Notch-RBPJ Pathway for the Differentiation of Bone Marrow Mesenchymal Stem Cells in Femoral Head Necrosis.

Femoral head necrosis (FHN) is a common leg disease in broilers, resulting in economic losses in the poultry industry. The occurrence of FHN is closely related to the decrease in the number of bone marrow mesenchymal stem cells (BMSCs) and the change in differentiation direction. This study aimed to investigate the function of differentiation of BMSCs in the development of FHN. We isolated and cultured BMSCs from spontaneous FHN-affected broilers and normal broilers, assessed the ability of BMSCs into three lineages by multiple staining methods, and found that BMSCs isolated from FHN-affected broilers demonstrated enhanced lipogenic differentiation, activated Notch-RBPJ signaling pathway, and diminished osteogenic and chondrogenic differentiation. The treatment of BMSCs with methylprednisolone (MP) revealed a significant decrease in the expressions of Runx2, BMP2, Col2a1 and Aggrecan, while the expressions of p-Notch1/Notch1, Notch2 and RBPJ were increased significantly. Jagged-1 (JAG-1, Notch activator)/DAPT (γ-secretase inhibitor) could promote/inhibit the osteogenic or chondrogenic ability of MP-treated BMSCs, respectively, whereas the differentiation ability of BMSCs was restored after transfection with si-RBPJ. The above results suggest that the Notch-RBPJ pathway plays important role in FHN progression by modulating the osteogenic and chondrogenic differentiation of BMSCs.

Downregulation of miR-30b-5p Facilitates Chondrocyte Hypertrophy and Apoptosis via Targeting Runx2 in Steroid-Induced Osteonecrosis of the Femoral Head.

As a widely used steroid hormone medicine, glucocorticoids have the potential to cause steroid-induced osteonecrosis of the femoral head (SONFH) due to mass or long-term use. The non-coding RNA hypothesis posits that they may contribute to the destruction and dysfunction of cartilages as a possible etiology of SONFH. MiR-30b-5p was identified as a regulatory factor in cartilage degeneration caused by methylprednisolone (MPS) exposure in our study through cell transfection. The luciferase reporter assay confirmed that miR-30b-5p was downregulated and runt-related transcription factor 2 (Runx2) was mediated by miR-30b-5p. The nobly increased expression of matrix metallopeptidase 13 (MMP13) and type X collagen (Col10a1) as Runx2 downstream genes contributed to the hypertrophic differentiation of chondrocytes, and the efficiently upregulated level of matrix metallopeptidase 9 (MMP9) may trigger chondrocyte apoptosis with MPS treatments. The cell transfection experiment revealed that miR-30b-5p inhibited chondrocyte hypertrophy and suppressed MPS-induced apoptosis. As a result, our findings showed that miR-30b-5p modulated Runx2, MMP9, MMP13, and Col10a1 expression, thereby mediating chondrocyte hypertrophic differentiation and apoptosis during the SONFH process. These findings revealed the mechanistic relationship between non-coding RNA and SONFH, providing a comprehensive understanding of SONFH and other bone diseases.

Discrimination of indoor versus outdoor environmental state with machine learning algorithms in myopia observational studies.

BACKGROUND: Wearable smart watches provide large amount of real-time data on the environmental state of the users and are useful to determine risk factors for onset and progression of myopia. We aim to evaluate the efficacy of machine learning algorithm in differentiating indoor and outdoor locations as collected by use of smart watches. METHODS: Real time data on luminance, ultraviolet light levels and number of steps obtained with smart watches from dataset A: 12 adults from 8 scenes and manually recorded true locations. 70% of data was considered training set and support vector machine (SVM) algorithm generated using the variables to create a classification system. Data collected manually by the adults was the reference. The algorithm was used for predicting the location of the remaining 30% of dataset A. Accuracy was defined as the number of correct predictions divided by all. Similarly, data was corrected from dataset B: 172 children from 3 schools and 12 supervisors recorded true locations. Data collected by the supervisors was the reference. SVM model trained from dataset A was used to predict the location of dataset B for validation. Finally, we predicted the location of dataset B using the SVM model self-trained from dataset B. We repeated these three predictions with traditional univariate threshold segmentation method. RESULTS: In both datasets, SVM outperformed the univariate threshold segmentation method. In dataset A, the accuracy and AUC of SVM were 99.55% and 0.99 as compared to 95.11% and 0.95 with the univariate threshold segmentation (p < 0.01). In validation, the accuracy and AUC of SVM were 82.67% and 0.90 compared to 80.88% and 0.85 with the univariate threshold segmentation method (p < 0.01). In dataset B, the accuracy and AUC of SVM and AUC were 92.43% and 0.96 compared to 80.88% and 0.85 with the univariate threshold segmentation (p < 0.01). CONCLUSIONS: Machine learning algorithm allows for discrimination of outdoor versus indoor environments with high accuracy and provides an opportunity to study and determine the role of environmental risk factors in onset and progression of myopia. The accuracy of machine learning algorithm could be improved if the model is trained with the dataset itself.

