Institute of Animal Sciences

Bidirectional Encoder Representations from Transformers (BERT) has shown marvelous improvements across various NLP tasks, and its consecutive variants have been proposed to further improve the performance of the pre-trained language models. In this paper, we aim to first introduce the whole word masking (wwm) strategy for Chinese BERT, along with a series of Chinese pre-trained language models. Then we also propose a simple but effective model called MacBERT, which improves upon RoBERTa in several ways. Especially, we propose a new masking strategy called MLM as correction (Mac). To demonstrate the effectiveness of these models, we create a series of Chinese pre-trained language models as our baselines, including BERT, RoBERTa, ELECTRA, RBT, etc. We carried out extensive experiments on ten Chinese NLP tasks to evaluate the created Chinese pre-trained language models as well as the proposed MacBERT. Experimental results show that MacBERT could achieve state-of-the-art performances on many NLP tasks, and we also ablate details with several findings that may help future research. We open-source our pre-trained language models for further facilitating our research community.

Mortality in piglets during the perinatal period, especially the first days after birth, is frequently caused by non-infectious conditions, such as hypoglucemia or low birth weight, which can be associated with hypothermia experienced at birth. The thermal stability of newborn piglets is a fundamental aspect of neonatal care, so maintaining a constant, ideal temperature will substantially reduce newborn mortality. Species-specific characteristics, such as a limited capacity for thermoregulation, low energy reserves, a lack of brown adipose tissue (BAT) (-, and environmental conditions that are adverse for the piglet around the time of birth, including the absence of a microclimate, all of them contribute to difficulties in reaching thermal homeostasis in the first hours post-birth. Shivering thermogenesis and behavioral modifications to regulate body temperature through innate mechanisms allow animals to reduce their energy expenditures. Some body postures are effective in reducing contact with the floor and also nestling are useful to avoid heat loss, and also decreases heat dissipation. Achieving optimal development of thermoregulation is a challenge that newborns must confront to successfully adapt to extrauterine life. The objectives of this review, are to discuss the adverse factors that can lead to a death event due to hypothermia by analyzing the thermoregulation mechanisms at the central and cutaneous levels, also to analyze the harmful impacts that surviving neonate piglets confront in an unfavorable thermal environment, and to describe the pathophysiological mechanisms of death caused by hypothermia.

Abstract BACKGROUND Black soldier fly larvae are converters of organic waste into edible biomass, of which the composition may depend on the substrate. In this study, larvae were grown on four substrates: chicken feed, vegetable waste, biogas digestate, and restaurant waste. Samples of prepupae and substrates were freeze‐dried and proximate, amino acid, fatty acid and mineral analyses were performed. RESULTS Protein content of prepupae varied between 399 and 431 g kg −1 dry matter ( DM ) among treatments. Differences in amino acid profile of prepupae were small. On the other hand, the ether extract ( EE ) and ash contents differed substantially. Prepupae reared on digestate were low in EE and high in ash (218 and 197 g kg −1 DM , respectively) compared to those reared on vegetable waste (371 and 96 g kg −1 DM , respectively), chicken feed (336 and 100 g kg −1 DM , respectively) and restaurant waste (386 and 27 g kg −1 DM , respectively). Prepupal fatty acid profiles were characterised by high levels of C12 :0 in all treatments. CONCLUSION Since protein content and quality were high and comparable for prepupae reared on different substrates, black soldier fly could be an interesting protein source for animal feeds. However, differences in EE and ash content as a function of substrate should be considered. © 2016 Society of Chemical Industry

Oxidative stress defines a condition in which the prooxidant-antioxidant balance in the cell is disturbed, resulting in DNA hydroxylation, protein denaturation, lipid peroxidation, and apoptosis, ultimately compromising cells' viability. Probiotics have been known for many beneficial health effects, and the consumption of probiotics alone or in food shows that strain-specific probiotics can present antioxidant activity and reduce damages caused by oxidation. However, the oxidation-resistant ability of probiotics, especially the underling mechanisms, is not properly understood. In this view, there is interest to figure out the antioxidant property of probiotics and summarize the mode of action of probiotic bacteria in antioxidation. Therefore, in the present paper, the antioxidant mechanisms of probiotics have been reviewed in terms of their ability to improve the antioxidant system and their ability to decrease radical generation. Since in recent years, oxidative stress has been associated with an altered gut microbiota, the effects of probiotics on intestinal flora composition are also elaborated.

