The pathophysiological mechanisms responsible for male subfertility/infertility caused by or complicated by genital heat stress remains unclear in many respects. Because seminal plasma creates the environment for the proper functioning of spermatozoa, in this study, we verified the associations among standard spermiograms, seminal biochemical parameters (neutral alpha-glucosidase, fructose, and citric acid) and oxidative stress markers (total antioxidant capacity, catalase activity, superoxide dismutase activity, and malondialdehyde concentration) in distinct entities associated with male infertility with and without long-time exposure to local hyperthermia. We demonstrated that men exposed to prolonged environmental or clinically recognized local heat stress in adulthood may suffer from dysregulation of seminal antioxidant components, which can be directly associated with epididymal and prostate function. The comparative analysis of the studied parameters showed numerous correlations among all biochemical parameters (particularly neutral alpha-glucosidase) with low standard semen quality in almost all the investigated infertile groups. In light of the data obtained in this originally designed study, we conclude that more attention should be paid to the epididymis and accessory gland function in subfertile and infertile men exposed to genital heat stress, especially in the context of novel treatment algorithms (targeted therapies).

Physiological and psychological stresses cause anxiety disorders such as depression and post-traumatic stress disorder (PTSD) and induce drastic changes at a molecular level in the brain. To counteract this stress, the heat-shock protein (HSP) network plays a vital role in restoring the homeostasis of the system. To study the stress-induced dynamics of heat-shock network, we analyzed three modules of the HSP90 network--namely trimerization reactions, phosphorylation-dephosphorylation reactions, and the conversion of HSP90 from an open to a closed conformation--and constructed a corresponding nonlinear differential equation model based on mass action kinetics laws. The kinetic parameters of the model were obtained through global optimization, and sensitivity analyses revealed that the most sensitive parameters are the kinase and phosphatase that drive the phosphorylation-dephosphorylation reactions. Bifurcation analysis carried out with the estimated kinetic parameters of the model with stress as bifurcation parameter revealed the occurrence of "mushroom", a type of complex dynamics in which S-shaped and Z-shaped hysteretic bistable forms are present together. We mapped the molecular events responsible for generating the mushroom dynamics under stress and interpreted the occurrence of the S-shaped hysteresis to a normal level of stress, and the Z-shaped hysteresis to the HSP90 variations under acute and chronic stress in the fear conditioned system, and further, we hypothesized that this can be extended to stress-related disorders such as depression and PTSD in humans. Finally, we studied the effect of parameter variations on the mushroom dynamics to get insight about the role of phosphorylation-dephosphorylation parameters in HSP90 network in bringing about complex dynamics such as isolas, where the stable steady states in a bistable system are isolated and separated from each other and not connected by an unstable steady state.

This study was conducted to explore underlying mechanism of microcirculation dysfunction and protectiverole of Xuebijing in heat stroke. Forty rats were divided into: control, vehicle + heat stress (HS), superoxide dismutase (SOD) + HS, and Xuebijing + HS groups. Rats in heat stress groups were subjected to continuous heat stress in infant incubator 1 h after tail vein injection of the tested compound and spinotrapezius preparation. Velocity of blood flow through micro-vessels and vascular diameter were detected in real time. Another 27 rats were divided into: vehicle, SOD, and Xuebijing groups, then further divided into three subgroups each: control, Tcore = 38 °C, Tcore = 41 °C. Rats were sacrificed, and spinotrapezius single-cell suspensions were prepared for detecting SOD and reactive oxygen species (ROS). The results showed that heat stress decreased SOD activity, increased ROS levels, and reduced the blood flow rate. Xuebijing increased SOD activity, decreased ROS levels and exhibited a protective effect in terms of blood flow rate but was less protective than SOD. The survival time in Xuebijing + HS group was longer than that in vehicle group but shorter than that in SOD + HS group. The results suggested Xuebijing could decrease ROS levels and have protective effects in severe heat stroke.

