Global proteomic analysis of serum during early pregnancy in the pig using data-independent acquisition mass spectrometry with verification by parallel reaction monitoring.

CONTEXT: The current pregnancy diagnosis is generally not ideal in accuracy and efficiency, and the physiological process of early pregnancy in pig remains unclarified. AIMS: This study aimed to evaluate protein expression profiles and identify typical proteins of early pregnancy for more understanding of physiological processes. METHODS: Data-independent acquisition-based (DIA) quantitative proteomic analysiswas performed to compare the serum proteome profiles on days 0, 5, 12, 16, and 19 of gestation in Tibetan pig.Parallel reaction monitoring (PRM) was subsequently performed to verify relative expression level. KEY RESULTS: 396 proteins were detected, of which 113 differentially expressed proteins (DEPs) were identified. Functional annotation and pathway analysis indicated that the DEPs were mainly involved in catalytic activity, metabolic processes and the proteasome. Four candidate DEPs (talin 1, profilin, carbonic anhydrase, and HGF activator) showed consistent expression trends in both DIA and PRM approaches. CONCLUSIONS: The DIA based proteomic methods indicate the involvement of numerous serum proteins in early pregnancy physiological function in pigs. The combination of DIA-PRM based global proteomic analysis may provide insights for function study and pregnancy diagnosis biomarkers. IMPLICATIONS: The global proteomic analyses performed here have increased the knowledge of early pregnancy in Tibetan swine and provide potential methods for pregnancy detection.

Effects of Long-Chain Fatty Acyl-CoA Synthetase 1 on Diglyceride Synthesis and Arachidonic Acid Metabolism in Sheep Adipocytes.

Long-chain fatty acyl-CoA synthetase (ACSLs) is an essential enzyme for the synthesis of fatty acyl-CoA. ACSL1 plays a key role in the synthesis of triglycerides, phospholipids, and cholesterol esters. BACKGROUND: In the current study, triglyceride content did not increase after overexpression of the ACSL1 gene. METHODS: RNA-seq and lipid metabolome profiling were performed to determine why triglyceride levels did not change with ACSL1 overexpression. RESULTS: Fatty acyl-CoA produced by ACSL1 was determined to be involved in the diglyceride synthesis pathway, and diglyceride content significantly increased when ACSL1 was overexpressed. Moreover, the arachidonic acid (AA) content in sheep adipocytes significantly increased, and the level of cyclooxygenase 2 (COX2) expression, the downstream metabolic gene, was significantly downregulated. Knocking down the ACSL1 gene was associated with an increase in COX2 mRNA expression, as well as an increase in prostaglandin content, which is the downstream metabolite of AA. CONCLUSIONS: The overexpression of the ACSL1 gene promotes the production of AA via downregulation of COX2 gene expression.

In-vitro differentiation of early pig spermatogenic cells to haploid germ cells.

Spermatogonial stem cells (SSCs) self-renew and contribute genetic information to the next generation. Pig is wildly used as a model animal for understanding reproduction mechanisms of human being. Inducing directional differentiation of porcine SSCs may be an important strategy in exploring the mechanisms of spermatogenesis and developing better treatment methods for male infertility. Here, we established an in-vitro culture model for porcine small seminiferous tubule segments, to induce SSCs to differentiate into single-tail haploid spermatozoa. The culture model subsequently enabled spermatozoa to express the sperm-specific protein acrosin and oocytes to develop to blastocyst stage after round spermatid injection. The addition of retinoic acid (RA) to the differentiation media promoted the efficiency of haploid differentiation. RT-PCR analysis indicated that RA stimulated the expression of Stra8 but reduced the expression of NANOS2 in spermatogonia. Genes involved in post-meiotic development, transition protein 1 (Tnp1) and protamine 1 (Prm1) were upregulated in the presence of RA. The addition of an RA receptor (RAR) inhibitor, BMS439, showed that RA enhanced the expression of cAMP responsive-element binding protein through RAR and promoted the formation of round spermatids. We established an efficient culture system for in-vitro differentiation of pig SSCs. Our study represents a model for human testis disease and toxicology screening. Molecular regulators of SSC differentiation revealed in this study might provide a therapeutic strategy for male infertility.

Screening of live yeast and yeast derivatives for their impact of strain and dose on in vitro ruminal fermentation and microbial profiles with varying media pH levels in high-forage beef cattle diet.

