-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
The iNatureH7N9 influenza virus emerged in China in 2013 and infected more than 1,560 people, 39% of which were fatal
.
The “cytokine storm” in the lungs of H7N9 patients is associated with poor prognosis and death; however, the underlying mechanism that triggers the cytokine storm is unclear
.
On July 30, 2021, Chen Hualan from the Harbin Veterinary Research Institute of the Chinese Academy of Agricultural Sciences and Shao Feng from the Beijing Institute of Biological Sciences jointly published an online publication entitled "H7N9 virus infection triggers lethal cytokine storm by activating gasdermin E-mediated pyroptosis of lung" in National Science Review.
Alveolar epithelial cells" research paper, the study found that the effective replication of H7N9 virus in mouse lungs activates Gasdermin E (GSDME)-mediated pyrolysis of alveolar epithelial cells, and the released cytoplasmic contents subsequently trigger a cytokine storm
.
Knockout of Gsdme changed the death mode of A549 and human primary alveolar epithelial cells from pyrolysis after H7N9 virus infection to apoptosis.
Gsdme knockout mice survived lethal H7N9 virus infection
.
The results of this study indicate that GSDME activation is the key and unique mechanism for the death of lung cytokine storm and H7N9 virus infection, thus opening a new door for the development of antiviral drugs against H7N9 virus
.
Influenza A virus spreads widely in nature and continues to pose a challenge to human health
.
Although H1N1 and H3N2 viruses are still actively circulating in humans around the world, other subtypes of avian influenza viruses have crossed the avian-human species barrier and infected humans; it is particularly noteworthy that H5N1 and H7N9 avian influenza viruses have caused Serious human diseases and deaths raise concerns that these avian influenza viruses may cause future human influenza pandemics and bring disastrous consequences
.
Understanding the pathogenesis of infections caused by these viruses will help the development of antiviral drugs
.
The H7N9 virus that emerged in China in 2013 has infected 1,568 people, including 616 deaths
.
Most H7N9 patients develop severe pneumonia and acute respiratory distress syndrome
.
Analysis of bronchoalveolar lavage samples showed that the levels of cytokines/chemokines in the lung were increased 1,000-fold relative to the levels in plasma, and the increase in the levels of these cytokines/chemokines in the lungs was not favorable or fatal The results are relevant
.
However, how these increased cytokine/chemokine levels (referred to as "cytokine storm" in this study) are triggered in the lungs remains largely unknown
.
In this study, animal models were used to explore the underlying mechanism of the abnormal innate immune response caused by the H7N9 virus, and to gain important insights into the pathogenesis of human H7N9 infection
.
The study found that the effective replication of H7N9 virus in mouse lungs activates Gasdermin E (GSDME)-mediated pyrolysis of alveolar epithelial cells, and the released cytoplasmic contents subsequently trigger a cytokine storm
.
Knockout of Gsdme changed the death mode of A549 and human primary alveolar epithelial cells from pyrolysis after H7N9 virus infection to apoptosis.
Gsdme knockout mice survived lethal H7N9 virus infection
.
The results of this study indicate that GSDME activation is the key and unique mechanism for the death of lung cytokine storm and H7N9 virus infection, thus opening a new door for the development of antiviral drugs against H7N9 virus
.
Reference message: https://academic.
oup.
com/nsr/advance-article/doi/10.
1093/nsr/nwab137/6332297?searchresult=1#
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
The iNatureH7N9 influenza virus emerged in China in 2013 and infected more than 1,560 people, 39% of which were fatal
.
The “cytokine storm” in the lungs of H7N9 patients is associated with poor prognosis and death; however, the underlying mechanism that triggers the cytokine storm is unclear
.
On July 30, 2021, Chen Hualan from the Harbin Veterinary Research Institute of the Chinese Academy of Agricultural Sciences and Shao Feng from the Beijing Institute of Biological Sciences jointly published an online publication entitled "H7N9 virus infection triggers lethal cytokine storm by activating gasdermin E-mediated pyroptosis of lung" in National Science Review.
Alveolar epithelial cells" research paper, the study found that the effective replication of H7N9 virus in mouse lungs activates Gasdermin E (GSDME)-mediated pyrolysis of alveolar epithelial cells, and the released cytoplasmic contents subsequently trigger a cytokine storm
.
Knockout of Gsdme changed the death mode of A549 and human primary alveolar epithelial cells from pyrolysis after H7N9 virus infection to apoptosis.
Gsdme knockout mice survived lethal H7N9 virus infection
.
The results of this study indicate that GSDME activation is the key and unique mechanism for the death of lung cytokine storm and H7N9 virus infection, thus opening a new door for the development of antiviral drugs against H7N9 virus
.
Influenza A virus spreads widely in nature and continues to pose a challenge to human health
.
Although H1N1 and H3N2 viruses are still actively circulating in humans around the world, other subtypes of avian influenza viruses have crossed the avian-human species barrier and infected humans; it is particularly noteworthy that H5N1 and H7N9 avian influenza viruses have caused Serious human diseases and deaths raise concerns that these avian influenza viruses may cause future human influenza pandemics and bring disastrous consequences
.
Understanding the pathogenesis of infections caused by these viruses will help the development of antiviral drugs
.
The H7N9 virus that emerged in China in 2013 has infected 1,568 people, including 616 deaths
.
Most H7N9 patients develop severe pneumonia and acute respiratory distress syndrome
.
Analysis of bronchoalveolar lavage samples showed that the levels of cytokines/chemokines in the lung were increased 1,000-fold relative to the levels in plasma, and the increase in the levels of these cytokines/chemokines in the lungs was not favorable or fatal The results are relevant
.
However, how these increased cytokine/chemokine levels (referred to as "cytokine storm" in this study) are triggered in the lungs remains largely unknown
.
In this study, animal models were used to explore the underlying mechanism of the abnormal innate immune response caused by the H7N9 virus, and to gain important insights into the pathogenesis of human H7N9 infection
.
The study found that the effective replication of H7N9 virus in mouse lungs activates Gasdermin E (GSDME)-mediated pyrolysis of alveolar epithelial cells, and the released cytoplasmic contents subsequently trigger a cytokine storm
.
Knockout of Gsdme changed the death mode of A549 and human primary alveolar epithelial cells from pyrolysis after H7N9 virus infection to apoptosis.
Gsdme knockout mice survived lethal H7N9 virus infection
.
The results of this study indicate that GSDME activation is the key and unique mechanism for the death of lung cytokine storm and H7N9 virus infection, thus opening a new door for the development of antiviral drugs against H7N9 virus
.
Reference message: https://academic.
oup.
com/nsr/advance-article/doi/10.
1093/nsr/nwab137/6332297?searchresult=1#