Exposure to intrauterine heat stress during late gestation affects offspring performance into adulthood. However, underlying mechanistic links between thermal insult in fetal life and postnatal outcomes are not completely understood. We examined morphology, DNA methylation, and gene expression of liver and mammary gland for bull calves and heifers that were gestated under maternal conditions of heat stress or cooling (i.e. in utero heat stressed vs. in utero cooled calves). Mammary tissue was harvested from dairy heifers during their first lactation and liver from bull calves at birth. The liver of in utero heat stressed bull calves contained more cells and the mammary glands of in utero heat stressed heifers were comprised of smaller alveoli. We identified more than 1,500 CpG sites differently methylated between maternal treatment groups. These CpGs were associated with approximately 400 genes, which play a role in processes, such as development, innate immune defense, cell signaling, and transcription and translation. We also identified over 100 differentially expressed genes in the mammary gland with similar functions. Interestingly, fifty differentially methylated genes were shared by both bull calf liver and heifer mammary gland. Intrauterine heat stress alters the methylation profile of liver and mammary DNA and programs their morphology in postnatal life, which may contribute to the poorer performance of in utero heat stressed calves.

Mother's own milk is the first choice for the feeding and nutrition of preterm and term newborns. When mother's own milk is unavailable or in short supply donor human milk (DM) could represent a solution. Heat treatment and cold storage are common practices in Human Milk Banks (HMBs). Currently, Holder pasteurization process is the recommended heat treatment in all international guidelines. This method is thought to lead to a good compromise between the microbiological safety and nutritional/biological quality of DM. Moreover, storage of refrigerated milk is a common practice in HMBs and in NICUs. Depending on the length and on the type of storage, human milk may lose some important nutritional and functional properties. The available data on oxidative stress markers confirm that pasteurization and refrigeration affected this important elements to variable degrees, even though it is rather difficult to quantify the level of deterioration. Nonetheless, clinical practice demonstrates that many beneficial properties of human milk are preserved, even after cold storage and heat treatment. Future studies should be focused on the evaluation of new pasteurization techniques, in order to achieve a better compromise between biological quality and safety of DM.

Ageing is associated with the reduced performance of physiological processes and has been proposed as a major risk factor for disease. An age-related decline in stress response pathways has been widely documented in lower organisms. In particular, the heat shock response (HSR) becomes severely compromised with age in Caenorhabditis elegans. However, a comprehensive analysis of the consequences of ageing on the HSR in higher organisms has not been documented. We used both HS and inhibition of HSP90 to induce the HSR in wild-type mice at 3 and 22 months of age to investigate the extent to which different brain regions, and peripheral tissues can sustain HSF1 activity and HS protein (HSP) expression with age. Using chromatin immunoprecipitation, quantitative reverse transcription polymerase chain reaction, western blotting and enzyme linked immunosorbent assay (ELISA), we were unable to detect a difference in the level or kinetics of HSP expression between young and old mice in all brain regions. In contrast, we did observe an age-related reduction in chaperone levels and HSR-related proteins in the heart. This could result in a decrease in the protein folding capacity of old hearts with implications for age-related cardiac disorders.

As sessile organisms, plants are highly sensitive to environmental stresses. In response to stresses, globally repressed translation initiation leads to stress granule (SG) formation. Protein liquid-liquid phase separation (LLPS) contributes to SG formation, but a direct link between protein LLPS and stress resistance has not yet been found in plants. Here, we report that two RNA-binding proteins, RBGD2 and RBGD4, function redundantly to improve heat resistance in Arabidopsis. RBGD2 and RBGD4 undergo LLPS in vitro and condense into heat-induced SGs in vivo via tyrosine residue array (TRA). Importantly, disrupting LLPS by mutating TRA abolishes RBGD2/4 condensation in SGs and impairs their protective function against heat stress (HS). Further study found that upon HS, the RBGD2/4 interaction network expands with additional SG proteins and heat-responsive mRNA. Our work shows a mechanistic basis that underlies protein LLPS in HS response in plants and suggests manipulation of protein LLPS as a general strategy to improve plant stress resistance.