Protective effects of anthocyanin against apoptosis and oxidative stress induced by arsanilic acid in DF-1 cells.

Anthocyanin is a natural plant pigment that acts as an antioxidant and scavenges free radicals. This study aimed to investigate the potential protective role of nightshade anthocyanin (NA), a natural flavonoid compound, against the arsanilic acid (ASA)-induced cell death of DF-1 cells. DF-1 cells were initially exposed to ASA, and then NA was applied to the treated cells. Cell viability, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and apoptosis were examined. Results showed that NA inhibited the ASA-induced decrease in cell viability, increase in ROS, and loss of MMP in DF-1 cells. Moreover, caspase-3 activation was inhibited by ASA supplementation and NA attenuated the ASA-induced increase in the percentage of apoptotic cells. In summary, our study suggested that NA can enhance ASA-induced cytotoxicity and apoptosis, thereby providing a basis for the molecular mechanisms of NA-mediated protection.

Effects of Cr(VI)-induced calcium-sensing receptor activation on DF-1 cell pyroptosis.

This study aims to investigate the effects of Cr(VI)-induced calcium-sensing receptor (CaSR) activation on DF-1 cell pyroptosis. Previous studies show that Cr(VI) could accumulate in the body of chickens and change Ca levels. Hence, a Ca-related pathway may be an important mechanism participating in some pathological processes. Pyroptosis level, which is meditated by CaSR, increases under Cr(VI) accumulation. In the present study, pyroptosis was determined by flow cytometry to detect SYTOX blue and caspase-1 staining followed by morphological observation. Interleukin (IL)-1ß and IL-18 levels were detected by ELISA, while CaSR protein and [Ca2+]i contents were detected by Western blot and fluorescence microplate spectrophotometry, respectively. The results showed that Cr(VI) causes DF-1 cell pyroptosis in a time- and dose-dependent manner and that this effect is caspase-1 dependent. Further experiments indicated that pyroptosis could be induced by Cr(VI) and is accompanied by up-regulated [Ca2+]i content. CaSR inhibition led to decreases in pyroptosis level. Some mechanisms may be involved in Cr(VI)-triggered CaSR activation and enhance DF-1 cell pyroptosis. Taken together, the results of this study support future investigations on Cr(VI)-induced pyroptosis in DF-1 cells.

The regulatory role of COX-2 in the interaction between Cr(VI)-induced endoplasmic reticulum stress and autophagy in DF-1 cells.

Hexavalent chromium (Cr(VI)) is a common environmental pollutant. Exposure of Cr(VI) can lead to cell autophagy, but the preventive measures for diminishing Cr(VI)-induced autophagy need further study. COX-2 can be induced by several heavy metals and can lead to endoplasmic reticulum (ER) stress and autophagy; thus, COX-2, ER stress, and autophagy may be related. This study mainly investigated the role of COX-2 in the eIF2α-ATF4 pathway, which is a major pathway in cell autophagy. In this study, Cr(VI) was used as a xenobiotic to determine changes in the parameters of ER stress, autophagy, and COX-2 levels. At the same time, a clear contrast was obtained by assigning positive and negative controls of ER stress and autophagy. The results showed that during Cr(VI) invasion, the parameters of ER stress and autophagy (such as BiP, PERK, p62, LC3-II, and mTOR) were enhanced, similarly to the positive control of ER stress and/or the autophagy controls. Such enhancement is a protective mechanism for cell survival. Additionally, the COX-2 levels increased. Moreover, when COX-2 was inhibited, the PERK level remained high, whereas the LC3-II level decreased. This finding suggests that COX-2 specifically affects the interaction between ER stress and autophagy. Notably, this study reveals that Cr(VI) can induce ER stress and autophagy in DF-1 cells and that COX-2 plays an essential role in the interaction between ER stress and autophagy.

HIV and stigma in Liuzhou, China.