The microbiological quality of experimental animals can critically influence animal welfare and the validity and reproducibility of research data. It is therefore important for breeding and experimental facilities to establish a laboratory animal health monitoring (HM) programme as an integrated part of any quality assurance system. FELASA has published recommendations for the HM of rodent and rabbit colonies in breeding and experimental units (Nicklas et al. Laboratory Animals, 2002), with the intention of harmonizing HM programmes. As stated in the preamble, these recommendations need to be adapted periodically to meet current developments in laboratory animal medicine. Accordingly, previous recommendations have been revised and shall be replaced by the present recommendations. These recommendations are aimed at all breeders and users of laboratory mice, rats, Syrian hamsters, guinea pigs and rabbits as well as diagnostic laboratories. They describe essential aspects of HM, such as the choice of agents, selection of animals and tissues for testing, frequency of sampling, commonly used test methods, interpretation of results and HM reporting. Compared with previous recommendations, more emphasis is put on the role of a person with sufficient understanding of the principles of HM, opportunistic agents, the use of sentinel animals (particularly under conditions of cage-level containment) and the interpretation and reporting of HM results. Relevant agents, testing frequencies and literature references are updated. Supplementary information on specific agents and the number of animals to be monitored and an example of a HM programme description is provided in the appendices.

Copper is an essential micronutrient that is necessary for healthy immune function. This requirement is underscored by an increased susceptibility to bacterial infection in copper-deficient animals; however, a molecular understanding of its importance in immune defense is unknown. In this study, we investigated the effect of proinflammatory agents on copper homeostasis in RAW264.7 macrophages. Interferon-gamma was found to increase expression of the high affinity copper importer, CTR1, and stimulate copper uptake. This was accompanied by copper-stimulated trafficking of the ATP7A copper exporter from the Golgi to vesicles that partially overlapped with phagosomal compartments. Silencing of ATP7A expression attenuated bacterial killing, suggesting a role for ATP7A-dependent copper transport in the bactericidal activity of macrophages. Significantly, a copper-sensitive mutant of Escherichia coli lacking the CopA copper-transporting ATPase was hypersensitive to killing by RAW264.7 macrophages, and this phenotype was dependent on ATP7A expression. Collectively, these data suggest that copper-transporting ATPases, CopA and ATP7A, in both bacteria and macrophage are unique determinants of bacteria survival and identify an unexpected role for copper at the host-pathogen interface.

Abstract Comparative population genomics offers an opportunity to discover the signatures of artificial selection during animal domestication, however, their function cannot be directly revealed. We discover the selection signatures using genome-wide comparisons among 40 mallards, 36 indigenous-breed ducks, and 30 Pekin ducks. Then, the phenotypes are fine-mapped based on resequencing of 1026 ducks from an F 2 segregating population generated by wild × domestic crosses. Interestingly, the two key economic traits of Pekin duck are associated with two selective sweeps with fixed mutations. A novel intronic insertion most possibly leads to a splicing change in MITF accounted for white duck down feathers. And a putative long-distance regulatory mutation causes continuous expression of the IGF2BP1 gene after birth which increases body size by 15% and feed efficiency by 6%. This study provides new insights into genotype–phenotype associations in animal research and constitutes a promising resource on economically important genes in fowl.

This volume examines the raising of dairy calves, giving an account of all aspects of calf rearing from the rudiments of anatomy and development through the practicalities of feeding and housing. Beginning with an overview of how the calf's digestive system develops, it highlights the period of transition from preruminant to ruminant digestion. The authors provide information necessary to understand the nutritional needs and restrictions during the liquid-feeding phase in the young calf, as well as those factors that govern the development of a functional rumen. Major emphasis is given to the energy and protein requirements of the young calf, with attention to the effects of environmental temperature on energy requirements. The book discusses the management, nutrition, and care of the pregnant cow as well as calving management necessary to deliver a healthy calf. Other topics include liquid feeding systems, formulation and use of milk replacers and starter feeds, the weaning process, housing principles, and the interactions of nutrition and disease.