BACKGROUND: Yeast products showed beneficial effects with respect to stabilizing ruminal pH, stimulating ruminal fermentation and improving production efficiency. Batch cultures were conducted to evaluate the effects of yeast products on gas production (GP), dry matter disappearance (DMD) and fermentation characteristics of high-forage substrate. The study was a two media pH (5.8 and 6.5) × five yeasts (three live yeasts, LY: LY1, LY2, LY3; two yeast derivatives, YD: YD4, YD5) × four dosages factorial arrangement, with monensin (Mon) assigned as a positive control. RESULTS: Greater (P < 0.01) GP, DMD, volatile fatty acid (VFA) concentration, ratio of acetate to propionate (A:P) and copy numbers of Fibrobacter succinogenes and Ruminococcus flavefaciens were observed at pH 6.5 than at pH 5.8. The GP kinetics, DMD, VFA concentration, A:P and NH3 -N concentration differed (P < 0.05) among yeasts but varied with media pH or yeast dosages. Increasing doses of LY3 linearly increased DMD (P < 0.04) and VFA concentration (P < 0.001) at media pH 5.8. The DMD linearly (P < 0.02) increased with increased addition of YD4 (pH 6.5) and YD5 (pH 5.8) and the ratio of A:P linearly decreased (P < 0.01) with the addition of YD4 or YD5 at pH 5.8. Overall greater (P < 0.05) GP, A:P (pH 5.8) and DMD (pH 6.5) were observed with yeast products than with Mon. CONCLUSION: LY3 appeared to be an interesting candidate for improving rumen digestibility and fermentation efficiency, particularly at low media pH. YD4 or YD5 improved fermentation efficiency and can be potentially fed as an alternative to Mon. © 2019 Her Majesty the Queen in Right of Canada Journal of the Science of Food and Agriculture © 2019 Society of Chemical Industry.

Overexpression of Toll-Like Receptor 4 Contributes to Phagocytosis of Salmonella Enterica Serovar Typhimurium via Phosphoinositide 3-Kinase Signaling in Sheep.

BACKGROUND/AIMS: Phagocytosis of bacteria by monocytes/macrophages can trigger the immune response and the clearance of bacteria. This innate immune response involves Toll-like receptor 4 (TLR4). However, much remains unknown about the mechanism of TLR4-regulated phagocytosis of Salmonella enterica serovar Typhimurium (S. typhimurium) within sheep monocytes/macrophages. Here, we aimed to address these knowledge gaps by infecting transgenic sheep overexpressing TLR4 with S. typhimurium and examining the phagocytic mechanisms involved. METHODS: Transgenic sheep were generated by microinjection of the constructed plasmids into fertilized eggs. Monocytes/macrophages isolated from sheep blood were stimulated with LPS and S. typhimurium. Phagocytosis-related factor expression, phagocytic ability, and adhesion were then determined. TLR4/phosphatidylinositide 3-kinase (PI3K) signaling was inhibited to investigate if this pathway is involved in changes in bacterial internalization in sheep. RESULTS: We found that TLR4 overexpression effectively activated the PI3K signaling pathway and upregulated the expression of scavenger receptors. Additionally, actin polymerization and adhesive capacity were both enhanced in TLR4-overexpressing sheep monocytes/macrophages. TLR4 inhibition decreased S. typhimurium phagocytosis by reducing the actin polymerization and adhesive capacity of cells. Furthermore, inhibition of PI3K markedly impaired TLR4-dependent phagocytosis by restraining actin polymerization and scavenger receptor expression and reduced the adhesive capacity of the monocytes/macrophages. CONCLUSION: Our findings indicate that overexpression of TLR4 enhances phagocytosis through PI3K signaling and the subsequent activation of actin polymerization and scavenger receptors in sheep monocytes/macrophages infected with S. typhimurium.

TLR4 signalling in ischemia/reperfusion injury: a promising target for linking inflammation, oxidative stress and programmed cell death to improve organ transplantation outcomes.

Transplantations represent the principal therapeutic interventions for terminal organ failure, a procedure that has salvaged myriad lives annually. Ischemia/reperfusion injury (IRI) is frequently correlated with an unfavourable prognosis and is relevant for early graft dysfunction and graft survival. IRI constitutes a complex pathological state influenced by a series of factors such as oxidative stress, metabolic stress, leukocytic infiltration, programmed cell death pathways, and inflammatory immune responses. Reducing ischemia/reperfusion injury is one of the main directions of transplantation research. Toll-like receptors (TLRs) are important pattern-recognition receptors expressed on various organs that orchestrate the immune responses upon recognising PAMPs and DAMPs. Targeting the TLR4 signalling has recently been suggested as a promising approach for alleviating IRI by affecting inflammation, oxidative stress and programmed cell death (PCD). In this minireview, we summarise the role of TLR4 signalling in regulating inflammation, oxidative stress and PCD in organ transplantation and discuss their interactions during IRI. A detailed understanding of the multiple functions of TLR4 in IRI provides novel insights into developing therapies to improve organ transplantation outcomes.

