Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway

Background/Aim. Staphylococcus aureus (S. aureus) is a gram-positive pathogen that causes various human diseases. S. aureus causes pneumonia, which is characterized by localized tissue necrosis. The aim of the study was to explore the expression of mouse β-defensin 3 (mBD-3) induced by S. aureus in...

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Main Authors: Ni Yongqing, Bi Xiaoduo, Zhao Pengwei
Format: Article
Language:English
Published: Ministry of Defence of the Republic of Serbia, University of Defence, Belgrade 2023-01-01
Series:Vojnosanitetski Pregled
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Online Access:https://doiserbia.nb.rs/img/doi/0042-8450/2023/0042-84502200051N.pdf
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author Ni Yongqing
Bi Xiaoduo
Zhao Pengwei
author_facet Ni Yongqing
Bi Xiaoduo
Zhao Pengwei
author_sort Ni Yongqing
collection DOAJ
description Background/Aim. Staphylococcus aureus (S. aureus) is a gram-positive pathogen that causes various human diseases. S. aureus causes pneumonia, which is characterized by localized tissue necrosis. The aim of the study was to explore the expression of mouse β-defensin 3 (mBD-3) induced by S. aureus in mouse lungs and the effect of mBD-3 expression on the mitogen-activated protein kinase (MAPK) pathway. Methods. An experimental model of S. aureus pneumonia in mice was developed, and the expression of mBD-3 and activation of the MAPK pathway were investigated using the methods of immunofluorescence and western blot. Results. The experimental model was created successfully. The number of white blood cells was elevated 48 and 72 hrs after the introduction of bacteria through mouse airways, and bronchiolar mucosal hyperemia was observed, along with a large number of white blood cells and mucus in the bronchioles. The mBD-3 expression levels 48 and 72 hrs after the induction of infection were greater than the levels in the control group and 24 hrs after the induction. The amount of phosphorylated extracellular signal-regulated kinase (ERK1/2) was increased 48 and 72 hrs after infection induction, compared with the levels in the control group and 24 hrs after induction. The expression of mBD-3 was lower when ERK1/2 phosphorylation was inhibited by the U0126 inhibitor. Conclusion. S. aureus in experimental pneumonia mouse model accelerates mBD-3 expression in the mouse lung mainly through an ERK1/2-dependent signaling pathway.
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institution Kabale University
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spelling doaj-art-4b54fa08f9b341dbaaf1b2b13c9d738d2025-08-20T03:36:27ZengMinistry of Defence of the Republic of Serbia, University of Defence, BelgradeVojnosanitetski Pregled0042-84502406-07202023-01-0180434334810.2298/VSP210601051N0042-84502200051NEffect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathwayNi Yongqing0Bi Xiaoduo1Zhao Pengwei2Affiliated Hospital of Inner Mongolia Medical University, Hohhot, PR ChinaAffiliated Hospital of Inner Mongolia Medical University, Hohhot, PR ChinaInner Mongolia Medical University, Laboratory of Microbiology and Immunology, Hohhot, PR ChinaBackground/Aim. Staphylococcus aureus (S. aureus) is a gram-positive pathogen that causes various human diseases. S. aureus causes pneumonia, which is characterized by localized tissue necrosis. The aim of the study was to explore the expression of mouse β-defensin 3 (mBD-3) induced by S. aureus in mouse lungs and the effect of mBD-3 expression on the mitogen-activated protein kinase (MAPK) pathway. Methods. An experimental model of S. aureus pneumonia in mice was developed, and the expression of mBD-3 and activation of the MAPK pathway were investigated using the methods of immunofluorescence and western blot. Results. The experimental model was created successfully. The number of white blood cells was elevated 48 and 72 hrs after the introduction of bacteria through mouse airways, and bronchiolar mucosal hyperemia was observed, along with a large number of white blood cells and mucus in the bronchioles. The mBD-3 expression levels 48 and 72 hrs after the induction of infection were greater than the levels in the control group and 24 hrs after the induction. The amount of phosphorylated extracellular signal-regulated kinase (ERK1/2) was increased 48 and 72 hrs after infection induction, compared with the levels in the control group and 24 hrs after induction. The expression of mBD-3 was lower when ERK1/2 phosphorylation was inhibited by the U0126 inhibitor. Conclusion. S. aureus in experimental pneumonia mouse model accelerates mBD-3 expression in the mouse lung mainly through an ERK1/2-dependent signaling pathway.https://doiserbia.nb.rs/img/doi/0042-8450/2023/0042-84502200051N.pdfdefensinsdisease models, animalpneumonia, staphylococcalsignal transductionstaphylococcus aureus
spellingShingle Ni Yongqing
Bi Xiaoduo
Zhao Pengwei
Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
Vojnosanitetski Pregled
defensins
disease models, animal
pneumonia, staphylococcal
signal transduction
staphylococcus aureus
title Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
title_full Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
title_fullStr Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
title_full_unstemmed Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
title_short Effect of Staphylococcus aureus in experimental pneumonia mouse model on promotion of mBD-3 expression through activation of the ERK1/2 pathway
title_sort effect of staphylococcus aureus in experimental pneumonia mouse model on promotion of mbd 3 expression through activation of the erk1 2 pathway
topic defensins
disease models, animal
pneumonia, staphylococcal
signal transduction
staphylococcus aureus
url https://doiserbia.nb.rs/img/doi/0042-8450/2023/0042-84502200051N.pdf
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