Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis
Phenol-soluble modulin α and β display divergent roles in staphylococcal infection and its associated septic arthritis - whereas PSMα is a virulence factor for neutrophils that worsens infection, PSMβ protects from the development of septic arthritis.
Main Authors: | , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2022-09-01
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Series: | Communications Biology |
Online Access: | https://doi.org/10.1038/s42003-022-03839-2 |
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author | Zhicheng Hu Pradeep Kumar Kopparapu Patrick Ebner Majd Mohammad Simon Lind Anders Jarneborn Claes Dahlgren Michelle Schultz Meghshree Deshmukh Rille Pullerits Mulugeta Nega Minh-Thu Nguyen Ying Fei Huamei Forsman Friedrich Götz Tao Jin |
author_facet | Zhicheng Hu Pradeep Kumar Kopparapu Patrick Ebner Majd Mohammad Simon Lind Anders Jarneborn Claes Dahlgren Michelle Schultz Meghshree Deshmukh Rille Pullerits Mulugeta Nega Minh-Thu Nguyen Ying Fei Huamei Forsman Friedrich Götz Tao Jin |
author_sort | Zhicheng Hu |
collection | DOAJ |
description | Phenol-soluble modulin α and β display divergent roles in staphylococcal infection and its associated septic arthritis - whereas PSMα is a virulence factor for neutrophils that worsens infection, PSMβ protects from the development of septic arthritis. |
first_indexed | 2024-12-10T14:42:41Z |
format | Article |
id | doaj.art-798d297117de42cb9eb21e795269552e |
institution | Directory Open Access Journal |
issn | 2399-3642 |
language | English |
last_indexed | 2024-12-10T14:42:41Z |
publishDate | 2022-09-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Communications Biology |
spelling | doaj.art-798d297117de42cb9eb21e795269552e2022-12-22T01:44:39ZengNature PortfolioCommunications Biology2399-36422022-09-015111110.1038/s42003-022-03839-2Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritisZhicheng Hu0Pradeep Kumar Kopparapu1Patrick Ebner2Majd Mohammad3Simon Lind4Anders Jarneborn5Claes Dahlgren6Michelle Schultz7Meghshree Deshmukh8Rille Pullerits9Mulugeta Nega10Minh-Thu Nguyen11Ying Fei12Huamei Forsman13Friedrich Götz14Tao Jin15Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine Tübingen (IMIT), University of TübingenDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine Tübingen (IMIT), University of TübingenInstitute of Medical Microbiology, University Hospital of MünsterCenter for Clinical Laboratories, the Affiliated Hospital of Guizhou Medical UniversityDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgDepartment of Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine Tübingen (IMIT), University of TübingenDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of GothenburgPhenol-soluble modulin α and β display divergent roles in staphylococcal infection and its associated septic arthritis - whereas PSMα is a virulence factor for neutrophils that worsens infection, PSMβ protects from the development of septic arthritis.https://doi.org/10.1038/s42003-022-03839-2 |
spellingShingle | Zhicheng Hu Pradeep Kumar Kopparapu Patrick Ebner Majd Mohammad Simon Lind Anders Jarneborn Claes Dahlgren Michelle Schultz Meghshree Deshmukh Rille Pullerits Mulugeta Nega Minh-Thu Nguyen Ying Fei Huamei Forsman Friedrich Götz Tao Jin Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis Communications Biology |
title | Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
title_full | Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
title_fullStr | Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
title_full_unstemmed | Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
title_short | Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
title_sort | phenol soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis |
url | https://doi.org/10.1038/s42003-022-03839-2 |
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