Autophagy is a promising process for linking inflammation and redox homeostasis in Down syndrome.

Trisomy 21, characterized by the presence of an additional chromosome 21, leads to a set of clinical features commonly referred to as Down syndrome (DS). The pathological phenotypes observed in DS are caused by a combination of factors, such as mitochondrial dysfunction, neuroinflammation, oxidative stress, disrupted metabolic patterns, and changes in protein homeostasis and signal transduction, and these factors collectively induce neurological alterations. In DS, the triplication of chromosome 21 and the micronuclei arising from the missegregation of chromosomes are closely associated with inflammation and the development of redox imbalance. Autophagy, an essential biological process that affects cellular homeostasis, is a powerful tool to facilitate the degradation of redundant or dysfunctional cytoplasmic components, thereby enabling the recycling of their constituents. Targeting the autophagy process has been suggested as a promising method to balance intracellular inflammation and oxidative stress and improve mitochondrial dysfunction. In this review, we summarize the role of autophagy in regulating inflammation and redox homeostasis in DS and discuss their crosslinks. A comprehensive elucidation of the roles of autophagy in DS offers novel insights for the development of therapeutic strategies aimed at aneuploidy-associated diseases.

The cGAS-STING pathway in viral infections: a promising link between inflammation, oxidative stress and autophagy.

The host defence responses play vital roles in viral infection and are regulated by complex interactive networks. The host immune system recognizes viral pathogens through the interaction of pattern-recognition receptors (PRRs) with pathogen-associated molecular patterns (PAMPs). As a PRR mainly in the cytoplasm, cyclic GMP-AMP synthase (cGAS) senses and binds virus DNA and subsequently activates stimulator of interferon genes (STING) to trigger a series of intracellular signalling cascades to defend against invading pathogenic microorganisms. Integrated omic and functional analyses identify the cGAS-STING pathway regulating various host cellular responses and controlling viral infections. Aside from its most common function in regulating inflammation and type I interferon, a growing body of evidence suggests that the cGAS-STING signalling axis is closely associated with a series of cellular responses, such as oxidative stress, autophagy, and endoplasmic reticulum stress, which have major impacts on physiological homeostasis. Interestingly, these host cellular responses play dual roles in the regulation of the cGAS-STING signalling axis and the clearance of viruses. Here, we outline recent insights into cGAS-STING in regulating type I interferon, inflammation, oxidative stress, autophagy and endoplasmic reticulum stress and discuss their interactions with viral infections. A detailed understanding of the cGAS-STING-mediated potential antiviral effects contributes to revealing the pathogenesis of certain viruses and sheds light on effective solutions for antiviral therapy.

Novel perspectives on autophagy-oxidative stress-inflammation axis in the orchestration of adipogenesis.

Adipose tissue, an indispensable organ, fulfils the pivotal role of energy storage and metabolism and is instrumental in maintaining the dynamic equilibrium of energy and health of the organism. Adipocyte hypertrophy and adipocyte hyperplasia (adipogenesis) are the two primary mechanisms of fat deposition. Mature adipocytes are obtained by differentiating mesenchymal stem cells into preadipocytes and redifferentiation. However, the mechanisms orchestrating adipogenesis remain unclear. Autophagy, an alternative cell death pathway that sustains intracellular energy homeostasis through the degradation of cellular components, is implicated in regulating adipogenesis. Furthermore, adipose tissue functions as an endocrine organ, producing various cytokines, and certain inflammatory factors, in turn, modulate autophagy and adipogenesis. Additionally, autophagy influences intracellular redox homeostasis by regulating reactive oxygen species, which play pivotal roles in adipogenesis. There is a growing interest in exploring the involvement of autophagy, inflammation, and oxidative stress in adipogenesis. The present manuscript reviews the impact of autophagy, oxidative stress, and inflammation on the regulation of adipogenesis and, for the first time, discusses their interactions during adipogenesis. An integrated analysis of the role of autophagy, inflammation and oxidative stress will contribute to elucidating the mechanisms of adipogenesis and expediting the exploration of molecular targets for treating obesity-related metabolic disorders.