We have read with great interest the Correspondence by Shibo Jiang and colleagues,1Jiang S Shi Z Shu Y et al.A distinct name is needed for the new coronavirus.Lancet. 2020; (published online Feb 19.)https://doi.org/10.1016/S0140-6736(20)30419-0Summary Full Text Full Text PDF Scopus (216) Google Scholar in which they propose a name change for the newly emerged coronavirus,2Zhu N Zhang D Wang W et al.A novel coronavirus from patients with pneumonia in China, 2019.N Engl J Med. 2020; 382: 727-733Crossref PubMed Scopus (18588) Google Scholar which was recently designated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the Coronavirus Study Group of the International Committee on Taxonomy of Viruses.3Gorbalenya AE Baker SC Baric RS et al.Severe acute respiratory syndrome-related coronavirus: the species and its viruses - a statement of the Coronavirus Study Group.bioRxiv. 2020; (published online Feb 11.) (preprint).DOI: 10.1101/2020.02.07.937863Google Scholar The authors argued that the use of SARS in the virus name could confuse the public about the disease that it causes; in addition, they noted that the name SARS-CoV-2 is not consistent with the disease name chosen by WHO, coronavirus disease 2019. The authors also indicated that scientifically, SARS-CoV-2 is naturally occurring and different from other SARS-like or SARS-related coronaviruses that are mainly characterised by their genome sequences. Furthermore, given the probability of future attenuation of this virus to a low-pathogenic form, the authors predict that the use of the name SARS-CoV-2 might have adverse effects, both socially and economically. On these grounds, the authors suggest that the name of the new virus is changed to human coronavirus 2019 (HCoV-19). Although these concerns and suggestions are appreciated, we feel that the adoption of SARS-CoV-2 by the Coronavirus Study Group was appropriate. To facilitate good practice and scientific exchange, the International Committee on Taxonomy of Viruses has established standardised formats for classifying viruses. Under these rules, a newly emerged virus is normally assigned to a species based on phylogeny and taxonomy.4Simmonds P Adams MJ Benko M et al.Consensus statement: virus taxonomy in the age of metagenomics.Nat Rev Microbiol. 2017; 15: 161-168Crossref PubMed Scopus (476) Google Scholar Through DivErsity pArtitioning by hieRarchical Clustering-based analyses,5Lauber C Gorbalenya AE Partitioning the genetic diversity of a virus family: approach and evaluation through a case study of picornaviruses.J Virol. 2012; 86: 3890-3904Crossref PubMed Scopus (59) Google Scholar the newly emerged coronavirus was deemed not sufficiently novel but is a sister virus to SARS-CoV, the primary viral isolate defining the species. The SARS-CoV species includes viruses such as SARS-CoV, SARS-CoV_PC4-227, and SARSr-CoV-btKY72. SARS-CoV-2 is the newest member of this viral species. The use of SARS in naming SARS-CoV-2 does not derive from the name of the SARS disease but is a natural extension of the taxonomic practice for viruses in the SARS species. The use of SARS for viruses in this species mainly refers to their taxonomic relationship to the founding virus of this species, SARS-CoV. In other words, viruses in this species can be named SARS regardless of whether or not they cause SARS-like diseases. The relationship between the name of a viral pathogen and its associated diseases is complex. Although the International Committee on Taxonomy of Viruses is responsible for naming viral species, WHO is responsible for naming the diseases caused by newly emerging viruses. For various reasons, the name of a disease and its causative viral pathogen can be different, as exemplified by acquired immunodeficiency syndrome (AIDS) and human immunodeficiency virus (HIV). We also believe that the use of the name SARS-CoV-2 will not affect social stability and economic development in the affected countries, as the authors envision. Given that the cross-species transmission of SARS-CoV-2 is currently not well understood, and no effective approach to stop such zoonotic transmission has been established, SARS-related coronaviruses, such as SARS-CoV-2 (or even SARS-CoV-3 in the future), might continue to emerge and re-emerge. This has been exemplified in the transmission of Middle East respiratory syndrome-related coronavirus, in which multiple spillover events occurred from camels to humans, resulting in human infections.6Sharif-Yakan A Kanj SS Emergence of MERS-CoV in the Middle East: origins, transmission, treatment, and perspectives.PLoS Pathog. 2014; 10e1004457Crossref PubMed Scopus (65) Google Scholar Thus, keeping SARS in the names of viruses of that species would be beneficial to keep the general public vigilant and prepared to respond quickly in the event of a new viral emergence. Should SARS-CoV-2 be significantly attenuated to the point of becoming a new low-pathogenic or non-pathogenic virus, such attenuated viral isolates could be named as low-pathogenic human coronaviruses, such as LPH-CoV. We believe that the naming of SARS-CoV-2 by the Coronavirus Study Group is aligned with the goals of the International Committee on Taxonomy of Viruses to facilitate good practice and scientific exchange. Given that SARS-CoV-2 is already being used in the scientific literature, a name change at this stage would cause confusion in the scientific community. With all the uncertainties about this newly emerged pathogenic virus, we suggest keeping SARS-CoV-2 as its name. We declare no competing interests. The opinions expressed in this Correspondence are the personal opinions of the authors.

