Autophagy is a defense mechanism controlling Streptococcus suis serotype 2 infection in murine microglia cells

Yue, Chao-xiong; Hu, C.; Xiang, Peng; Zhang, Siming; Xiao, Haiyan; Zhou, Wei; Jin, Hui; shi, Deshi; Li, Jinquan; Xu, Li‐Yan; Chen, Yu‐Shan; Zeng, Yan

doi:10.1016/j.vetmic.2021.109103

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…Notably, mixed infection can exacerbate PCV2 pathogenicity [62]. Previous reports have shown that co-infection of different viruses and bacteria usually synergistically exacerbates the pathogenicity of microorganisms [62], causing high morbidity and mortality in animals [63,64]. For example, simultaneous infection of S. suis with PRRSV and swine influenza virus promoted more serious respiratory disease [65,66].…”

Section: Discussionmentioning

confidence: 99%

Epidemiology and Genetic Diversity of PCV2 Reveals That PCV2e Is an Emerging Genotype in Southern China: A Preliminary Study

Zhang

Sun

et al. 2022

Viruses

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Porcine circovirus-associated disease (PCVAD), caused by porcine circovirus type 2 (PCV2), has ravaged the pig industry, causing huge economic loss. At present, PCV2b and PCV2d are highly prevalent genotypes worldwide, while in China, in addition to PCV2b and PCV2d, a newly emerged PCV2e genotype detected in the Fujian province has attracted attention, indicating that PCV2 genotypes in China are more abundant. A preliminary study was conducted to better understand the genetic diversity and prevalence of PCV2 genotypes in southern China. We collected 79 random lung samples from pigs with respiratory signs, from 2018 to 2021. We found a PCV2-positivity rate of 29.1%, and frequent co-infections of PCV2 with PCV3, Streptococcus suis (S. suis), and other porcine pathogens. All PCV2-positive samples were sequenced and subjected to whole-genome analysis. Phylogenetic analysis, based on the PCV2 ORF2 gene and complete genomes, found that PCV2 strains identified in this study belonged to genotypes PCV2a (1), PCV2b (6), PCV2d (10), and PCV2e (6). Importantly, PCV2e was identified for the first time in some provinces, including Guangdong and Jiangxi. Additionally, we found two positively selected sites in the ORF2 region, located on the previously reported antigenic epitopes. Moreover, codon 63, one of the positively selected sites, has different types of amino acids in different genotypes. In conclusion, this study shows that PCV2e is an emerging genotype circulating in southern China, which warrants urgent, specific surveillance to aid the development of prevention and control strategies in China.

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Section: Discussionmentioning

confidence: 99%

Epidemiology and Genetic Diversity of PCV2 Reveals That PCV2e Is an Emerging Genotype in Southern China: A Preliminary Study

Zhang

Sun

et al. 2022

Viruses

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“…And ablation of NOD2 partly reversed above changes to improve neuroinflammation via suppressing TAK1/NF-κB signal and hyperactivated autophagy [ 75 ]. Besides, autophagy was induced accompanied by an accumulation of LC3 dots and autophagosomes, and an increase expression of LC3-II protein, which were reversed by siRNA targeting ATG5, Beclin1, ATG9 and ATG12 in streptococcus suis serotype 2-infected BV2 cells and mice [ 76 ]. Moreover, ULK1 gene knockout alleviated TBI-induced behavior impairment, reduced neuro-inflammation and apoptosis along with inhibition of microglia and astrocytes activation, an increase in Bcl-2 expression, a decrease in proinflammatory cytokines and the expression of Bax, cytochrome c, cleaved Caspase-3 and cleaved PARP in hippocampus.…”