This paper describes emergent stigma-related themes from individual descriptions of living with HIV in Liuzhou, China. Qualitative interviews were conducted with 23 people living with HIV (PLHIV). To provide contextual information, 14 public health personnel and 4 community workers in Liuzhou were also interviewed. PLHIV experienced enacted, anticipated, and internalized HIV-related stigma, which resulted in negative affective, behavioral, and physical health outcomes, including barriers to health care, preemptive self-isolation, suicidal ideation, and poverty. To lessen stigma, future programs should aim to increase HIV knowledge and empathy for PLHIV among family members, community workers, and health professionals. HIV programs should also include suicide risk assessment for PLHIV, especially immediately after diagnosis and at the onset of HIV-related symptoms.

Allelopathic effects of Eucalyptus extract and wood vinegar on germination and sprouting of rapeseed (Brassica rapa L.).

Eucalyptus plantations are usually characterized by low biodiversity due to allelopathy effects. Wood vinegar is considered a complex growth regulator that can promote plant growth at low concentrations. However, there is information scarcity about the co-application of eucalypt leaf water extract and wood vinegar on plants. This study aimed at clarifying whether wood vinegar can protect seed germination against suppression by eucalypt-induced allelopathy. We examined germination behavior and seedling elongation characteristics in rapeseed (Brassica rapa L.) treated with different solutions of wood vinegar and eucalypt leaf water extract. The results showed that eucalypt leaf water extracts, wood vinegar solutions, and their mixture allelopathically suppressed seed germination rate. After rapeseed sprouting, eucalypt leaf water extracts promoted root elongation, stem elongation, and fresh weight elongation. Malondialdehyde content was also lower under the influence of eucalypt leaf water extract. Mixture of high concentration of eucalypt leaf water extract and lower concentration of wood vinegar significantly promoted root elongation. Therefore, both eucalypt leaf water extract and wood vinegar are complex plant growth regulators, which can be used to inhibit or stimulate plants at different ontogenic stages. During the seed germination period, both eucalypt leaf extracts and wood vinegar could be used as weed inhibitors. Conversely, during the period of sprouting (seedling establishment), low concentrations of eucalypt leaf extracts and wood vinegar can promote growth.

Nationwide meta-analysis of microplastic distribution and risk assessment in China's aquatic ecosystems, soils, and sediments.

Microplastic (MP) accumulation has recently become a pressing global environmental challenge. As a major producer and consumer of plastic products, China's MP pollution has garnered significant attention from researchers. However, accurate and comprehensive investigations of national-level MP pollution are still lacking. In this study, we systematically collated a national MP pollution dataset consisting of 7766 water, soil, and sediment sampling sites from 544 publicly published studies, revealing the spatiotemporal distribution and potential risks of MP pollution in China. The results indicate that MP distribution is influenced by various regional factors, including economic development level, population distribution, and geographical environment, exhibiting considerable range and complexity. MP concentrations are generally higher in economically prosperous areas, but the degree of pollution varies significantly across different environmental media. Given the uncertainty and lack of standardized data in traditional microplastic risk assessment methods, this article highlights the urgency of developing a comprehensive big data and artificial intelligence (AI)-based regulatory framework. This work provides a substantial amount of accurate MP pollution data and offers a fresh perspective on leveraging AI for microplastic pollution regulation.

Human PBMC scRNA-seq-based aging clocks reveal ribosome to inflammation balance as a single-cell aging hallmark and super longevity.

Quantifying aging rate is important for evaluating age-associated decline and mortality. A blood single-cell RNA sequencing dataset for seven supercentenarians (SCs) was recently generated. Here, we generate a reference 28-sample aging cohort to compute a single-cell level aging clock and to determine the biological age of SCs. Our clock model placed the SCs at a blood biological age to between 80.43 and 102.67 years. Compared to the model-expected aging trajectory, SCs display increased naive CD8+ T cells, decreased cytotoxic CD8+ T cells, memory CD4+ T cells, and megakaryocytes. As the most prominent molecular hallmarks at the single-cell level, SCs contain more cells and cell types with high ribosome level, which is associated with and, according to Bayesian network inference, contributes to a low inflammation state and slow aging of SCs. Inhibiting ribosomal activity or translation in monocytes validates such translation against inflammation balance revealed by our single-cell aging clock.

Effects of Simvastatin on Cartilage Homeostasis in Steroid-Induced Osteonecrosis of Femoral Head by Inhibiting Glucocorticoid Receptor.

