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Recently, the journal Nature-Communications published the latest research results of Yangzhou University Professor Jia Xin'an's team in cooperation with the German University of Gissen and other units.
they discovered the genetic evolutionary law of the new super toxic mononucleosis hypernuclear cell hyperstitus and its composition of the HSL-II genealogy, and revealed the molecular pathogenic mechanism of Listeria, which provided an important theoretical basis for the prevention and control of Listeria disease.
mononucleosis listeria is an important human-animal co-disease of the original bacteria, serious harm to livestock and poultry breeding industry, can also cause public health problems.
the team found mononucleosis hypertoxic strains of listeriosis in sheep that were infested with listeria, which formed the new genetic ally subspectral HSL-II, and were 240-400 times more capable of planting in mouse organs than known super-toxic strains.
co-author of the paper, Yangzhou University Professor Yin Yuelan, said that through comparative genomics analysis, it was found that the HSL-II strain carried both single-core cell hyperpluse listeria 1 (LIPI-1) and Elister toxicity island 2 (LIPI-2), and clarified that the smcL gene encoded phospholipidase in LIPI-2 played an important role in its host implantation. Further research
found that the HSL-II strain has a unique semi-lactose-modified sympic synonytic acid, which gives the listeria a new phenotype characteristic of serotype 4h, which can significantly enhance the strain's invasive pathogenicity to the host.
the paper's communication author, Jia Xin'an, told China Science Daily that the new HSL-II strains of listeria after natural recombination of two pathogenic species have unique genetic evolution and phenotype characteristics, and traditional biochemical identification and internationally used serotype identification methods cannot effectively identify them. The
's discovery of the genetic evolution of HSL-II strains and their molecular pathogenic mechanisms has laid an important foundation for the establishment of listeria rapid identification methods, the development of diagnostic reagents and the development of vaccines.
the research was funded by the National Natural Science Foundation of China and the National Key Research and Development Program.
's Institute for Nutrition and Health found a new mechanism for the abduction of macrophages mitochondrial autophagy, the international academic journal Nature Immunology published online the latest research results of the Qianyou Depository Task Force of the Shanghai Institute of Nutrition and Health of the Chinese Academy of Sciences, "Liste raprias host mitophagy through a novelmitophagy to fan".
the study found that monotolitus to promote its own survival by inducing mitochondrial autophagy reactions in macrophages, and identified a new mitochondrial autophagy receptor NLRX1.
mitochondrial autophagy (mitophagy) is a selective autophagy process that specifically degrades damaged or excess mitochondria within cells to complete the regulation of cell metabolism levels and fate decisions.
However, which substances can induce mitochondrial autophagy reactions under physiological or pathological conditions, and which molecular specificity mediates the activation of mitochondrial autophagy pathways, is a key scientific question that is still urgently needed in this research field.
Qianyou Depository Task Force for many years around the innate immune family NOD-like receptors (NOD-like receptors, NLRs) research and exploration work, the previous research found that nLR family members NLRC5 by regulating tissue compatibility complex protein MHC class I gene expression to promote the body Resistance to listeriosis infection (Yao, et al., Cell Research 2012), while NLRP3 inflammatory small cells can be activated by Perforin in killer T cells to promote anti-tumor immunity (Yao, et al., Nature Communications 2017).
however, the function of NLRX1, the only NLR family member positioned in the mitochondria, remains unclear.
To explore whether bacterial infection can activate the mitochondrial autophagy pathway, the researchers infected macrophages with intracellular bacteria (listeria, salmonella) and extracellular bacteria (E. coli, Bacillus Citrate) respectively, and systematically analyzed the occurrence of mitochondrial autophagy, which showed that intracellular infection can significantly induce mitochondrial autophagic reactions. further studies
found that Listeria induces the development of calcium ion intraflow, mitochondrial damage, and mitochondrial autophagy in cells by secreting hemolytic O (listeriolysin O, LLO).
found that NLRX1's NACHT (nucleotide binding and oligomerization domain) domain contained a conservative autophagy marker LC3 binding site (LC3-interacting region, LIR) through bioinformatics prediction and RNA interference, and relied on this site specificity to mediate the mitochondrial autophagy process of Listeria and LLO-induced.
at the physiological functional level, by using the NLRX1 gene systemic knockout and macrophage-specific knockout mice, as well as mitochondrial autophagy inhibitor Mdivi-1, studies have shown that inhibiting the activation of mitochondrial autophagy pathways leads to the accumulation of intracellular granulocytosis, thereby inhibiting the survival of Listeria.
at the mechanism level, the LRR (leucine-rich) domain of NLRX1 interacts with the NACHT domain in a resting state to form a stable monomer state, closing its LIR and LC3 binding, while listeria infection or LLO stimulation leads to intracellular NLRX1 polypolymerization, promoting the binding of its LIR domain and LC3 and then interlocuting the autoplascomere autophagery.
, this study is the first to report that NLR family members NLRX1 participate in the steady state regulation of mitochondrial autophagy as a new type of mitochondrial autophagy receptor, and also deepen sedative understanding of the function of mitochondrial autophagy physiology, and provide new molecular targets and therapeutic ideas for anti-infection treatment. Zhang Yifan, assistant researcher at the Institute of Nutrition and Health of
, and Yao Yikun, a postdoctoral fellow, are co-authors of the paper, and researcher Qian Youxuan is the author of the newsletter.
the study was supported by Stephen E. Girardin, a professor at the University of Toronto in Canada, Houhui Song of Zhejiang University of Agriculture and Forestry, and Wang Jianrong, a professor at Suzhou University.
funding support from the Ministry of Science and Technology, the National Natural Science Foundation of China, the Chinese Academy of Sciences, etc., while the research received the support and assistance of the public technology platform and animal platform of the Institute of Nutrition and Health.
: Listeria induces mitochondrial damage through its secreted toxin protein LLO, promotes the polymerization of NLRX1 and binds to autophagy protein LC3, which in turn promotes the activation of the mitochondrial autophagy pathway.
study found that listeria is super-toxic in the form of thousands of listeria strains that can cause severe foodborne diseases.
a genomics study that identified strains that are more likely to cause disease and identified the factors associated with previously unknown bacterial infections and disease-causing causes, could allow people to better monitor these bacteria.
results were recently published in Nature-Genetics.
eating foods infected with Listeria can cause foodborne diseases, which are particularly dangerous for pregnant women and can cause miscarriages or life-threatening illnesses in newborns.
listeria is also a potentially significant threat to the elderly, newborns and people with compromised immune systems.
regulators have long believed that the bacteria are consistent in all types of toxicity and that their pathogenicity is not different.
Marc Lecuit team at the Pasteur Institute in Paris, France, collected 6,633 listeriosis strains from clinical samples and food, and compared this highly diverse sample set to the medical records of listeria patients to determine which strains were most likely to cause disease.
they found that some strains can cause disease in people with good immune systems, meaning these bacteria are more toxic than other bacteria in their class and can escape the immune system.
researchers compared the genomes of 104 representative strains and found that genes make germs more virulent, including a group of genes called LIPI-4 that may play a role in bacteria's ability to infect the central nervous system.
Source: Shanghai Institute of Nutrition and Health, China Science Daily.