Yunhang Gao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
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Research Subjects
Yunhang Gao has a total of 172 co-authors. Here are the top co-authors by number of shared publications:
- Xiqing Zhang
Animal Husbandry and Veterinary Research Institute, Jilin Academy of Agricultural Sciences, Changchun 130033, China
14 shared publications - Yunna Jia
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China
10 shared publications - Zhenhua Ma
College of Animal Science and Technology, Jilin Agricultural University, Changchun 130118, China
10 shared publications - Lixia Wang
State Key Laboratory of Black Soils Conservation and Utilization, Northeast Institute of Geography and Agroecology, Chinese Academy of Sciences, Changchun 130102, China
8 shared publications - Wangdui Basang
Institute of Animal Husbandry and Veterinary Medicine, Xizang Academy of Agriculture and Animal Husbandry Sciences, Lhasa, China
8 shared publications - Xiaojun Liang
Institute of Animal Science, Ningxia Academy of Agriculture and Forestry Sciences, Yinchuan 750002, China
8 shared publications
Latest Publications
- Open Access
- 25 October 2026
- Published by MDPI AG in Marine Drugs
- Vol. 24 (11) , 375
Deep-Learning-Assisted Discovery of Marine Antimicrobial Peptides: A Roadmap Integrating Omics Mining, Structure-Guided Diffusion Design, and Sustainable Aquaculture Translation
Antimicrobial peptides (AMPs) offer diverse antibacterial mechanisms, but candidate generation alone does not resolve the linked demands of potency, host safety, stability, manufacturability, and application-specific exposure. This review presents a roadmap that integrates two complementary computational routes for marine AMP discovery. De novo generation expands sequence space, whereas omics mining preserves biological provenance and enables recovery of encoded or encrypted peptides from marine organisms and microbiomes. Structure-guided diffusion is positioned as a selective third route when a defined target, motif, or stable structural template is available, rather than as a universal replacement for sequence-based AMP models. We further examine aquaculture as a translational setting in which efficacy must be evaluated together with salt and feed tolerance, environmental fate, tissue residues, resistance risk, and export-related requirements. Current evidence remains limited at the direct intersection of marine provenance and deep learning, particularly for target-conditioned structural design. We therefore propose an evidence-based workflow that links marine sequence resources, model selection, matched experimental validation, and application-specific deployment. This framework is intended to move marine AMP research from candidate prediction toward reproducible and testable translation.
- 25 October 2026
- Published by MDPI AG in Marine Drugs
- Vol. 24 (11) , 375
Open AccessDeep-Learning-Assisted Discovery of Marine Antimicrobial Peptides: A Roadmap Integrating Omics Mining, Structure-Guided Diffusion Design, and Sustainable Aquaculture Translation
Antimicrobial peptides (AMPs) offer diverse antibacterial mechanisms, but candidate generation alone does not resolve the linked demands of potency, host safety, stability, manufacturability, and application-specific exposure. This review presents a roadmap that integrates two complementary computational routes for marine AMP discovery. De novo generation expands sequence space, whereas omics mining preserves biological provenance and enables recovery of encoded or encrypted peptides from marine organisms and microbiomes. Structure-guided diffusion is positioned as a selective third route when a defined target, motif, or stable structural template is available, rather than as a universal replacement for sequence-based AMP models. We further examine aquaculture as a translational setting in which efficacy must be evaluated together with salt and feed tolerance, environmental fate, tissue residues, resistance risk, and export-related requirements. Current evidence remains limited at the direct intersection of marine provenance and deep learning, particularly for target-conditioned structural design. We therefore propose an evidence-based workflow that links marine sequence resources, model selection, matched experimental validation, and application-specific deployment. This framework is intended to move marine AMP research from candidate prediction toward reproducible and testable translation.
- Open Access
- 9 October 2026
- Published by MDPI AG in Microorganisms
- Vol. 14 (10) , 2294
Calcium Peroxide Addition Suppresses ARG Dissemination by Modulating Host Succession and MGE-Mediated Horizontal Transfer During Swine Manure Composting
Applying exogenous additives during composting can help to effectively mitigate the environmental dissemination of antibiotic resistance genes (ARGs). Calcium peroxide (CaO2)—a strong oxidizing agent—has achieved significant efficacy in degrading various pollutants. This study aims to evaluate the effects of CaO2 at varying doses (0, 1% and 3% DW) on the variation in ARGs, mobile genetic elements (MGEs), and bacterial community succession during swine manure composting. Compared to the control (CK), adding 1% and 3% CaO2 reduced total ARGs and MGEs by 50.29% and 64.62% in the LCP and by 68.96% and 79.74% in the HCP treatment, respectively. Adding 1% and 3% CaO2 significantly increased the relative abundances (RAs) of Actinobacteriota and Firmicutes while decreasing those of Proteobacteria and Bacteroidetes during the thermophilic phase, especially under the high-dose treatment. Redundancy analysis (RDA) revealed that MGEs accounted for 54.20% of the total variation in ARGs, followed by environmental factors (30.3%). Network analysis further revealed that 1% and 3% CaO2 treatments disrupted the association between ARGs and their host bacteria. Overall, adding CaO2 can reduce the risks of spreading ARGs in compost products.