Quantitative proteomic analysis and verification identify global protein profiling dynamics in pig during the estrous cycle.

The current estrus detection method is generally time-consuming and has low accuracy. As such, a deeper understanding of the physiological processes during the estrous cycle accelerates the development of estrus detection efficiency and accuracy. In this study, the label-free acquisition mass spectrometry was used to explore salivary proteome profiles during the estrous cycle (day -3, day 0, day 3, and day 8) in pigs, and the parallel reaction monitoring (PRM) was applied to verify the relative profiles of protein expression. A total of 1,155 proteins were identified in the label-free analysis, of which 115 were identified as differentially expressed proteins (DEPs) among different groups (p ≤ 0.05). Functional annotation revealed that the DEPs were clustered in calcium ion binding, actin cytoskeleton, and lyase activity. PRM verified the relative profiles of protein expression, in which PHB domain-containing protein, growth factor receptor-bound protein 2, elongation factor Tu, carboxypeptidase D, carbonic anhydrase, and trefoil factor 3 were confirmed to be consistent in both label-free and PRM approaches. Comparative proteomic assays on saliva would increase our knowledge of the estrous cycle in sows and provide potential methods for estrus detection.

Differences in histomorphology and expression of key lipid regulated genes of four adipose tissues from Tibetan pigs.

Tibetan pigs, an indigenous pig breed in China, have high overall fat deposition and flavorful and tasty meat. They are thus good models for studying adipogenesis. Few studies have been conducted focusing on expression of lipid regulated genes in different adipose tissues of Tibetan pigs. Therefore, we compared the difference of histomorphology and expression level of lipid regulated genes through qPCR and western blot in subcutaneous fat, perirenal fat, omental adipose tissue, and inguinal fat of Tibetan pigs. Our results showed that the area of subcutaneous adipocytes in Tibetan pigs was smaller, while the other three adipose tissues (perirenal fat, greater omentum fat, inguinal fat) had cell areas of similar size. The gene expression of FABP4, FASN, FABP3, and ME1 in subcutaneous fat was significantly higher than that in perirenal fat. Furthermore, the protein expression of FABP4 was significantly lower in subcutaneous fat than in perirenal fat (p < 0.05), and the expression of FASN was higher in greater omentum fat than in subcutaneous fat (p = 0.084). The difference in adipocyte cell size and expression of lipid-regulated genes in adipose tissues from the various parts of the pig body is likely due to the different cellular lipid metabolic processes. Specially, FABP4 and FASN may be involved in the regulation of fat deposition in different adipose tissues of Tibetan pigs.

Effects of Dietary Supplementation with Mulberry Leaf Powder on the Growth Performance, Lipid Metabolism Parameters, Immunity Indicators, and Gut Microbiota of Dogs.

Overfeeding and a lack of exercise are increasingly causing obesity in dogs, which has become a big problem threatening the health of dogs. Therefore, it is necessary to investigate how dietary regulations can help to improve dogs' body conditions and minimize obesity. This study was carried out to investigate the effects of dietary mulberry leaf powder (MLP) supplementation on the growth performance, lipid metabolism parameters, and gut microbiota of Chinese indigenous dogs. Fifteen Chinese indigenous dogs (6.34 ± 0.56 kg) were randomly assigned to three treatment groups and received either the control diet (CON), high-fat diet (HF), or high-fat diet containing 6% Mulberry leaf powder (MLP) for four weeks. The CON group received a basal diet, the HF group received a basal diet supplemented with 10% lard, and the MLP group received a basal diet supplemented with 10% lard and 6% MLP. The trial lasted for four weeks. The growth performance, lipid metabolism parameters, immune globulins, cytokines, and fecal microbiota were measured. Results showed that there was no significant difference in growth performance. The MLP group appeared to have decreased (p < 0.05) the serum level of low-density lipoprotein cholesterol (LDL-C) and apoliprotein-A1(APO-A1) in serum. The MLP group appeared to have higher (p < 0.05) serum immune globulin A (IgA) levels. UPGMA results showed that the MLP group was closer to the CON group than to the HF group. LEfSe analysis showed that dietary supplementation with MLP contributed to an alteration in the genus Alloprevotella, Sarcina, and species belonging to the Bacteroides and Lactobacillus genus. Overall, the dietary supplementation of 6% MLP can improve lipid metabolism conditions and immunity in high-fat-diet-fed dogs, and can alter the gut microbial composition of dogs.

