplement neither altered the dairy cow’s body temperature, skin temperature and respiration rate, nor affected their milk yield and milk quality; however, it reduced the level of triglyceride and urea in serum.

The effect of mild heat stress of different frequencies on the adaptability of Drosophila melanogaster females.

In natural populations, insects regularly face an adverse impact of different natures: harsh weather swings, lack of food resources, the insecticidal treatment. We studied the effect of repeated episodes of mild heat stress of different frequencies on stress resistance of Drosophila melanogaster females. We found out that the mild heat stress (38°С, 1 hr) repeated daily within 2 weeks resulted in (a) an increased activity of the dopamine (DA) metabolism enzymes, DA-dependent arylalkylamine N-acetyltransferase and alkaline phosphatase, which suggested a decrease in DA level, and (b) an increased survival rate under acute heat stress (38°С, 4 hr). The same mild heat stress repeated weekly had no effect on these parameters.

Effects of copper hydroxychloride and choice white grease on growth performance and blood characteristics of weanling pigs kept at normal ambient temperature or under heat stress

An experiment was conducted to test the hypothesis that copper (Cu) hydroxychloride improves growth performance and blood characteristics, and reduces diarrhea incidence in weanling pigs without or with exposure to heat stress. One hundred sixty pigs (6.14 ± 0.90 kg) were allotted to a 2 × 2 factorial arrangement with 2 levels of choice white grease (CWG; 0 or 50 g/kg) and 2 levels of Cu from Cu hydroxychloride (0 or 100 mg/kg). There were 5 pigs per pen and 8 pen replicates per diet. Fecal scores were visually assessed using a score from 1 to 5 (1 = normal feces to 5 = watery feces). On day 40 until the end of the experiment, ambient temperature was increased from 24 °C to 32 °C to create a mild heat stress. On day 14, day 28, day 40, and on day 44, blood samples were collected from 1 pig per pen and tumor necrosis factor-α (TNF-α), peptide YY, immunoglobulin G, blood urea nitrogen, total protein, and albumin were analyzed. Results indicated that there were no interactions between CWG and Cu hydroxychloride for overall growth performance. Greater (P < 0.05) gain:feed was observed from day 29 to 40 and from day 41 to 44 for pigs fed diets with 50 g/kg CWG compared with pigs fed diets without supplemental fat. Average daily gain was greater (P < 0.05) from day 15 to 28 and also during exposure to heat stress, and fecal scores were reduced over the entire period (P < 0.05) for pigs fed diets with Cu hydroxychloride compared with pigs fed diets without Cu hydroxychloride. There was also an increase (P < 0.05) in concentration of peptide YY and a reduction (P < 0.05) in TNF-α concentration on day 14 for pigs fed Cu hydroxychloride diets compared with pigs fed diets without Cu hydroxychloride. This may be attributed to the effect of Cu in enhancing the expression of hypothalamic appetite regulators and its bacteriostatic property in reducing inflammation caused by pathogens. In conclusion, supplementation of Cu hydroxychloride to diets fed to weanling pigs without or with addition of CWG reduces diarrhea incidence and improves growth performance and some blood characteristics.

An Overview of Hydration Status and Its Relation to Occupational Heat Stress among Workers

Working in high temperature environment is unavoidable condition for an outdoor worker, especially the outdoor workers in to tropical countries such as Indonesia. Heat stress leads to various heat-related illnesses, such as heat stroke, hyperthermia, heat exhaustion, heat cramps or heat rashes. A mild and moderate heat stress usually less serious and did not harm general health condition, however it could cause individual fatigue and unfocused, which will interfere the working performance and productivity. Heat stress will had caused physiologic response of the body, as it needs to reduce the increased temperature inside the body; known as heat strain condition.

Effect of a post-hatch lipopolysaccharide challenge in Turkey poults and ducklings after a primary embryonic heat stress