- 9 October 2026
- Published by MDPI AG in Microorganisms
- Vol. 14 (10) , 2294
Open AccessCalcium Peroxide Addition Suppresses ARG Dissemination by Modulating Host Succession and MGE-Mediated Horizontal Transfer During Swine Manure Composting
Applying exogenous additives during composting can help to effectively mitigate the environmental dissemination of antibiotic resistance genes (ARGs). Calcium peroxide (CaO2)—a strong oxidizing agent—has achieved significant efficacy in degrading various pollutants. This study aims to evaluate the effects of CaO2 at varying doses (0, 1% and 3% DW) on the variation in ARGs, mobile genetic elements (MGEs), and bacterial community succession during swine manure composting. Compared to the control (CK), adding 1% and 3% CaO2 reduced total ARGs and MGEs by 50.29% and 64.62% in the LCP and by 68.96% and 79.74% in the HCP treatment, respectively. Adding 1% and 3% CaO2 significantly increased the relative abundances (RAs) of Actinobacteriota and Firmicutes while decreasing those of Proteobacteria and Bacteroidetes during the thermophilic phase, especially under the high-dose treatment. Redundancy analysis (RDA) revealed that MGEs accounted for 54.20% of the total variation in ARGs, followed by environmental factors (30.3%). Network analysis further revealed that 1% and 3% CaO2 treatments disrupted the association between ARGs and their host bacteria. Overall, adding CaO2 can reduce the risks of spreading ARGs in compost products.
- Open Access
- 31 July 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (8) , 958
Tylosin Removal Under Pb2+ Stress Using Kurthia gibsonii TYL-A1: Redox Adaptation and Transcriptomic Insights
With the increasing prevalence of antibiotic–heavy metal co-contamination in agricultural wastewater, elucidating the antibiotic removal capacity of degrading bacteria under heavy metal stress, as well as their adaptive mechanisms, is of considerable theoretical significance and practical value. In this study, the highly efficient TYL-degrading strain TYL-A1 was selected as a model organism, and the effects of Pb2+ exposure on its TYL removal performance, oxidative stress response, cell surface characteristics, and transcriptional regulation were systematically investigated. The results showed that TYL removal remained above 85% after 72 h under a nominal Pb2+ concentration of 100 mg/L in the phosphate-containing MSM system. The phosphate may have reduced Pb2+ bioavailability. Nominal Pb2+ exposure increased the activities of superoxide dismutase (SOD) and catalase (CAT), accompanied by elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as a decrease in adenosine triphosphate (ATP) content. This indicates that the strain experienced pronounced oxidative stress and altered energy metabolism. Meanwhile, cell membrane permeability increased. Scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy (FTIR) analyses showed that the overall cellular morphology remained intact, whereas the membrane surface structure and related cellular components underwent adaptive changes. According to a transcriptomic analysis, the differentially expressed genes were mainly enriched in pathways associated with primary metabolism, transmembrane transport, ABC transporters, and two-component systems. In summary, strain TYL-A1 maintained high TYL removal performance under the tested nominal Pb2+ concentrations in the present phosphate-containing culture system, suggesting its potential applicability in the bioremediation of water bodies co-contaminated with antibiotics and heavy metals.
