Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung

Summary 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...

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Main Authors: Ming‐Shan Kao, Jen‐Ho Yang, Arun Balasubramaniam, Supitchaya Traisaeng, Albert Jackson Yang, John Jackson Yang, Benjamin Prethiviraj Salamon, Deron R. Herr, Chun‐Ming Huang
Format: Article
Language:English
Published: Wiley 2022-07-01
Series:Microbial Biotechnology
Online Access:https://doi.org/10.1111/1751-7915.13994
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author Ming‐Shan Kao
Jen‐Ho Yang
Arun Balasubramaniam
Supitchaya Traisaeng
Albert Jackson Yang
John Jackson Yang
Benjamin Prethiviraj Salamon
Deron R. Herr
Chun‐Ming Huang
author_facet Ming‐Shan Kao
Jen‐Ho Yang
Arun Balasubramaniam
Supitchaya Traisaeng
Albert Jackson Yang
John Jackson Yang
Benjamin Prethiviraj Salamon
Deron R. Herr
Chun‐Ming Huang
author_sort Ming‐Shan Kao
collection DOAJ
description Summary 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.
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spelling doaj.art-6c0008feec09492aba2fc07bfa46044c2022-12-22T00:33:29ZengWileyMicrobial Biotechnology1751-79152022-07-011571984199410.1111/1751-7915.13994Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lungMing‐Shan Kao0Jen‐Ho Yang1Arun Balasubramaniam2Supitchaya Traisaeng3Albert Jackson Yang4John Jackson Yang5Benjamin Prethiviraj Salamon6Deron R. Herr7Chun‐Ming Huang8Department of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Life Sciences National Central University Taoyuan 32001 TaiwanDepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanDepartment of Biology San Diego State University San Diego CA 92182 USADepartment of Biomedical Sciences and Engineering National Central University Taoyuan 32001 TaiwanSummary 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.https://doi.org/10.1111/1751-7915.13994
spellingShingle Ming‐Shan Kao
Jen‐Ho Yang
Arun Balasubramaniam
Supitchaya Traisaeng
Albert Jackson Yang
John Jackson Yang
Benjamin Prethiviraj Salamon
Deron R. Herr
Chun‐Ming Huang
Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
Microbial Biotechnology
title Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
title_full Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
title_fullStr Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
title_full_unstemmed Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
title_short Colonization of nasal cavities by Staphylococcus epidermidis mitigates SARS‐CoV‐2 nucleocapsid phosphoprotein‐induced interleukin (IL)‐6 in the lung
title_sort colonization of nasal cavities by staphylococcus epidermidis mitigates sars cov 2 nucleocapsid phosphoprotein induced interleukin il 6 in the lung
url https://doi.org/10.1111/1751-7915.13994
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