The neuropeptide urocortin 3 (UCN3) has a beneficial effect on metabolic disorders, such as obesity, diabetes, and cardiovascular disease. It has been reported that UCN3 regulates insulin secretion and is dysregulated with increasing severity of obesity and diabetes. However, its function in the adipose tissue is unclear. We investigated the overexpression of UCN3 in 3T3-L1 preadipocytes and differentiated adipocytes and its effects on heat shock response, ER stress, inflammatory markers, and glucose uptake in the presence of stress-inducing concentrations of palmitic acid (PA). UCN3 overexpression significantly downregulated heat shock proteins (HSP60, HSP72 and HSP90) and ER stress response markers (GRP78, PERK, ATF6, and IRE1α) and attenuated inflammation (TNFα) and apoptosis (CHOP). Moreover, enhanced glucose uptake was observed in both preadipocytes and mature adipocytes, which is associated with upregulated phosphorylation of AKT and ERK but reduced p-JNK. Moderate effects of UCN3 overexpression were also observed in the presence of 400 μM of PA, and macrophage conditioned medium dramatically decreased the UCN3 mRNA levels in differentiated 3T3-L1 cells. In conclusion, the beneficial effects of UCN3 in adipocytes are reflected, at least partially, by the improvement in cellular stress response and glucose uptake and attenuation of inflammation and apoptosis.

Heat stress (HS) causes serious physiological dysfunction associated with cardiovascular diseases. Curcumin (CUR) may increase animal survival and lifespan under HS. However, its effects and mechanism on mammal are underexplored. The goal of this study was to examine the protective effect of CUR on the cardiac health of mice exposed to HS. Mice were divided into six groups (n=8 per group): no-heat treatment (NHT), heat treatment (HT), aspirin, CUR 50 mg/kg/day, CUR 100 mg/kg/day and CUR 200 mg/kg/day. After administration for 4 weeks, except for NHT, other groups were exposed once to HS at 41°C for 20 min. After HS treatment, the physiological-related indexes of blood pressure, rectal temperature and heart rate were measured. Serum biochemical indexes and the levels of cardiac troponin I (cTn-I) in serum and angiotensin II (Ang II) in cardiomyocytes were analyzed. Furthermore, the mRNA and proteins levels of angiotensin receptor 1 (AT1), 78-kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP) and B-cell lymphoma 2 (Bcl-2) were measured. Our results indicated that CUR supplementation could alleviate HS-induced physiological disorders and the increasing of cTn-I and Ang II. The expression of AT1 gene in HT group was significantly higher than that of CUR groups, indicating the cardioprotective effects of CUR. Moreover, the levels of GRP78 and CHOP proteins in the HT group were significantly higher than those of CUR groups, indicating that CUR supplementation reversed the endoplasmic reticulum HS-mediated apoptosis. In summary, CUR supplementation alleviates physiological stress and cardiac damage caused by HS.

Global temperature change causes heat stress related disorders in humans. A constituent of red ginseng has been known the beneficial effect on the resistance to many diseases. However, the mechanism of red ginseng (RG) against heat stress still remains unclear. To determine the effect of RG on heat stress, we examined the effect of the RG on the gene expression profiles in rats subjected to environmental heat stress. We evaluated the transcripts associated with hepatic lipid accumulation and oxidative stress in rats subjected to heat stress. We also analyzed the reactive oxygen species (ROS) contents. Our results suggested RG inhibited heat stress mediated altering mRNA expressions include HSPA1, DEAF1, HMGCR, and FMO1. We also determined RG attenuated fat accumulation in the liver by altering C/EBPβ expression. RG promoted to repress the heat stress mediated hepatic cell death by inhibiting of Bcl-2 expression in rats subjected to heat stress. Moreover, RG administered group during heat stress dramatically decreased the malondialdehyde (MDA) contents and ROS associated genes compared with the control group. Thus, we suggest that RG might influence inhibitory effect on environmental heat stress induced abnormal conditions in humans.