We previously localized a quantitative trait locus (QTL) on chromosome 6 affecting milk fat and protein concentration to a 4-cM confidence interval, centered on the microsatellite BM143. We characterized the genes and sequence variation in this region and identified common haplotypes spanning five polymorphic sites in the genes IBSP, SPP1, PKD2, and ABCG2 for two sires heterozygous for this QTL. Expression of SPP1 and ABCG2 in the bovine mammary gland increased from parturition through lactation. SPP1 and all the coding exons of ABCG2 and PKD2 were sequenced for these two sires. The single nucleotide change capable of encoding a substitution of tyrosine-581 to serine (Y581S) in the ABCG2 transporter was the only polymorphism corresponding to the segregation status of all 3 heterozygous and 15 homozygous sires for the QTL in the Israeli and U.S. Holstein populations. The allele substitution fixed effects on the genetic evaluations of 335 Israeli sires were -341 kg milk, +0.16% fat, and +0.13% protein (F-value = 200). No other polymorphism gave significant effect for fat and protein concentration in models that also included Y581S. The allele substitution effects on the genetic evaluations of 670 cows, daughters of two heterozygous sires, were -226 kg milk, 0.09% fat, and 0.08% protein (F-value = 394), with partial dominance towards the 581S homozygotes. We therefore propose that Y581S in ABCG2 is the causative site for this QTL.

Luteolin, a flavonoid found in high concentrations in celery and green pepper, has been shown to reduce production of proinflammatory mediators in LPS-stimulated macrophages, fibroblasts, and intestinal epithelial cells. Because excessive production of proinflammatory cytokines by activated brain microglia can cause behavioral pathology and neurodegeneration, we sought to determine whether luteolin also regulates microglial cell production of a prototypic inflammatory cytokine, IL-6. Pretreatment of primary murine microlgia and BV-2 microglial cells with luteolin inhibited LPS-stimulated IL-6 production at both the mRNA and protein levels. To determine how luteolin inhibited IL-6 production in microglia, EMSAs were performed to establish the effects of luteolin on LPS-induced binding of transcription factors to the NF-kappaB and activator protein-1 (AP-1) sites on the IL-6 promoter. Whereas luteolin had no effect on the LPS-induced increase in NF-kappaB DNA binding activity, it markedly reduced AP-1 transcription factor binding activity. Consistent with this finding, luteolin did not inhibit LPS-induced degradation of IkappaB-alpha but inhibited JNK phosphorylation. To determine whether luteolin might have similar effects in vivo, mice were provided drinking water supplemented with luteolin for 21 days and then they were injected i.p. with LPS. Luteolin consumption reduced LPS-induced IL-6 in plasma 4 h after injection. Furthermore, luteolin decreased the induction of IL-6 mRNA by LPS in hippocampus but not in the cortex or cerebellum. Taken together, these data suggest luteolin inhibits LPS-induced IL-6 production in the brain by inhibiting the JNK signaling pathway and activation of AP-1 in microglia. Thus, luteolin may be useful for mitigating neuroinflammation.

