A5001829459- Prion Diseases and Protein Misfolding
- Tuberculosis Research and Epidemiology
- Mycobacterium research and diagnosis
- Neurological diseases and metabolism
- interferon and immune responses
- Trace Elements in Health
- Neuroinflammation and Neurodegeneration Mechanisms
- Inflammasome and immune disorders
- Alzheimer's disease research and treatments
- RNA regulation and disease
- Autophagy in Disease and Therapy
- Cytokine Signaling Pathways and Interactions
- Immune Response and Inflammation
- Immune responses and vaccinations
- Gut microbiota and health
- Bacteriophages and microbial interactions
- Clostridium difficile and Clostridium perfringens research
- Cell Adhesion Molecules Research
- Antimicrobial Peptides and Activities
- Endoplasmic Reticulum Stress and Disease
- HIV Research and Treatment
- Pneumocystis jirovecii pneumonia detection and treatment
- Pharmacological Effects of Natural Compounds
- Nuclear Receptors and Signaling
- Galectins and Cancer Biology
China Agricultural University
2016-2025
Guiyang Medical University
2025
Affiliated Hospital of Guizhou Medical University
2025
Jishou University
2025
Hunan Cancer Hospital
2025
Central South University
2025
China National Center for Food Safety Risk Assessment
2023
University of Nottingham
2013-2022
Zero to Three
2022
Ningbo Entry-Exit Inspection And Quarantine Bureau
2018
Prion diseases are neurodegenerative disorders characterized by the accumulation of misfolded prion protein, spongiform changes in brain, and brain inflammation as a result wide-spread activation microglia. Autophagy is highly conserved catabolic process for clearance cytoplasmic components, including protein aggregates damaged organelles; this also eliminates pathological PrPSc it accumulates during infection. The NALP3 inflammasome multiprotein complex that component innate immune system...
ABSTRACT The gut microbiota is closely associated with inflammatory bowel disease (IBD) and colorectal cancer (CRC). Probiotics such as Clostridium butyricum (CB) or Akkermansia muciniphila (AKK) have the potential to treat However, research on combined therapeutic effects immunomodulatory mechanisms of CB AKK in treating IBD CRC has never been studied. This study evaluates co-administration DSS/AOM-induced colitis-associated CRC. Our results indicate that compared mono-administration, not...
The occurrence of necrosis during Mycobacterium bovis (M. bovis) infection is regarded as harmful to the host because it promotes spread M. bovis. Ferroptosis a controlled type cell death that occurs when there an excessive buildup both free iron and lipid peroxides. Here, we demonstrate mammalian entry (Mce) 4 family protein Mb3523c triggers ferroptosis promote pathogenicity dissemination. Mechanistically, Mb3523c, through its Y237 G241 site, interacts with HSP90 stabilize LAMP2A on...
Prion diseases are neurodegenerative disorders characterized by the accumulation of an abnormal disease-associated prion protein, PrPSc. In prion-infected brains, activated microglia often present in vicinity PrPSc aggregates, and microglial activation is thought to play a key role pathogenesis diseases. Although interleukin (IL)-1β release prion-induced has been widely reported, mechanism which primed become secrete IL-1β not yet elucidated. this study, we investigated NACHT, LRR PYD...
Abstract Prion diseases caused by the cellular prion protein (PrP C ) conversion into a misfolded isoform Sc are associated with multiple mitochondrial damages. We previously reported dynamic abnormalities and cell death in via modulation of variety factors. Optic atrophy 1 (OPA1) is one factors that control fusion, DNA (mtDNA) maintenance, bioenergetics, cristae integrity. In this study, we observed downregulation OPA1 disease models vitro vivo, mitochondria structure damage dysfunction,...
Mycobacterium bovis, the causative agent of bovine tuberculosis, infects host macrophages and triggers production proinflammatory cytokine interleukin 1β (IL-1β). The mechanism by which become activated secrete IL-1β in tuberculosis has not yet been elucidated.In this study, we investigated role absence melanoma 2 (AIM2) inflammasome release from infected with pathogenic M. bovis strain.We found that AIM2 activation is involved primary immortalized mouse macrophage upon infection; process...
Mycobacterium bovis (M. bovis) is highly adapted to macrophages and has developed multiple mechanisms resist intracellular assaults. However, the host cells in turn deploy a multipronged defense mechanism control bacterial infection. Endoplasmic reticulum (ER) stress-mediated apoptosis one such primary mechanism. However role of interferon regulatory factor 3 (IRF3) between ER stress during M. infection unknown. Here, we demonstrate that effectively induced murine macrophages. Caspase-12,...
Mitophagy is a selective autophagy mechanism for eliminating damaged mitochondria and plays crucial role in the immune evasion of some viruses bacteria. Here, we report that Mycobacterium bovis (M. bovis) utilizes host mitophagy to suppress xenophagy enhance its intracellular survival. M. causative agent animal tuberculosis human tuberculosis. In current study, show induces macrophages, induction impaired by PINK1 knockdown, indicating PINK1-PRKN/Parkin pathway involved induced bovis....
To further unravel the mechanisms responsible for attenuation of tuberculosis vaccine Mycobacterium bovis BCG, comparative genomics was used to identify single nucleotide polymorphisms (SNPs) that differed between sequenced strains and M. BCG. SNPs were assayed in isolates from France United Kingdom different BCG vaccines order those arose during process which gave rise Informative data sets obtained 658 21 virulent 13 strains; these showed phylogenetic clustering consistent with...
Nilotinib, a tyrosine kinase inhibitor, has been studied extensively in various tumor models; however, no information exists about the pharmacological action of nilotinib bacterial infections. Mycobacterium bovis (M. bovis) and avium subspecies paratuberculosis (MAP) are etiological agents bovine tuberculosis Johne’s disease, respectively. Although M. MAP cause distinct tissue tropism, both them infect, reside, replicate mononuclear phagocytic cells infected host. Autophagy is an innate...
Evidence of the gut microbiota influencing neurodegenerative diseases has been reported for several neural diseases. However, there is little insight regarding relationship between and prion disease. Here, using fecal samples 12 prion-infected mice 25 healthy controls, we analyzed structure metabolic changes by 16S rRNA sequencing LC-MS–based metabolomics respectively as multi-omic analyses. Additionally, SCFAs common amino acids were detected GC–MS UPLC respectively. Enteric induced disease...
Mycobacterium bovis (M. bovis) is the pathogen of animals and humans that can replicate in phagosomes myeloid cells. Cytosolic detection bacterial products plays a crucial role initiating innate immune response, including autophagy activation interferon-β (IFN-β) release. Although IFN-β release have been reported during mycobacterium infection, mechanisms underlying remains poorly defined. Here, we demonstrated increases macrophages exposed to M. this requires DNA sensor interferon-γ...
Mycobacterium bovis is the causative agent of tuberculosis in a wide range mammals, including humans. Macrophages are first line host defense. They secrete proinflammatory cytokines, such as interleukin-1 beta (IL-1β), response to mycobacterial infection, but underlying mechanisms by which human macrophages activated and release IL-1β following M. infection poorly understood. Here we show that 'nucleotide binding oligomerization domain-like receptor (NLR) family pyrin domain containing 7...