Steroid-induced osteonecrosis of femoral head (SONFH) is one of the most common bone disorders in humans. Statin treatment is beneficial in preventing the development of SONFH through anti-inflammation effects and inhibition of the glucocorticoid receptor (GR). However, potential mechanisms of statin action remain to be determined. In this study, pulse methylprednisolone (MP) treatment was used to induce SONFH in broilers, and then MP-treated birds were administrated with simvastatin simultaneously to investigate the changes in cartilage homeostasis. Meanwhile, chondrocytes were isolated, cultured, and treated with MP, simvastatin, or GR inhibitor in vitro. The changes in serum homeostasis factors, cell viability, and expression of GR were analyzed. The results showed that the morbidity of SONFH in the MP-treated group increased significantly compared with the simvastatin-treated and control group. Furthermore, MP treatment induced apoptosis and high-level catabolism and low-level anabolism in vitro and vivo, while simvastatin significantly decreased catabolism and slightly recovered anabolism via inhibiting GR and the hypoxia-inducible factor (HIF) pathway. The GR inhibitor or its siRNA mainly affected the catabolism of cartilage homeostasis in vitro. In conclusion, the occurrence of SONFH in broilers was related to the activation of GR and HIF pathway, and imbalance of cartilage homeostasis. Simvastatin and GR inhibitor maintained cartilage homeostasis via GR and the HIF pathway.

Dietary sodium butyrate and/or vitamin D3 supplementation alters growth performance, meat quality, chemical composition, and oxidative stability in broilers.

The present study was conducted to elucidate the effects of sodium butyrate (SB) and vitamin D3 (VD3) supplementation on meat quality, oxidative stability, and nutritional value of the broiler chicken. The results indicated that dietary SB decreased lightness (L*), cooking and drip loss, free fatty acids (FFA), C14:0, C16:0, saturated fatty acids (SFA), C20:4n6, and n-6: n3 polyunsaturated fatty acids (PUFA) and increased DPPH and ABTS in chicken meat. The PUFAs content in the chicken meat increased only when SB was added along with higher VD3 levels. However, the amino acid content was reduced with an increase in the VD3 levels. In conclusion, dietary SB supplementation improved chicken meat quality by enhancing the antioxidant capacity and physical properties. Moreover, adding SB or combined with higher VD3 levels optimized the fatty acid composition. However, higher VD3 levels reduced the amino acid content of the chicken meat.

Comprehensive landscape of the functions and prognostic value of RNA binding proteins in uterine corpus endometrial carcinoma.

Background: The dysregulation of RNA binding proteins (RBPs) is involved in tumorigenesis and progression. However, information on the overall function of RNA binding proteins in Uterine Corpus Endometrial Carcinoma (UCEC) remains to be studied. This study aimed to explore Uterine Corpus Endometrial Carcinoma-associated molecular mechanisms and develop an RNA-binding protein-associated prognostic model. Methods: Differently expressed RNA binding proteins were identified between Uterine Corpus Endometrial Carcinoma tumor tissues and normal tissues by R packages (DESeq2, edgeR) from The Cancer Genome Atlas (TCGA) database. Hub RBPs were subsequently identified by univariate and multivariate Cox regression analyses. The cBioPortal platform, R packages (ggplot2), Human Protein Atlas (HPA), and TIMER online database were used to explore the molecular mechanisms of Uterine Corpus Endometrial Carcinoma. Kaplan-Meier (K-M), Area Under Curve (AUC), and the consistency index (c-index) were used to test the performance of our model. Results: We identified 128 differently expressed RNA binding proteins between Uterine Corpus Endometrial Carcinoma tumor tissues and normal tissues. Seven RNA binding proteins genes (NOP10, RBPMS, ATXN1, SBDS, POP5, CD3EAP, ZC3H12C) were screened as prognostic hub genes and used to construct a prognostic model. Such a model may be able to predict patient prognosis and acquire the best possible treatment. Further analysis indicated that, based on our model, the patients in the high-risk subgroup had poor overall survival (OS) compared to those in the low-risk subgroup. We also established a nomogram based on seven RNA binding proteins. This nomogram could inform individualized diagnostic and therapeutic strategies for Uterine Corpus Endometrial Carcinoma. Conclusion: Our work focused on systematically analyzing a large cohort of Uterine Corpus Endometrial Carcinoma patients in the The Cancer Genome Atlas database. We subsequently constructed a robust prognostic model based on seven RNA binding proteins that may soon inform individualized diagnosis and treatment.

Hydrogen-Rich Medium Regulates Cr(VI)-Induced ER Stress and Autophagy Signaling in DF-1 Cells.