Implantation in all mammals involves shedding of the zona pellucida, followed by orientation, apposition, attachment and adhesion of the blastocyst to the endometrium. Endometrial invasion does not occur in domestic ruminants; thus, definitive implantation is achieved by adhesion of the mononuclear trophoblast cells to the endometrial lumenal epithelium (LE) and formation of syncytia by the fusion of trophoblast binucleate cells with the LE. This review highlights new information on mechanisms regulating the implantation cascade in sheep. The embryo enters the uterus on day 4 at the morula stage of development and then develops into a blastocyst by day 6. The blastocyst sheds the zona pellucida (day 8), elongates to a filamentous form (days 11-16), and adheres to the endometrial LE (day 16). Between days 14 and 16, the binucleate cells begin to differentiate in the trophoblast and subsequently migrate and fuse with the endometrial LE to form syncytia. Continuous exposure of the endometrium to progesterone in early pregnancy downregulates the progesterone receptors in the epithelia, a process which is associated with loss of the cell-surface mucin MUC1 and induction of several secreted adhesion proteins. Recurrent early pregnancy loss in the uterine gland knockout ewe model indicates that secretions of the endometrial epithelia have a physiologic role in blastocyst elongation and implantation. A number of endometrial proteins have been identified as potential regulators of blastocyst development and implantation in sheep, including glycosylated cell adhesion molecule 1 (GlyCAM-1), galectin-15, integrins and osteopontin. The epithelial derived secreted adhesion proteins (GlyCAM-1, galectin-15 and osteopontin) are expressed in a dynamic temporal and spatial manner and regulated by progesterone and/or interferon tau, which is the pregnancy recognition signal produced by the trophoblast during blastocyst elongation. The noninvasive and protracted nature of implantation in domestic animals provides valuable opportunities to investigate fundamental processes of implantation that are shared among all mammals. Understanding of the cellular and molecular signals that regulate uterine receptivity and implantation can be used to diagnose and identify causes of recurrent pregnancy loss and to improve pregnancy outcome in domestic animals and humans.

The effects of addition of bacitracin methylene disalicylate (BMD) or virginiamycin (VM) to a corn-soybean meal diet on broiler performance and gastrointestinal tract (GIT) growth parameters and morphology were studied at various ages during growth and finishing. Male and female birds were killed at 1, 3, 5, or 7 wk of age for gross and histologic examination of the duodenum and ileum. Feeding either antibiotic increased BW and decreased intestinal length and weight at all times compared with control birds. However, intestinal length and weight decreases were greater in birds fed VM than BMD at 1 and 3 wk of age. The only change found in the duodenum resulting from dietary treatment was an increase in the number of villi per unit length in birds given VM but not BMD or control. In the ileum, the muscularis mucosa was thinner in birds given VM than in those fed the control diet. Chicks supplemented with VM had a smaller total villus area and shorter villus height and crypt depth in the ileum than birds fed the control diet or BMD. Physical changes in the intestine of birds given either antibiotic growth promoter, although not the same, resulted in improved performance.

The aging brain is characterized by a shift from the homeostatic balance of inflammatory mediators to a proinflammatory state. This increase in neuroinflammation is marked by increased numbers of activated and primed microglia, increased steady-state levels of inflammatory cytokines and decreases in anti-inflammatory molecules. These conditions sensitize the aged brain to produce an exaggerated response to the presence of an immune stimulus in the periphery or following exposure to a stressor. In the brain, proinflammatory cytokines can have profound effects on behavioral and neural processes. As the aged brain is primed to respond to inflammatory stimuli, infection or stress may produce more severe detriments in cognitive function in the aged. Typically after an immune stimulus, aged animals display prolonged sickness behaviors, increased cytokine induction and greater cognitive impairments compared to adults. Additionally, aging can also augment the central response to stressors leading to exaggerated cytokine induction and increased decrements in learning and memory. This alteration in neuroinflammation and resultant sensitization to extrinsic and intrinsic stressors can have considerable effects upon the elderly's recovery and coping during disease and stress.