Sun-related physiological disorders such as sun damage on apples (Malus domestica Borkh) are caused by cumulative photooxidative and heat stress during their growing season triggering morphological, physiological, and biochemical changes in fruit tissues not only while it is on the tree but also after it has been harvested. The objective of the work was to establish the interaction of auxin (indole-3-acetic acid; IAA), abscisic acid (ABA), jasmonic acid (JA), salicylic acid (SA), and ethylene (ET) and its precursor ACC (free and conjugated, MACC) during development of sun-injury-related disorders pre- and post-harvest on apples. Peel tissue was extracted from fruit growing under different sun exposures (Non-exposed, NE; Exposed, EX) and with sun injury symptoms (Moderate, Mod). Sampling was carried out every 15 days from 75 days after full bloom (DAFB) until 120 days post-harvest in cold storage (1°C, > 90%RH). Concentrations of IAA, ABA, JA, SA, were determined using UHPLC mass spectrometry, and ET and ACC (free and conjugated MACC) using gas chromatography. IAA was found not to be related directly to sun injury development, but it decreased 60% in sun exposed tissue, and during fruit development. ABA, JA, SA, and ethylene concentrations were significantly higher (P ≤ 0.05) in Mod tissue, but their concentration, except for ethylene, were not affected by sun exposure. ACC and MACC concentrations increased until 105 DAFB in all sun exposure categories. During post-harvest, ethylene climacteric peak was delayed on EX compared to Mod. ABA and SA concentrations remained stable throughout storage in both tissue. JA dramatically increased post-harvest in both EX and Mod tissue, and orchards, confirming its role in low temperature tolerance. The results suggest that ABA, JA, and SA together with ethylene are modulating some of the abiotic stress defense responses on sun-exposed fruit during photooxidative and heat stress on the tree.

Despite progress in the use of hyperthermia in clinical practice, the thermosensitivity of cancer cells is poorly understood. In a previous study, we found that sensitivity to hyperthermia varied between ovarian and uterine cancer cell lines. Upon hyperthermia, glycolytic enzymes decreased in hyperthermia-resistant SKOV3 cells. However, the mechanisms of glycolysis inhibition and their relationship with thermoresistance remain to be explored. In this study, metabolomic analysis indicated the downregulation of glycolytic metabolites in SKOV3 cells after hyperthermia. Proteomic and pathway analyses predicted that the ubiquitin pathway was explicitly activated in resistant SKOV3 cells, compared with hyperthermia-sensitive A2780 cells, and STUB1, a ubiquitin ligase, potentially targeted PKM, a glycolytic rate-limiting enzyme. PKM is degraded via ubiquitination upon hyperthermia. Although glycolysis is inactivated by hyperthermia, ATP production is maintained. We observed that oxygen consumption and mitochondrial membrane potential were activated in SKOV3 cells but suppressed in A2780 cells. The activation of mitochondria could compensate for the loss of ATP production due to the suppression of glycolysis by hyperthermia. Although the physiological significance has not yet been elucidated, our results demonstrated that metabolomic adaptation from the Warburg effect to mitochondrial oxidative phosphorylation could contribute to thermoresistance in ovarian and uterine cancer cells.

This paper investigated the effects of heat stress on gut-microbial metabolites, gastrointestinal peptides, glycolipid metabolism, and performance of broilers. Thus, 132 male Arbor Acres broilers, 28-days-old, were randomly distributed to undergo two treatments: thermoneutral control (TC, 21 °C) and high temperature (HT, 31 °C). The results showed that the average daily gain (ADG), average daily feed intake (ADFI), and gastric inhibitory polypeptide (GIP) concentration in the jejunum significantly decreased the core temperature, feed conversion ratio (FCR), and ghrelin of the hypothalamus, and cholecystokinin (CCK) in jejunum, and serum significantly increased in the HT group (p < 0.05). Exploration of the structure of cecal microbes was accomplished by sequencing 16S rRNA genes. The sequencing results showed that the proportion of Christensenellaceae and Lachnospiraceae decreased significantly whereas the proportion of Peptococcaceae increased at the family level (p < 0.05). Ruminococcus and Clostridium abundances significantly increased at the genus level. Furthermore, the content of acetate in the HT group significantly increased. Biochemical parameters showed that the blood glucose concentration of the HT group significantly decreased, and the TG (serum triglycerides), TC (total cholesterol), insulin concentration, and the insulin resistance index significantly increased. Nonesterified fatty acid (NEFA) in the HT group decreased significantly. In conclusion, the results of this paper suggest that the poor production performance of broilers under heat stress may be related to short-chain fatty acids (SCFAs) fermented by intestinal microbiota involved in regulating metabolic disorders.