Section: Autophagy In Neuroinflammation and Related Cns Diseasesmentioning

confidence: 99%

Autophagy in Neuroinflammation: A Focus on Epigenetic Regulation

Chen

Xing

et al. 2024

Aging and disease

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Neuroinflammation, characterized by the secretion of abundant inflammatory mediators, pro-inflammatory polarization of microglia, and the recruitment of infiltrating myeloid cells to foci of inflammation, drives or exacerbates the pathological processes of central nervous system disorders, especially in neurodegenerative diseases. Autophagy plays an essential role in neuroinflammatory processes, and the underlaying physiological mechanisms are closely correlated with neuroinflammation-related signals. Inhibition of mTOR and activation of AMPK and FOXO1 enhance autophagy and thereby suppress NLRP3 inflammasome activity and apoptosis, leading to the relief of neuroinflammatory response. And autophagy mitigates neuroinflammation mainly manifested by promoting the polarization of microglia from a pro-inflammatory to an anti-inflammatory state, reducing the production of pro-inflammatory mediators, and up-regulating the levels of anti-inflammatory factors. Notably, epigenetic modifications are intimately associated with autophagy and the onset and progression of various brain diseases. Non-coding RNAs, including microRNAs, circular RNAs and long noncoding RNAs, and histone acetylation have been reported to adjust autophagy-related gene and protein expression to alleviate inflammation in neurological diseases. The present review primarily focuses on the role and mechanisms of autophagy in neuroinflammatory responses, as well as epigenetic modifications of autophagy in neuroinflammation to reveal potential therapeutic targets in central nervous system diseases.

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“…Microglia are born to sculpt neural networks throughout life via synaptic remodeling [reviewed in [1]], and to phagocytose toxic debris [2], including other microglia. They act as immune sentinels, often being the first responders to information requiring immediate neuroprotective actions, including regulation of blood-brain barrier function [reviewed in [3]], the recruitment of pathogen-specific lymphocytes [4] and exhibit autophagy-mediated destruction of phagocytosed pathogens [5]. Microglia, which comprise approximately 0.5–16% of cells in the human brain [6] or 5–12% in the mouse brain [7], depending on the anatomic region, may also act as antigen presenting cells (APCs) within infected brain parenchyma, and induce apoptosis of virally infected neurons [8].…”

Section: Introductionmentioning

confidence: 99%

Microglia at the scene of the crime: what their transcriptomics reveal about brain health

Arutyunov

Klein

2023

Current Opinion in Neurology

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Purpose of reviewMicroglia, which arise from primitive myeloid precursors that enter the central nervous system (CNS) during early development, are the first responders to any perturbance of homeostasis. Although their activation has become synonymous with neurologic disease, it remains unclear whether microglial responses are the cause of or response to neuropathology. Here, we review new insights in the roles of microglia during CNS health and disease, including preclinical studies that transcriptionally profile microglia to define their functional states.Recent findingsConverging evidence suggests that innate immune activation of microglia is associated with overlapping alterations in their gene expression profiles regardless of the trigger. Thus, recent studies examining neuroprotective microglial responses during infections and aging mirror those observed during chronic neurologic diseases, including neurodegeneration and stroke. Many of these insights derive from studies of microglial transcriptomes and function in preclinical models, some of which have been validated in human samples. During immune activation, microglia dismantle their homeostatic functions and transition into subsets capable of antigen presentation, phagocytosis of debris, and management of lipid homeostasis. These subsets can be identified during both normal and aberrant microglial responses, the latter of which may persist long-term. The loss of neuroprotective microglia, which maintain a variety of essential CNS functions, may therefore, in part, underlie the development of neurodegenerative diseases.SummaryMicroglia exhibit a high level of plasticity, transforming into numerous subsets as they respond to innate immune triggers. Chronic loss of microglial homeostatic functions may underlie the development of diseases with pathological forgetting.

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Autophagy is a defense mechanism controlling Streptococcus suis serotype 2 infection in murine microglia cells

Cited by 5 publications

References 36 publications

Epidemiology and Genetic Diversity of PCV2 Reveals That PCV2e Is an Emerging Genotype in Southern China: A Preliminary Study

Epidemiology and Genetic Diversity of PCV2 Reveals That PCV2e Is an Emerging Genotype in Southern China: A Preliminary Study

Autophagy in Neuroinflammation: A Focus on Epigenetic Regulation

Microglia at the scene of the crime: what their transcriptomics reveal about brain health

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