Progress toward understanding the pathogenesis of cystic fibrosis (CF) and developing effective therapies has been hampered by lack of a relevant animal model. CF mice fail to develop the lung and pancreatic disease that cause most of the morbidity and mortality in patients with CF. Pigs may be better animals than mice in which to model human genetic diseases because their anatomy, biochemistry, physiology, size, and genetics are more similar to those of humans. However, to date, gene-targeted mammalian models of human genetic disease have not been reported for any species other than mice. Here we describe the first steps toward the generation of a pig model of CF. We used recombinant adeno-associated virus (rAAV) vectors to deliver genetic constructs targeting the CF transmembrane conductance receptor (CFTR) gene to pig fetal fibroblasts. We generated cells with the CFTR gene either disrupted or containing the most common CF-associated mutation (DeltaF508). These cells were used as nuclear donors for somatic cell nuclear transfer to porcine oocytes. We thereby generated heterozygote male piglets with each mutation. These pigs should be of value in producing new models of CF. In addition, because gene-modified mice often fail to replicate human diseases, this approach could be used to generate models of other human genetic diseases in species other than mice.

We investigated the effect of a 12-d exposure to 34°C plus dietary inclusion of the probiotic Bacillus licheniformis on the egg production, gut morphology, and intestinal mucosal immunity of laying hens. Ninety-six commercial hens (Hy-Line Brown) at the age of 60 wk were randomly allocated to 4 groups. After a period of laying rate adjustment (14 d), all the hens were subjected to 2 temperature treatments (12 d). Birds in 1 group were raised at 21°C and fed a basal diet, and birds in the other 3 groups were raised at 34°C and fed a basal diet supplemented with 0, 10(6), or 10(7) cfu of B. licheniformis per gram of feed, respectively. Rearing at 34°C depressed egg production and feed intake (P < 0.05). Compared with birds kept at 21°C, birds kept at 34°C had elevated serum levels of tumor necrosis factor-α (d 6), IL-1 (d 6 and 12), and corticosterone (d 6); decreased villus height (ileum: d 6; cecum: d 6 and 12) and ratio of villus height to crypt depth (ileum: d 6; cecum: d 6 and 12); fewer intraepithelial lymphocytes (ileum: d 6; cecum: d 6) and IgA-secreting cells (ileum: d 6; cecum: d 6 and 12); and more mast cells (ileum: d 6; cecum: d 6 and 12; P < 0.05). The number of goblet cells in the cecum increased at d 6 in heat-treated birds, and then deceased at d 12 (P < 0.05). Moreover, morphological examination showed injury to the villi of birds kept at 34°C. In general, inclusion of 10(7) cfu/g of B. licheniformis in the diet of heat-stressed hens was effective in overcoming the observed decline in egg production and feed intake, restoring the impaired villus structure, and sustaining a balanced mucosal immune response. Therefore, the probiotic B. licheniformis may be useful for ameliorating the adverse influence of heat on the egg production and gut health of laying hens.

Proinflammatory cytokines inhibit learning and memory but the significance of interleukin-6 (IL-6) in acute cognitive deficits induced by the peripheral innate immune system is not known. To examine the functional role of IL-6 in hippocampus-mediated cognitive impairments associated with peripheral infections, C57BL6/J (IL-6(+/+)) and IL-6 knock-out (IL-6(-/-)) mice were trained in a matching-to-place version of the water maze. After an acquisition phase, IL-6(+/+) mice injected intraperitoneally with lipopolysaccharide (LPS) exhibited deficits in working memory. However, IL-6(-/-) mice were refractory to the LPS-induced impairment in working memory. To determine the mechanism by which IL-6 deficiency conferred protection from disruption in working memory, plasma IL-1beta and tumor necrosis factor alpha (TNFalpha), c-Fos immunoreactivity in the nucleus of the solitary tract (NTS), and steady-state levels of IL-1beta and TNFalpha mRNA in neuronal layers of the hippocampus were determined in IL-6(+/+) and IL-6(-/-) mice after injection of LPS. Plasma IL-1beta and TNFalpha and c-Fos immunoreactivity in the NTS were increased similarly in IL-6(+/+) and IL-6(-/-) mice after LPS, indicating high circulating levels of IL-1beta and TNFalpha and activation of vagal afferent pathways were not sufficient to disrupt working memory in the absence of IL-6. However, the LPS-induced upregulation of IL-1beta and TNFalpha mRNA that was evident in hippocampal tissue of IL-6(+/+) mice was greatly attenuated or entirely absent in IL-6(-/-) mice. Collectively, these data suggest that humoral and neural immune-to-brain communication pathways are intact in IL-6-deficient mice but that, in the absence of IL-6, the central cytokine compartment is hyporesponsive.