Nano‑selenium (nano-Se) shows high biological activity and low toxicity, and has emerged as an ideal antioxidant. Our goal was to determine the underlying mechanism of nano-Se-mediated heat stress tolerance in rainbow trout (Oncorhynchus mykiss). Using liquid chromatography-mass spectrometry (LC-MS) metabolomics, histomorphology, and conventional biochemical assays, we investigated the physiological responses of heat-stressed rainbow trout to nano-Se. Fish were fed to two levels nano-Se at 18 °C for 9 days: CG18 (0 mg/kg) and Se18 (5 mg/kg). The water temperature of all groups was increased to 24 °C and maintained for 8 h (CG24, Se24). The results showed that most glycerophospholipids and CoA levels were decreased in CG18-CG24, and pathway enrichment analysis showed that it mainly interfered with glycerophospholipids and fatty acid metabolism. Meanwhile, hematoxylin and eosin and Oil Red O staining showed significant damage to CG18-CG24, which was ameliorated by Se18-Se24. The results combining analysis of antioxidant enzymes and heat shock proteins further support the notion that nano-Se supplementation inhibited galactose metabolism and activated the glutamate-glutamine metabolic pathway as the key metabolic strategy against heat stress. These results could establish heat stress defense strategies and increase our understanding of the mechanism of nutrient participation in fish's response to adverse environments. SIGNIFICANCE: Global warming is affecting the distribution and survival of cold-water fish worldwide, through seasonal water temperature increases and an increase in the frequency of extreme heat wave events. Surprisingly, Nano‑selenium (Nano-Se) with its outstanding advantages of high biological activity and low toxicity, making it a good Se nutrient supplement and free radical scavenger, and also an ideal and ecological way to supplement Se. How to utilize the metabolome to better address the complexity of the interactions that may occur with Nano-Se during the process of heat stress resistance is an important challenge. In the present study, this is the first publicly available metabonomics study of the anti-heat stress effect of Nano-Se as a nutrient on rainbow trout liver. These data indicated that Nano-Se effectively alleviated stress damage in rainbow trout, in which heat stress interfered with the metabolism of glycerophospholipids and fatty acids significantly, causing liver cell membrane damage and lipid metabolism disorders in rainbow trout. Meanwhile, supplementation of Nano-Se downregulated galactose metabolism and activated glutamate and glutamine metabolic pathways, which seems to be a key metabolic strategy to combat heat stress. The results provide a scientific basis for the development of an anti-heat-stress feed for rainbow trout that help maintain their health, productivity and welfare under unfavorable heat conditions.

Clinical studies clearly indicate that early-life stress (ELS) may cause physical and mental health problems later in life. Therefore, the identification of universal biomarkers of ELS-related diseases is very important. The 70-kDa heat shock proteins (HSP70s), specifically HSPA5 and HSPA1B, have been recently shown to be potentially associated with occurrence of anxiety, mood disorders, and schizophrenia; thus, we hypothesized that HSP70s are potential candidate biomarkers of ELS-induced psychopathologies. A maternal separation (MS) procedure in rats was used to model ELS, and the expression of HSPA5 and HSPA1B was investigated in the blood, medial prefrontal cortex (mPFC), and hippocampus of juvenile, preadolescent, and adult animals. We also studied the effects of MS on the long-term potentiation (LTP) and behavioral phenotypes of adult rats. We found that MS enhanced the expression of HSPA1B mRNA in the blood and mPFC of juvenile and preadolescent rats. This increase was accompanied by an increase in the HSPA1A/1B protein levels in the mPFC and hippocampus of juvenile rats that persisted in the mPFC until adulthood. MS juvenile and adult rats showed enhanced HSPA5 mRNA expression in the blood and increased HSPA5 protein expression in the mPFC (juveniles) and hippocampus (adults). Concurrently, MS adult rats exhibited aberrations in LTP in the mPFC and hippocampus and a less anxious behavioral phenotype. These results indicate that MS may produce enduring overexpression of HSPA1B and HSPA5 in the brain and blood. Therefore, both HSP70 family members may be potential candidate peripheral and brain biomarkers of ELS-induced changes in brain functioning.

