tetano
Editor, Senior Moderator
Microb Biotechnol
. 2022 Apr 14.
doi: 10.1111/1751-7915.13994. Online ahead of print.
Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS-CoV-2 nucleocapsid phosphoprotein-induced interleukin (IL)-6 in the lung
Ming-Shan Kao[SUP] 1 [/SUP], Jen-Ho Yang[SUP] #[/SUP][SUP] 1 [/SUP], Arun Balasubramaniam[SUP] #[/SUP][SUP] 1 [/SUP], Supitchaya Traisaeng[SUP] 2 [/SUP], Albert Jackson Yang[SUP] 1 [/SUP], John Jackson Yang[SUP] 1 [/SUP], Benjamin Prethiviraj Salamon[SUP] 1 [/SUP], Deron R Herr[SUP] 3 [/SUP], Chun-Ming Huang[SUP] 1 4 [/SUP]
Affiliations
Abstract
Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can trigger excessive interleukin (IL)-6 signalling, leading to a myriad of biological effects including a cytokine storm that contributes to multiple organ failure in severe coronavirus disease 2019 (COVID-19). Using a mouse model, we demonstrated that nasal inoculation of nucleocapsid phosphoprotein (NPP) of SARS-CoV-2 increased IL-6 content in bronchoalveolar lavage fluid (BALF). Nasal administration of liquid coco-caprylate/caprate (LCC) onto Staphylococcus epidermidis (S. epidermidis)-colonized mice significantly attenuated NPP-induced IL-6. Furthermore, S. epidermidis-mediated LCC fermentation to generate electricity and butyric acid that promoted bacterial colonization and activated free fatty acid receptor 2 (Ffar2) respectively. Inhibition of Ffar2 impeded the effect of S. epidermidis plus LCC on the reduction of NPP-induced IL-6. Collectively, these results suggest that nasal S. epidermidis is part of the first line of defence in ameliorating a cytokine storm induced by airway infection of SARS-CoV-2.
. 2022 Apr 14.
doi: 10.1111/1751-7915.13994. Online ahead of print.
Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS-CoV-2 nucleocapsid phosphoprotein-induced interleukin (IL)-6 in the lung
Ming-Shan Kao[SUP] 1 [/SUP], Jen-Ho Yang[SUP] #[/SUP][SUP] 1 [/SUP], Arun Balasubramaniam[SUP] #[/SUP][SUP] 1 [/SUP], Supitchaya Traisaeng[SUP] 2 [/SUP], Albert Jackson Yang[SUP] 1 [/SUP], John Jackson Yang[SUP] 1 [/SUP], Benjamin Prethiviraj Salamon[SUP] 1 [/SUP], Deron R Herr[SUP] 3 [/SUP], Chun-Ming Huang[SUP] 1 4 [/SUP]
Affiliations
- PMID: 35426250
- DOI: 10.1111/1751-7915.13994
Abstract
Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can trigger excessive interleukin (IL)-6 signalling, leading to a myriad of biological effects including a cytokine storm that contributes to multiple organ failure in severe coronavirus disease 2019 (COVID-19). Using a mouse model, we demonstrated that nasal inoculation of nucleocapsid phosphoprotein (NPP) of SARS-CoV-2 increased IL-6 content in bronchoalveolar lavage fluid (BALF). Nasal administration of liquid coco-caprylate/caprate (LCC) onto Staphylococcus epidermidis (S. epidermidis)-colonized mice significantly attenuated NPP-induced IL-6. Furthermore, S. epidermidis-mediated LCC fermentation to generate electricity and butyric acid that promoted bacterial colonization and activated free fatty acid receptor 2 (Ffar2) respectively. Inhibition of Ffar2 impeded the effect of S. epidermidis plus LCC on the reduction of NPP-induced IL-6. Collectively, these results suggest that nasal S. epidermidis is part of the first line of defence in ameliorating a cytokine storm induced by airway infection of SARS-CoV-2.