- 31 July 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (8) , 958
Open AccessTylosin Removal Under Pb2+ Stress Using Kurthia gibsonii TYL-A1: Redox Adaptation and Transcriptomic Insights
With the increasing prevalence of antibiotic–heavy metal co-contamination in agricultural wastewater, elucidating the antibiotic removal capacity of degrading bacteria under heavy metal stress, as well as their adaptive mechanisms, is of considerable theoretical significance and practical value. In this study, the highly efficient TYL-degrading strain TYL-A1 was selected as a model organism, and the effects of Pb2+ exposure on its TYL removal performance, oxidative stress response, cell surface characteristics, and transcriptional regulation were systematically investigated. The results showed that TYL removal remained above 85% after 72 h under a nominal Pb2+ concentration of 100 mg/L in the phosphate-containing MSM system. The phosphate may have reduced Pb2+ bioavailability. Nominal Pb2+ exposure increased the activities of superoxide dismutase (SOD) and catalase (CAT), accompanied by elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as a decrease in adenosine triphosphate (ATP) content. This indicates that the strain experienced pronounced oxidative stress and altered energy metabolism. Meanwhile, cell membrane permeability increased. Scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy (FTIR) analyses showed that the overall cellular morphology remained intact, whereas the membrane surface structure and related cellular components underwent adaptive changes. According to a transcriptomic analysis, the differentially expressed genes were mainly enriched in pathways associated with primary metabolism, transmembrane transport, ABC transporters, and two-component systems. In summary, strain TYL-A1 maintained high TYL removal performance under the tested nominal Pb2+ concentrations in the present phosphate-containing culture system, suggesting its potential applicability in the bioremediation of water bodies co-contaminated with antibiotics and heavy metals.
- Open Access
Key Molecular Events in PM2.5-Induced Lung Injury: Autophagy and Ferroptosis Mediated by the miR-212-5p/RASSF1 Axis
Fine particulate matter (PM2.5) can directly impact pulmonary epithelial cells, resulting in lung injury. While it is known that PM2.5 can alter the expression profile of microRNAs in the lung, its specific role in damaging pulmonary epithelial cells remains unclear. This study, therefore, employed RT-qPCR, Western blotting, and dual luciferase reporter assays to investigate the regulatory role of microRNAs in PM2.5-induced cellular damage. PM2.5 exposure induces oxidative stress, autophagy, and ferroptosis in rat lung alveolar epithelial cells (RLE-6TN). Further functional rescue experiments confirm that the ferroptosis-specific inhibitor Fer-1 can block PM2.5-induced ferroptosis. Bioinformatics analysis and validation indicate that miR-212-5p plays a crucial role by negatively regulating RASSF1 through targeted inhibition. Overexpression of miR-212-5p activates the PI3K/AKT signaling pathway, thereby promoting autophagy and ferroptosis. However, when the expression of both miR-212-5p and RASSF1 is suppressed, PM2.5-induced autophagy and ferroptosis are significantly alleviated by inhibiting the PI3K/AKT/mTOR signaling pathway. Rescue validation experiments demonstrated that, under PM2.5 exposure combined with RASSF1 overexpression, miR-212-5p exacerbates the aforementioned cellular damage process. This study reveals that miR-212-5p regulates autophagy and ferroptosis by targeting RASSF1. These findings provide a multi-target intervention strategy for PM2.5-related lung diseases.
Open AccessKey Molecular Events in PM2.5-Induced Lung Injury: Autophagy and Ferroptosis Mediated by the miR-212-5p/RASSF1 Axis
Fine particulate matter (PM2.5) can directly impact pulmonary epithelial cells, resulting in lung injury. While it is known that PM2.5 can alter the expression profile of microRNAs in the lung, its specific role in damaging pulmonary epithelial cells remains unclear. This study, therefore, employed RT-qPCR, Western blotting, and dual luciferase reporter assays to investigate the regulatory role of microRNAs in PM2.5-induced cellular damage. PM2.5 exposure induces oxidative stress, autophagy, and ferroptosis in rat lung alveolar epithelial cells (RLE-6TN). Further functional rescue experiments confirm that the ferroptosis-specific inhibitor Fer-1 can block PM2.5-induced ferroptosis. Bioinformatics analysis and validation indicate that miR-212-5p plays a crucial role by negatively regulating RASSF1 through targeted inhibition. Overexpression of miR-212-5p activates the PI3K/AKT signaling pathway, thereby promoting autophagy and ferroptosis. However, when the expression of both miR-212-5p and RASSF1 is suppressed, PM2.5-induced autophagy and ferroptosis are significantly alleviated by inhibiting the PI3K/AKT/mTOR signaling pathway. Rescue validation experiments demonstrated that, under PM2.5 exposure combined with RASSF1 overexpression, miR-212-5p exacerbates the aforementioned cellular damage process. This study reveals that miR-212-5p regulates autophagy and ferroptosis by targeting RASSF1. These findings provide a multi-target intervention strategy for PM2.5-related lung diseases.