The effect of embryonic thermal manipulation on the post-hatch immune response to a lipopolysaccharide (LPS) challenge was studied in Pekin ducklings and turkey poults. Commercial duck and turkey eggs were distributed among four treatments: SS-Control (37.5 °C from embryonic day [ED] 1 to 25); SS-LPS (37.5 °C from ED1 to 25 + LPS at D0 [hatch]); HH-LPS (38 °C from ED1 to 25 + LPS at D0; SH-LPS (37.5 °C from ED1 to 10 and 38 °C from ED 11 to 25 + LPS at D0). At ED16 and ED24, the egg shell temperature of the duck and turkey eggs in the HH and SH treatments were higher (P ≤ 0.01) than the SS treatment. Ducklings and poults in the HH treatment had the lowest yolk free body weight at hatch (P ≤ 0.05). At 24, 48, and 72 h post-LPS injection, ducklings and poults in the HH-LPS treatment had significantly reduced BW compared with the SS-Con treatments (P ≤ 0.05). Ducklings and poults in the SH-LPS and HH-LPS treatments had increased plasma heat shock protein 70 (HSP70) and lower splenic HSP70 mRNA amounts than the SS-LPS treatments at 24, and 48 h post-challenge (P ≤ 0.05). At 48 and 72 h, macrophage nitric oxide (NO) production in ducklings and poults in the SH-LPS and HH-LPS treatments was lower than in the SS-LPS treatments (P ≤ 0.05). Ducklings and poults in the SH-LPS treatment had increased thymocyte proliferation compared to the SS-LPS treatment at 24, 48 and 72 h (P ≤ 0.05). At 24 h, ducklings in the SH-LPS treatment had increased splenic IL-10 and reduced IFNγ and IL-6 mRNA abundance. However, both ducklings and poults in the HH-LPS treatment had increased IFNγ, and IL-10 mRNA abundance compared to the SS-LPS treatment (P ≤ 0.05). At 48 h, SH-LPS ducklings and poults had lower splenic IL-10 mRNA abundance (P ≤ 0.05) while the HH-LPS treatment resulted in comparable splenic IL-10 mRNA compared to the SS-LPS treatment (P ≥ 0.05). Ducklings and poults in the SH-LPS treatment had increased thymic and splenic CD8+/CD4+ ratios at 24 h versus the SS-LPS treatment (P ≤ 0.05). In conclusion, embryonic thermal manipulation from ED11-25 increased extracellular HSP70 release, thymocyte proliferation and IL-10 but decreased splenic HSP70 and IFNγ mRNA amounts at 24 h post-LPS injection. This suggests that mild heat stress during the later stages of incubation could potentially prime the embryonic immune system thereby enhances the immune response as earlier than 24 h to eliminate the inflammatory response without affecting the growth performance by increase the extracellular release of HSP70 in both ducklings and poults. Continuous exposure to the small increase in temperature from ED 1–25 (HH) caused an imbalance between pro (IFNγ)- and anti-inflammatory cytokines(IL-10) which affects hatchling responses to an inflammatory challenge and increased mortality. The amount of extracellular HSP70 could potentially play an important role in modulating the immune response against inflammatory challenges.

The relationship between the number of consecutive days with heat stress and milk production of Holstein dairy cows raised in a humid continental climate

Heat stress is known to affect performance of dairy cows experiencing prolonged periods of high temperature and relative humidity. Less is known about its effects in cooler climates. The goals of the present study were to determine the prevalence of days susceptible to cause mild heat stress in dairy cows living in a humid continental climate and to investigate the relationship between the number of consecutive days of mild heat stress and milk, fat, protein, and lactose production. A 6-yr data set (2010-2015) containing 606,031 milk analysis records for 34,360 Holstein dairy cows at different parities was matched with the corresponding daily maximum temperature-humidity index. Exposure to heat stress conditions was divided into 5 categories corresponding to 0, 1 to 2, 3 to 4, 5 to 6, and 7 to 8 consecutive days before milk test date. On average, cows were exposed to heat stress conditions for 135.8 ± 5.9 d/yr in Southwest Quebec and 95.3 ± 10.2 d/yr in Eastern Quebec. Cows experiencing heat stress conditions produced on average less fat, protein, and energy-corrected milk and lower fat and protein concentrations. The decrease in milk fat reached 6% for category 7 to 8 exposure of cows in parity 3 or more. The association between exposure category and milk yield and lactose yield and concentration was weak. Heat stress lowered milk fat and protein production but had little effect on milk volume output. Further research is necessary to better understand the mechanism underlying the effects of sporadic low- to medium-intensity heat stress on dairy productivity.

Antioxidant supplements as a novel mean for blocking recurrent heat stress-induced kidney damage following rehydration with fructose-containing beverages

Recently repeated heat stress and dehydration have been reported to cause oxidative stress and kidney damage that is enhanced by rehydrating with fructose solutions. We hypothesized that antioxidants might provide a novel way to prevent kidney damage. To test this hypothesis, mild heat stress was induced by exposing rats to 37 °C during 1 h in a closed chamber. The supplementation with water-soluble antioxidants (Antiox), ascorbic acid 1% plus N-acetyl cysteine 600 mg/L was done either in the 10% fructose 2 h rehydration fluid immediately after heat stress (Fructose 10% + Antiox), and/or in the tap water (Water + Antiox) for the remainder of the day, or in both fluids. After 4 weeks, control rats exposed to heat with fructose rehydration developed impaired renal function, tubular injury, intrarenal oxidative stress, a reduction in Nrf2-Keap1 antioxidant pathway, stimulation of vasopressin and the intrarenal polyol-fructokinase pathway. In contrast, dosing the antioxidants in the tap water (i.e., before the heat exposure and rehydration with fructose) preserved renal function, prevented renal tubule dysfunction and avoided the increase in systemic blood pressure. These effects were likely due to the amplification of the antioxidant defenses through increased Nrf2 nuclear translocation stimulated by the antioxidants and by the prevention of polyol fructokinase pathway overactivation. More studies to understand the mechanisms implicated in this pathology are warranted as there is recent evidence that they may be operating in humans as well.