Related studies have shown that chromium (Cr) is toxic to cells, and hydrogen can protect cells by regulating endoplasmic reticulum (ER) stress and autophagy. However, there are few reports on the protective effects of hydrogen on heavy metal-induced cell damage. The objective of this study was to investigate the protection of hydrogen-rich medium (HRM) on Cr(VI)-induced ER stress and autophagy in DF-1 cells. Therefore, HRM were pretreated for 30 min before Cr(VI) treatment, and detected the autophagy and ER stress-related indicators to determine the role of HRM. The results showed that HRM could reduce the cell damage caused by Cr(VI), and 3-methyladenine (3-MA) could protect cells by inhibiting over autophagy. HRM can reverse the changes of ER stress- and autophagy-related indexes caused by Cr(VI), and inhibit the excessive autophagy caused by Cr(VI). In conclusion, HRM can protect cells from damage induced by Cr(VI), and play a role by inhibiting ER stress-mediated autophagy.

Vacuum-Driven Orientation of Nanostructured Diblock Copolymer Thin Films.

This work aims to demonstrate a facile method for the controlled orientation of nanostructures of block copolymer (BCP) thin films. A simple diblock copolymer system, polystyrene-block-polydimethylsiloxane (PS-b-PDMS), is chosen to demonstrate vacuum-driven orientation for solving the notorious low-surface-energy problem of silicon-based BCP nanopatterning. By taking advantage of the pressure dependence of the surface tension of polymeric materials, a neutral air surface for the PS-b-PDMS thin film can be formed under a high vacuum degree (∼10-4 Pa), allowing the formation of the film-spanning perpendicular cylinders and lamellae upon thermal annealing. In contrast to perpendicular lamellae, a long-range lateral order for forming perpendicular cylinders can be efficiently achieved through the self-alignment mechanism for induced ordering from the top and bottom of the free-standing thin film.

Endoplasmic reticulum stress, chondrocyte apoptosis and oxidative stress in cartilage of broilers affected by spontaneous femoral head necrosis.

With the promotion of the intensive breeding model, the incidence of leg diseases has risen in fast-growing commercial broilers with higher body weight, seriously affecting their feed efficiency and causing animal welfare problems. Femoral head necrosis (FHN) is the most common leg disease in broilers. Previous studies reported that hormone-induced FHN is related to endoplasmic reticulum (ER) stress, apoptosis, and oxidative stress, but no detailed study has been conducted in broilers with spontaneous FHN. In the study, the articular cartilage of 5-wk-old Ross 308 broilers with spontaneous FHN was used to investigate the pathogenesis of the disease. According to the degree of femoral head injury, the birds participating in the experiment were divided into 3 groups, namely a control group, femoral head separation group and femoral head separation with growth plate lacerations group. The morphological changes in articular cartilage were observed by hematoxylin and eosin, toluidine blue, alcian blue and safranine O-solid green staining, and the expressions of genes related to cartilage homeostasis, ER stress, autophagy, apoptosis and oxidative stress was detected using Real-Time Quantitative PCR. In the results, the expression of aggrecan and collagen-2 mRNA levels decreased in the articular cartilage of spontaneous FHN broilers, and the same changes were observed in the tissue staining results, indicating the disordered nature of articular cartilage homeostasis. At the same time, FHN in broilers causes ER stress in articular chondrocytes and regulates oxidative stress by activating the nuclear factor erythroid 2-related factor 2/antioxidant response element pathway through protein kinase RNA-like ER kinase. Autophagy can be activated through the protein kinase RNA-like ER kinase-activating transcription factor-4 pathway, and apoptosis can even be activated through CCAAT-enhancer-binding protein homologous protein. Therefore, the secretory activity of articular chondrocytes in spontaneous FHN broilers is negatively affected, which leads to the disorder of cartilage homeostasis and results in FHN due to ER-stress-mediated chondrocyte apoptosis and oxidative stress.

Abnormal Lipid Profile in Fast-Growing Broilers With Spontaneous Femoral Head Necrosis.

This study investigated lipid metabolism in broilers with spontaneous femoral head necrosis (FHN) by determining the levels of markers of the blood biochemistry and bone metabolism. The birds were divided into a normal group and FHN group according to the femoral head scores of 3-, 4-, and 5-week-old chickens with FHN, and a comparative study was conducted. The study showed that spontaneous FHN broilers had a lipid metabolism disorder, hyperlipidemia, and an accumulation of lipid droplets in the femur. In addition, there were significant changes in the bone parameters and blood bone biochemistry markers, and the expression of genes related to lipid metabolism in the femoral head was also significantly increased. Therefore, FHN may result from dyslipidemia, which affects the bone growth and development of broilers.