- Open Access
- 21 January 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (1) , 138
Differential Toxicity of Water-Soluble Versus Water-Insoluble Components of Cowshed PM2.5 on Ovarian Granulosa Cells and the Regulatory Role of Txnip in Overall Toxicity
Fine particulate matter (PM2.5)-induced ovarian damage has attracted widespread attention, but differences in cytotoxicity and underlying mechanisms of water-soluble (WS-PM2.5) and water-insoluble (WIS-PM2.5) fractions are unclear. To investigate potential effects of PM2.5 from livestock farming environments on animal ovaries, PM2.5 samples were collected from large-scale cattle barns. There were significant differences between fractions regarding elemental composition, proportion of water-soluble ions, polycyclic aromatic hydrocarbon content, and endotoxin concentrations. Based on transcriptome sequencing results, in a cowshed PM2.5 exposure model (rats), differentially expressed ovarian mRNAs were significantly enriched in signaling pathways such as cytokine interaction and the Hippo pathway, with the expression of thioredoxin-interacting protein (Txnip) significantly increased. In vitro (primary rat ovarian granulosa cells), short-term exposure to WS-PM2.5 (12 h) significantly induced inflammatory factor release, acute oxidative stress, mitochondrial dysfunction, and intracellular Ca2+ overload, with characteristics of rapid acute injury. However, extended (24 h) WIS-PM2.5 exposure had greater disruptive effects on estrogen homeostasis, intracellular enzyme release (LDH), and mitochondrial structure (subacute characteristics). Furthermore, downregulating Txnip expression via inhibitors effectively mitigated cowshed PM2.5-induced ovarian granulosa cell toxicity, oxidative stress, and mitochondrial and hormonal dysfunction. In summary, solubility of cowshed PM2.5 components affected cytotoxic characteristics, and Txnip was a key factor linking oxidative stress to granulosa cell damage. The study provided a mechanistic basis and potential targets for preventing and controlling PM2.5-induced ovarian damage in livestock environments.
- 21 January 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (1) , 138
Open AccessDifferential Toxicity of Water-Soluble Versus Water-Insoluble Components of Cowshed PM2.5 on Ovarian Granulosa Cells and the Regulatory Role of Txnip in Overall Toxicity
Fine particulate matter (PM2.5)-induced ovarian damage has attracted widespread attention, but differences in cytotoxicity and underlying mechanisms of water-soluble (WS-PM2.5) and water-insoluble (WIS-PM2.5) fractions are unclear. To investigate potential effects of PM2.5 from livestock farming environments on animal ovaries, PM2.5 samples were collected from large-scale cattle barns. There were significant differences between fractions regarding elemental composition, proportion of water-soluble ions, polycyclic aromatic hydrocarbon content, and endotoxin concentrations. Based on transcriptome sequencing results, in a cowshed PM2.5 exposure model (rats), differentially expressed ovarian mRNAs were significantly enriched in signaling pathways such as cytokine interaction and the Hippo pathway, with the expression of thioredoxin-interacting protein (Txnip) significantly increased. In vitro (primary rat ovarian granulosa cells), short-term exposure to WS-PM2.5 (12 h) significantly induced inflammatory factor release, acute oxidative stress, mitochondrial dysfunction, and intracellular Ca2+ overload, with characteristics of rapid acute injury. However, extended (24 h) WIS-PM2.5 exposure had greater disruptive effects on estrogen homeostasis, intracellular enzyme release (LDH), and mitochondrial structure (subacute characteristics). Furthermore, downregulating Txnip expression via inhibitors effectively mitigated cowshed PM2.5-induced ovarian granulosa cell toxicity, oxidative stress, and mitochondrial and hormonal dysfunction. In summary, solubility of cowshed PM2.5 components affected cytotoxic characteristics, and Txnip was a key factor linking oxidative stress to granulosa cell damage. The study provided a mechanistic basis and potential targets for preventing and controlling PM2.5-induced ovarian damage in livestock environments.