TLR4 Overexpression Aggravates Bacterial Lipopolysaccharide-Induced Apoptosis via Excessive Autophagy and NF-κB/MAPK Signaling in Transgenic Mammal Models.

Gram-negative bacterial infections pose a significant threat to public health. Toll-like receptor 4 (TLR4) recognizes bacterial lipopolysaccharide (LPS) and induces innate immune responses, autophagy, and cell death, which have major impacts on the body's physiological homeostasis. However, the role of TLR4 in bacterial LPS-induced autophagy and apoptosis in large mammals, which are closer to humans than rodents in many physiological characteristics, remains unknown. So far, few reports focus on the relationship between TLR, autophagy, and apoptosis in large mammal levels, and we urgently need more tools to further explore their crosstalk. Here, we generated a TLR4-enriched mammal model (sheep) and found that a high-dose LPS treatment blocked autophagic degradation and caused strong innate immune responses and severe apoptosis in monocytes/macrophages of transgenic offspring. Excessive accumulation of autophagosomes/autolysosomes might contribute to LPS-induced apoptosis in monocytes/macrophages of transgenic animals. Further study demonstrated that inhibiting TLR4 downstream NF-κB or p38 MAPK signaling pathways reversed the LPS-induced autophagy activity and apoptosis. These results indicate that the elevated TLR4 aggravates LPS-induced monocytes/macrophages apoptosis by leading to lysosomal dysfunction and impaired autophagic flux, which is associated with TLR4 downstream NF-κB and MAPK signaling pathways. This study provides a novel TLR4-enriched mammal model to study its potential effects on autophagy activity, inflammation, oxidative stress, and cell death. These findings also enrich the biological functions of TLR4 and provide powerful evidence for bacterial infection.

Bile acids and their receptors in regulation of gut health and diseases.

It is well established that bile acids play important roles in lipid metabolism. In recent decades, bile acids have also been shown to function as signaling molecules via interacting with various receptors. Bile acids circulate continuously through the enterohepatic circulation and go through microbial transformation by gut microbes, and thus bile acids metabolism has profound effects on the liver and intestinal tissues as well as the gut microbiota. Farnesoid X receptor and G protein-coupled bile acid receptor 1 are two pivotal bile acid receptors that highly expressed in the intestinal tissues, and they have emerged as pivotal regulators in bile acids metabolism, innate immunity and inflammatory responses. There is considerable interest in manipulating the metabolism of bile acids and the expression of bile acid receptors as this may be a promising strategy to regulate intestinal health and disease. This review aims to summarize the roles of bile acids and their receptors in regulation of gut health and diseases.

Modulation of Innate Antiviral Immune Response by Porcine Enteric Coronavirus.

Host's innate immunity is the front-line defense against viral infections, but some viruses have evolved multiple strategies for evasion of antiviral innate immunity. The porcine enteric coronaviruses (PECs) consist of porcine epidemic diarrhea virus (PEDV), porcine deltacoronavirus (PDCoV), transmissible gastroenteritis coronavirus (TGEV), and swine acute diarrhea syndrome-coronavirus (SADS-CoV), which cause lethal diarrhea in neonatal pigs and threaten the swine industry worldwide. PECs interact with host cells to inhibit and evade innate antiviral immune responses like other coronaviruses. Moreover, the immune escape of porcine enteric coronaviruses is the key pathogenic mechanism causing infection. Here, we review the most recent advances in the interactions between viral and host's factors, focusing on the mechanisms by which viral components antagonize interferon (IFN)-mediated innate antiviral immune responses, trying to shed light on new targets and strategies effective for controlling and eliminating porcine enteric coronaviruses.

Transcript variants of long-chain acyl-CoA synthase 1 have distinct roles in sheep lipid metabolism.