Cell and tissue degeneration, and the development of degenerative diseases, are influenced by genetic and environmental factors that affect protein misfolding and proteotoxicity. To better understand the role of the environment in degeneration, we developed a genetic model for heat shock (HS)-stress-induced degeneration in Drosophila This model exhibits a unique combination of features that enhance genetic analysis of degeneration and protection mechanisms involving environmental stress. These include cell-type-specific failure of proteostasis and degeneration in response to global stress, cell-nonautonomous interactions within a simple and accessible network of susceptible cell types, and precise temporal control over the induction of degeneration. In wild-type flies, HS stress causes selective loss of the flight ability and degeneration of three susceptible cell types comprising the flight motor: muscle, motor neurons and associated glia. Other motor behaviors persist and, accordingly, the corresponding cell types controlling leg motor function are resistant to degeneration. Flight motor degeneration was preceded by a failure of muscle proteostasis characterized by diffuse ubiquitinated protein aggregates. Moreover, muscle-specific overexpression of a small heat shock protein (HSP), HSP23, promoted proteostasis and protected muscle from HS stress. Notably, neurons and glia were protected as well, indicating that a small HSP can mediate cell-nonautonomous protection. Cell-autonomous protection of muscle was characterized by a distinct distribution of ubiquitinated proteins, including perinuclear localization and clearance of protein aggregates associated with the perinuclear microtubule network. This network was severely disrupted in wild-type preparations prior to degeneration, suggesting that it serves an important role in muscle proteostasis and protection. Finally, studies of resistant leg muscles revealed that they sustain proteostasis and the microtubule cytoskeleton after HS stress. These findings establish a model for genetic analysis of degeneration and protection mechanisms involving contributions of environmental factors, and advance our understanding of the protective functions and therapeutic potential of small HSPs.

Heat stress represents a major environmental factor that negatively affects the health and performance of dairy cows, causing huge economic losses to the dairy industry. Identifying and selecting animals that are thermotolerant is an attractive alternative for reducing the negative effects of heat stress on dairy cattle performance. As such, the objectives of the present study were to estimate genetic components of milk yield, fat yield, and protein yield considering heat stress and to perform whole-genome scans and a subsequent gene-set analysis for identifying candidate genes and functional gene-sets implicated in milk production under heat stress conditions. Data consisted of about 254k test-day records from 17,522 Holstein cows. Multi-trait repeatability test day models with random regressions on a function of temperature-humidity index (THI) values were used for genetic analyses. The models included herd-test-day and DIM classes as fixed effects, and general and thermotolerance additive genetic and permanent environmental as random effects. Notably, thermotolerance additive genetic variances for all milk traits increased across parities suggesting that cows become more sensitive to heat stress as they age. In addition, our study revealed negative genetic correlations between general and thermotolerance additive effects, ranging between -0.18 to -0.68 indicating that high producing cows are more susceptible to heat stress. The association analysis identified at least three different genomic regions on BTA5, BTA14, and BTA15 strongly associated with milk production under heat stress conditions. These regions harbor candidate genes, such as HSF1, MAPK8IP1, and CDKN1B that are directly involved in the cellular response to heat stress. Moreover, the gene-set analysis revealed several functional terms related to heat shock proteins, apoptosis, immune response, and oxidative stress, among others. Overall, the genes and pathways identified in this study provide a better understanding of the genetic architecture underlying dairy cow performance under heat stress conditions. Our findings point out novel opportunities for improving thermotolerance in dairy cattle through marker-assisted breeding.