- Open Access
- 14 January 2026
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 309, 119718
Expression and application of α/β hydrolase from Kurthia gibsonii TYL-A1
- 14 January 2026
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 309, 119718
Open AccessExpression and application of α/β hydrolase from Kurthia gibsonii TYL-A1
- Open Access
- 13 January 2026
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 309, 119733
PM2.5-induced lung injury in rats: Identification of differential circRNAs and analysis of circRNA–miRNA–mRNA regulatory networks
- 13 January 2026
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 309, 119733
Open AccessPM2.5-induced lung injury in rats: Identification of differential circRNAs and analysis of circRNA–miRNA–mRNA regulatory networks
- Open Access
- 31 July 2025
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 302, 118755
The long noncoding RNA lnc-H3f3b2 regulates cow barn PM2.5-induced apoptosis of rat alveolar Ⅱ epithelial cells through a ceRNA mechanism
- 31 July 2025
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 302, 118755
Open AccessThe long noncoding RNA lnc-H3f3b2 regulates cow barn PM2.5-induced apoptosis of rat alveolar Ⅱ epithelial cells through a ceRNA mechanism
- Open Access
- 9 July 2025
- Published by MDPI AG in Microorganisms
- Vol. 13 (7) , 1621
Removal of Chemical Oxygen Demand (COD) from Swine Farm Wastewater by Corynebacterium xerosis H1
Swine wastewater (SW) has a high chemical oxygen demand (COD) content and is difficult to degrade; an effective strategy to address this issue is through biodegradation, which poses negligible secondary pollution risks and ensures cost-efficiency. The objectives of this study were to isolate an effective COD-degrading strain of SW, characterize (at the molecular level) its transformation of SW, and apply it to practical production. A strain of Corynebacterium xerosis H1 was isolated and had a 27.93% ± 0.68% (mean ± SD) degradation rate of COD in SW. This strain precipitated growth in liquids, which has the advantage of not needing to be immobilized, unlike other wastewater-degrading bacteria. Based on analysis by Fourier-transform ion cyclotron resonance mass spectrometry (FT-ICR MS), this bacterium removed nitrogen-containing compounds in SW, with proteins and lipids decreasing from 41 to 10% and lignins increasing from 51 to 82%. Furthermore, the enhancement of the sequencing batch reactor (SBR) with strain H1 improved COD removal in effluent, with reductions in the fluorescence intensity of aromatic protein I, aromatic protein II, humic-like acids, and fulvic acid regions. In addition, based on 16S rRNA gene sequencing analysis, SBRH1 successfully colonized some H1 bacteria and had a higher abundance of functional microbiota than SBRC. This study confirms that Corynebacterium xerosis H1, as a carrier-free efficient strain, can be directly applied to swine wastewater treatment, reducing carrier costs and the risk of secondary pollution. The discovery of this strain enriches the microbial resource pool for SW COD degradation and provides a new scheme with both economic and environmental friendliness for large-scale treatment.
- 9 July 2025
- Published by MDPI AG in Microorganisms
- Vol. 13 (7) , 1621
Open AccessRemoval of Chemical Oxygen Demand (COD) from Swine Farm Wastewater by Corynebacterium xerosis H1
Swine wastewater (SW) has a high chemical oxygen demand (COD) content and is difficult to degrade; an effective strategy to address this issue is through biodegradation, which poses negligible secondary pollution risks and ensures cost-efficiency. The objectives of this study were to isolate an effective COD-degrading strain of SW, characterize (at the molecular level) its transformation of SW, and apply it to practical production. A strain of Corynebacterium xerosis H1 was isolated and had a 27.93% ± 0.68% (mean ± SD) degradation rate of COD in SW. This strain precipitated growth in liquids, which has the advantage of not needing to be immobilized, unlike other wastewater-degrading bacteria. Based on analysis by Fourier-transform ion cyclotron resonance mass spectrometry (FT-ICR MS), this bacterium removed nitrogen-containing compounds in SW, with proteins and lipids decreasing from 41 to 10% and lignins increasing from 51 to 82%. Furthermore, the enhancement of the sequencing batch reactor (SBR) with strain H1 improved COD removal in effluent, with reductions in the fluorescence intensity of aromatic protein I, aromatic protein II, humic-like acids, and fulvic acid regions. In addition, based on 16S rRNA gene sequencing analysis, SBRH1 successfully colonized some H1 bacteria and had a higher abundance of functional microbiota than SBRC. This study confirms that Corynebacterium xerosis H1, as a carrier-free efficient strain, can be directly applied to swine wastewater treatment, reducing carrier costs and the risk of secondary pollution. The discovery of this strain enriches the microbial resource pool for SW COD degradation and provides a new scheme with both economic and environmental friendliness for large-scale treatment.