The gastrointestinal tract is the site of nutrient digestion and absorption and is also colonized by diverse, highly mutualistic microbes. The intestinal microbiota has diverse effects on the development and function of the gut-specific immune system, and provides some protection from infectious pathogens. However, interactions between intestinal immunity and microorganisms are very complex, and recent studies have revealed that this intimate crosstalk may depend on the production and sensing abilities of multiple bioactive small molecule metabolites originating from direct produced by the gut microbiota or by the metabolism of dietary components. Here, we review the interplay between the host immune system and the microbiota, how commensal bacteria regulate the production of metabolites, and how these microbiota-derived products influence the function of several major innate and adaptive immune cells involved in modulating host immune homeostasis.

Several long-chain fatty acids (LCFA) are natural ligands of nonruminant peroxisome proliferator-activated receptor-gamma (PPARG), which, along with its lipogenic target genes, is upregulated in bovine mammary tissue during lactation. Thus, PPARG might represent an important control point of bovine milk fat synthesis. We tested lipogenic gene network expression via quantitative PCR of 19 genes in bovine mammary epithelial cells cultured with 16:0, 18:0, cis-9 18:1, trans-10 18:1, trans-10,cis-12 18:2 [t10c12 conjugated linoleic acid (CLA)], 20:5, ethanol (control), and the PPARG agonist rosiglitazone (ROSI). Triplicate cultures were maintained for 12 h with 50 muM ROSI or 100 muM LCFA. Responses common to 16:0 and 18:0 relative to the control included significantly greater expression of INSIG1 (+298%, +92%), AGPAT6 (+137%, +169%), FABP3 (+755%, +338%), and FABP4 (+171%, 157%). These were coupled with greater intracellular lipid droplet formation and mRNA of ACSS2, LPIN1, SCD, and SREBF2 in response to 16:0, and greater DGAT1 and THRSP with 18:0. Trans-10 18:1 and t10c12 CLA reduced expression of FASN (-60%, -31%), SCD (-100%, -357%), and SREBF1 (-49%, -189%). Furthermore, t10c12 CLA downregulated ACSS2, FABP3, INSIG1, SREBF2, and THRSP expression. Expression of SREBF1 was lower with cis-9 18:1 (-140%) and 20:5 (-125%) compared with the control. This latter LCFA also decreased SCD, SREBF2, and LPL expression. No effects of LCFA or ROSI on PPARG were observed, but ROSI upregulated (+39% to +269%) expression of ACACA, FASN, LPIN1, AGPAT6, DGAT1, SREBF1, SREBF2, and INSIG1. Thus, these genes are putative PPARG target genes in bovine mammary cells. This is the first report showing a direct effect of trans-10 18:1 on bovine mammary cell lipogenic gene expression. The coordinated upregulation of lipogenic gene networks in response to ROSI and saturated LCFA offers support for PPARG activation in regulating bovine milk fat synthesis.

Feelings of hunger and satiety are the key determinants for maintaining the life of humans and animals. Disturbed appetite control may disrupt the metabolic health of the host and cause various metabolic disorders. A variety of factors have been implicated in appetite control, including gut microbiota, which develop the intricate interactions to manipulate the metabolic requirements and hedonic feelings. Gut microbial metabolites and components act as appetite-related signaling molecules to regulate appetite-related hormone secretion and the immune system, or act directly on hypothalamic neurons. Herein, we summarize the effects of gut microbiota on host appetite and consider the potential molecular mechanisms. Furthermore, we propose that the manipulation of gut microbiota represents a clinical therapeutic potential for lessening the development and consequence of appetite-related disorders. Video abstract.