Developing effective strategies to prevent diarrhea and associated-gut disorders in mammals has gained great significance. Owing to the many health benefits provided by the commensal microbiota of the intestinal tract, such as against environmental perturbation, we explored the host phenotype-associated microbes and their probiotic potential. Based on the observations that the chronic heat stress-exposed weaned piglets present as heat stress-susceptible (HS-SUS) or heat stress-resistant (HS-RES) individuals, we confirmed the phenotypic difference between the two on growth performance (P < 0.05), diarrhea index (P < 0.001), intestinal heat shock protein 70 (HSP70) regulation (P < 0.01), and inflammatory responses (P < 0.01). By comparing the gut microbiome using 16S rRNA gene sequencing and KEGG functional analysis, we found that Lactobacillus johnsonii exhibited significantly higher relative abundance in the HS-RES piglets than in the HS-SUS ones (P < 0.05). Further experiments using a mouse model for chemical-induced inflammation and intestinal injury demonstrated that oral administration of a representative L. johnsonii N5 (isolated from the HS-RES piglets) ameliorated the clinical and histological signs of colitis while suppressing intestinal pro-inflammatory cytokines TNF-α and IL-6 production (P < 0.05). We found that N5 treatment enhanced tight junction proteins ZO-1 and occludin and cytoprotective HSP70 levels under physiological condition and restored their mucosal expressions in colitis (P < 0.05). In support of the high production of the anti-inflammatory cytokine IL-10, N5 promoted the intestinal Peyer's patches MHCII+ and CD103+ dendritic cell populations (P < 0.05), increased the regulatory T (Treg) cell numbers (P < 0.05), and decreased the Th17 population and its IL-17a production under physiological condition and during colitis (P < 0.01). Our results shed light on understanding the interaction between commensal Lactobacillus and the host health, and provide L. johnsonii N5 as an alternative to antibiotics for preventing diarrhea and intestinal diseases.

The purpose of this study was to clarify whether there is a synergistic effect on muscular strength and hypertrophy when low-intensity resistance training is performed after heat stress.

With the increasing of global mean surface air temperature, heat stress (HS) induced by extreme high temperature has become a key factor restricting the poultry industry. Liver is the main metabolic organ of broilers, HS induces liver damage and metabolic disorders, which impairs the health of broilers and affects food safety. As an essential trace element for animals, selenium (Se) involves in the formation of antioxidant system, and its biological functions are generally mediated by selenoproteins. However, the mechanism of Se against HS induced liver damage and metabolic disorders in broilers is inadequate. Therefore, we developed the chronic heat stress (CHS) broiler model and investigated the potential protection mechanism of organic Se (selenomethionine, SeMet) on CHS induced liver damage and metabolic disorders. In present study, CHS caused liver oxidative damage, and induced hepatic lipid accumulation and glycogen infiltration of broilers, which are accompanied by mitochondrial dysfunction, abnormal mitochondrial tricarboxylic acid (TCA) cycle and endoplasmic reticulum (ER) stress. Dietary SeMet supplementation increased the hepatic Se concentration and exhibited protective effects via promoting the expression of selenotranscriptome and several key selenoproteins (GPX4, TXNRD2, SELENOK, SELENOM, SELENOS, SELENOT, GPX1, DIO1, SELENOH, SELENOU and SELENOW). These key selenoproteins synergistically improved the antioxidant capacity, and mitigated the mitochondrial dysfunction, abnormal mitochondrial TCA cycle and ER stress, thus recovered the hepatic triglyceride and glycogen concentration. What's more, SeMet supplementation suppressed lipid and glycogen biosynthesis and promoted lipid and glycogen breakdown in liver of broilers exposed to CHS though regulating the AMPK signals. Overall, our present study reveals a potential mechanism that Se alleviates environment HS induced liver damage and glycogen and lipid metabolism disorders in broilers, which provides a preventive and/or treatment measure for environment HS-dependent hepatic metabolic disorders in poultry industry.