Mutton has recently been identified to be a consumer favorite, and intermuscular fat is the key factor in determining meat tenderness. Long-chain acyl-CoA synthetase 1 (ACSL1) is a vital subtype of the ACSL family that is involved in the synthesis of lipids from acyl-CoA and the oxidation of fatty acids. The amplification of the ACSL1 gene using rapid amplification of cDNA ends revealed that the alternative polyadenylation (APA) results in two transcripts of the ACSL1 gene. Exon 18 had premature termination, resulting in a shorter CDS region. In this study, the existence of two transcripts of varying lengths translated normally and designated ACSL1-a and ACSL1-b was confirmed. Overexpression of ACSL1-a can promote the synthesis of an intracellular diglyceride, while ACSL1-b can promote triglyceride synthesis. The transfection of ACSL1 shRNA knocks down both the transcripts, the triglyceride content was significantly reduced after differentiation and induction; and lipidome sequencing results exhibited a significant decrease in 14-22 carbon triglyceride metabolites. The results of the present study indicated that the ACSL1 gene played a crucial role in the synthesis of triglycerides. Furthermore, the two transcripts involved in various interactions in the triglyceride synthesis process may be the topic of interest for future research and provide a more theoretical basis for sheep breeding.

The multifunctional roles of autophagy in the innate immune response: Implications for regulation of transplantation rejection.

Organ transplantation is the main treatment for end-stage organ failure, which has rescued tens of thousands of lives. Immune rejection is the main factor affecting the survival of transplanted organs. How to suppress immune rejection is an important goal of transplantation research. A graft first triggers innate immune responses, leading to graft inflammation, tissue injury and cell death, followed by adaptive immune activation. At present, the importance of innate immunity in graft rejection is poorly understood. Autophagy, an evolutionarily conserved intracellular degradation system, is proven to be involved in regulating innate immune response following graft transplants. Moreover, there is evidence indicating that autophagy can regulate graft dysfunction. Although the specific mechanism by which autophagy affects graft rejection remains unclear, autophagy is involved in innate immune signal transduction, inflammatory response, and various forms of cell death after organ transplantation. This review summarizes how autophagy regulates these processes and proposes potential targets for alleviating immune rejection.

Application of Gene Editing Technology in Resistance Breeding of Livestock.

As a new genetic engineering technology, gene editing can precisely modify the specific gene sequence of the organism's genome. In the last 10 years, with the rapid development of gene editing technology, zinc-finger nucleases (ZFNs), transcription activator-like endonucleases (TALENs), and CRISPR/Cas9 systems have been applied to modify endogenous genes in organisms accurately. Now, gene editing technology has been used in mice, zebrafish, pigs, cattle, goats, sheep, rabbits, monkeys, and other species. Breeding for disease-resistance in agricultural animals tends to be a difficult task for traditional breeding, but gene editing technology has made this easier. In this work, we overview the development and application of gene editing technology in the resistance breeding of livestock. Also, we further discuss the prospects and outlooks of gene editing technology in disease-resistance breeding.

The Effects of Dietary Inclusion of Mulberry Leaf Powder on Growth Performance, Carcass Traits and Meat Quality of Tibetan Pigs.

This research was conducted to study the effects of dietary inclusion of mulberry leaf powder (MLP) on growth performance, meat quality, antioxidant activity, and carcass traits of Tibetan pigs. Eighteen Tibetan pigs (33.8 ± 1.1 kg) were assigned to two treatment groups randomly and received either the control diet (CON) or a basal diet containing 8% MLP (MLP) for two months. After the two-month feeding trial, the MLP group showed lower backfat thickness while a higher lean percentage. Compared with CON pigs, MLP pigs had higher serum CAT activity. In addition, dietary MLP supplementation significantly decreased the muscle shear force. Muscle fiber morphology analysis showed that MLP pigs had larger muscle fiber density while smaller muscle fiber cross-sectional area. Up-regulated gene expression of myosin heavy chain (MyHC)IIa was also observed in MLP pigs. These results indicate that the enhanced antioxidant activity and altered muscle fiber type and morphology appeared to contribute to the improvement of meat quality in Tibetan pigs fed diets containing MLP.

Autophagy and Mitochondrial Homeostasis During Infection: A Double-Edged Sword.

Autophagy, an essential biological process that affects immunity, is a powerful tool that host cells can use to defend against infections caused by pathogenic microorganisms. Autophagy can not only initiate innate immune responses but also degrade the cellular components that provide the conditions for removing the invaders. However, hyperactivated or inhibited autophagy leads to mitochondrial dysfunction, which is harmful to the host itself and is involved in many types of diseases. Mitochondria perform the functions of biological oxidation and energy exchange. In addition, mitochondrial functions are closely related to cell death, oxygen radical formation, and disease. Accumulation of mitochondrial metabolites affects survival of intracellular pathogens. In this mini-review, we focus on the crosstalk between autophagy and mitochondrial homeostasis during infection.