Changes of lipid and bone metabolism in broilers with spontaneous femoral head necrosis.

Blood biochemistry and bone metabolism were evaluated to investigate the etiology and mechanism of spontaneous femoral head necrosis (FHN) in broilers. According to the femoral head score of the fourth, fifth, and sixth week old FHN-affected broilers, they were divided into 3 groups, namely Normal group, femoral head separation group, and femoral head separation with growth plate lacerations group, and then carried out a comparative study. The results showed that the liver function (alanine aminotransferase and aspartate aminotransferase) and lipid metabolism (high-density lipoprotein and triglyceride) levels of broilers with spontaneous FHN were significant changed compared with the normal group. At the same time, accumulation of lipid droplets appeared in the liver, which illustrated that the occurrence of FHN may be related to lipid metabolism disorders. Tibia and femur parameters showed significant changes in bone mineral density and bone strength. The distribution of chondrocytes in the articular cartilage of broilers with FHN was irregular and vacuoles appeared, which indicated that cartilage homeostasis was destroyed. TUNEL staining showed that the apoptosis rate of articular chondrocytes in broilers with FHN in 6-week-old was significantly higher than that of normal broilers. Meanwhile, the bone markers (bone glaprotein and bone-specific alkaline phosphatase) changed significantly, indicating that the articular chondrocyte apoptosis and bone metabolism disorder may occur in FHN-affected birds. Therefore, FHN in broilers may be caused by dyslipidemia and abnormal bone metabolism.

Protective Effect of Purple Tomato Anthocyanidin on Chromium(VI)-Induced Autophagy in LMH Cells by Inhibiting Endoplasmic Reticulum Stress.

This study aimed to investigate the role of purple tomato anthocyanin (PTA) in autophagy induced by chromium(VI) in a chicken hepatocellular carcinoma cell line (LMH cells). LMH cells were exposed to Cr(VI), PTA, and Cr(VI) + PTA. The changes in endoplasmic reticulum (ER) stress, autophagy, related proteins, and COX-2 were detected. Results showed that the cell viability was reduced after Cr(VI) treatment, and the decrease was also restrained by 3-MA or PTA. Levels of ER stress-related proteins (GRP78/Bip and PERK) and COX-2 increased after Cr(VI) treatment, which resulted in an increase in autophagy-related proteins (Beclin1 and LC3-II), inhibition of autophagy pathway protein mTOR, and degradation of autophagy-related protein p62, leading to excessive autophagy and cell damage. Meanwhile, the changes of these indicators induced by Cr(VI) were alleviated by PTA. In conclusion, our study suggested that Cr(VI) can induce excessive autophagy in LMH cells, while PTA can ameliorate Cr(VI)-induced autophagy by inhibiting ER stress.

Autophagy of bovine mammary epithelial cell induced by intracellular Staphylococcus aureus.

Bovine mastitis is a common disease in the dairy industry that causes great economic losses. As the primary pathogen of contagious mastitis, Staphylococcus aureus (S. aureus) can invade bovine mammary epithelial cells, thus evading immune defenses and resulting in persistent infection. Recently, autophagy has been considered an important mechanism for host cells to clear intracellular pathogens. In the current study, autophagy caused by S. aureus was detected, and the correlation between autophagy and intracellular S. aureus survival was assessed. First, a model of intracellular S. aureus infection was established. Then, the autophagy of MAC-T cells was evaluated by confocal microscopy and western blot. Moreover, the activation of the PI3K-Akt-mTOR and ERK1/2 signaling pathways was determined by western blot. Finally, the relationship between intracellular bacteria and autophagy was analyzed by using autophagy regulators (3-methyladenine [3-MA], rapamycin [Rapa] and chloroquine [CQ]). The results showed that S. aureus caused obvious induction of autophagosome formation, transformation of LC3I/II, and degradation of p62/SQSTM1 in MAC-T cells; furthermore, the PI3K-Akt-mTOR and ERK1/2 signaling pathways were activated. The number of intracellular S. aureus increased significantly with autophagy activation by rapamycin, whereas the number decreased when the autophagy flux was inhibited by chloroquine. Therefore, this study indicated that intracellular S. aureus can induce autophagy and utilize it to survive in bovine mammary epithelial cells.