- Open Access
- 8 July 2025
- Published by Frontiers Media SA in Frontiers in Veterinary Science
- Vol. 12, 1631913
Interactions between particulate matter and bacteria during cowshed PM2.5-induced respiratory injury initiates GBP2/Caspase-11/NLRP3-mediated intracellular bacterial defense and pyroptosis
Introduction: Fine particulate matter (PM2.5) is an important factor in the induction of a variety of respiratory diseases and associated cellular damage. The composition of PM2.5 in the animal farm environments is complex, which poses a significant threat to the respiratory health of both workers and livestock, but the causative mechanisms are unclear.Methods: In order to investigate targeted treatment options, this study focused on the role of microbial components in cowshed PM2.5-induced respiratory damage. Utilizing the common pathogenic bacteria (Pasteurella multocida) in cowshed PM2.5 as a perspective, the intrinsic connection and interaction mechanism between PM2.5 particles and bacterial components were explored through in vivo and in vitro experiments. Bacterial components can interact with PM2.5 and are important factors in the respiratory toxicity of PM2.5 in farm animal environments by scanning electron microscopy (SEM), Fourier infrared spectroscopy (FTIR) and Zeta potential measurements.Results: We demonstrate that Bacteria adhered to PM2.5 particles and modified the original surface functional groups characteristics, significantly enhanced toxic effects of PM2.5 on cells (including oxidative stress levels, release of inflammatory factors, etc.). Furthermore, PM2.5 particles significantly enhanced bacterial intracellular invasion, initiated the guanylate-binding protein 2 (GBP2)-mediated intracellular bacterial defense mechanism, further triggered the non-canonical NLRP3 pathway, and ultimately induced a cascade of inflammatory responses and pyroptosis. To explore therapeutic strategies, siRNA silencing of GBP2 and inhibition of NLRP3 were done; GBP2 silencing initially delayed cytotoxicity, but eventually increased the inflammatory response. However, inhibition of NLRP3 expression maintained cell viability and delayed pyroptosis, with potential as an effective solution for treatment of PM2.5-induced lung injury in farm-animal environments.Conclusion: In conclusion, the results of this study demonstrated the interaction between particulate matter and bacteria during cowshed PM2.5-induced respiratory injury and clarified the signaling mechanisms among intracellular bacteria, GBP2, NLRP3, and pyroptosis. These findings provide a theoretical basis for developing therapeutic strategies against PM2.5-related respiratory diseases in farm-animal environments.
- 8 July 2025
- Published by Frontiers Media SA in Frontiers in Veterinary Science
- Vol. 12, 1631913
Open AccessInteractions between particulate matter and bacteria during cowshed PM2.5-induced respiratory injury initiates GBP2/Caspase-11/NLRP3-mediated intracellular bacterial defense and pyroptosis
Introduction: Fine particulate matter (PM2.5) is an important factor in the induction of a variety of respiratory diseases and associated cellular damage. The composition of PM2.5 in the animal farm environments is complex, which poses a significant threat to the respiratory health of both workers and livestock, but the causative mechanisms are unclear.Methods: In order to investigate targeted treatment options, this study focused on the role of microbial components in cowshed PM2.5-induced respiratory damage. Utilizing the common pathogenic bacteria (Pasteurella multocida) in cowshed PM2.5 as a perspective, the intrinsic connection and interaction mechanism between PM2.5 particles and bacterial components were explored through in vivo and in vitro experiments. Bacterial components can interact with PM2.5 and are important factors in the respiratory toxicity of PM2.5 in farm animal environments by scanning electron microscopy (SEM), Fourier infrared spectroscopy (FTIR) and Zeta potential measurements.Results: We demonstrate that Bacteria adhered to PM2.5 particles and modified the original surface functional groups characteristics, significantly enhanced toxic effects of PM2.5 on cells (including oxidative stress levels, release of inflammatory factors, etc.). Furthermore, PM2.5 particles significantly enhanced bacterial intracellular invasion, initiated the guanylate-binding protein 2 (GBP2)-mediated intracellular bacterial defense mechanism, further triggered the non-canonical NLRP3 pathway, and ultimately induced a cascade of inflammatory responses and pyroptosis. To explore therapeutic strategies, siRNA silencing of GBP2 and inhibition of NLRP3 were done; GBP2 silencing initially delayed cytotoxicity, but eventually increased the inflammatory response. However, inhibition of NLRP3 expression maintained cell viability and delayed pyroptosis, with potential as an effective solution for treatment of PM2.5-induced lung injury in farm-animal environments.Conclusion: In conclusion, the results of this study demonstrated the interaction between particulate matter and bacteria during cowshed PM2.5-induced respiratory injury and clarified the signaling mechanisms among intracellular bacteria, GBP2, NLRP3, and pyroptosis. These findings provide a theoretical basis for developing therapeutic strategies against PM2.5-related respiratory diseases in farm-animal environments.