Public articles linked to the same research event.
bioRxiv Using repeated intratracheal inoculation of mice with recombinant Staphylococcus aureus serine protease-like protein B (SplB) or an inactive mutant, this study found that SplB sensitized mice and caused eosinophilic airway inflammation and hyperresponsiveness, that asthma development required both the proteolytic activity of SplB and a functional adaptive immune system, and that the soluble protease sensor IL-33 was necessary for eosinophil tissue invasion whereas the membrane-bound protease sensor PAR2 was not, leading the authors to propose a third mechanism in which S. aureus releases allergens such as SplB that sensitize individuals and lead to asthma.
Using repeated intratracheal inoculation of mice with recombinant Staphylococcus aureus serine protease-like protein B (SplB) or an inactive mutant, this study found that SplB sensitized mice and caused eosinophilic airway inflammation and hyperresponsiveness, that asthma development required both the proteolytic activity of SplB and a functional adaptive immune system, and that the soluble protease sensor IL-33 was necessary for eosinophil tissue invasion whereas the membrane-bound protease sensor PAR2 was not, leading the authors to propose a third mechanism in which S. aureus releases allergens such as SplB that sensitize individuals and lead to asthma.
Using repeated intratracheal inoculation of mice with recombinant Staphylococcus aureus serine protease-like protein B (SplB) or an inactive mutant, this study found that SplB sensitized mice and caused eosinophilic airway inflammation and hyperresponsiveness, that asthma development required both the proteolytic activity of SplB and a functional adaptive immune system, and that the soluble protease sensor IL-33 was necessary for eosinophil tissue invasion whereas the membrane-bound protease sensor PAR2 was not, leading the authors to propose a third mechanism in which S. aureus releases allergens such as SplB that sensitize individuals and lead to asthma.
Using repeated intratracheal inoculation of mice with recombinant Staphylococcus aureus serine protease-like protein B (SplB) or an inactive mutant, this study found that SplB sensitized mice and caused eosinophilic airway inflammation and hyperresponsiveness, that asthma development required both the proteolytic activity of SplB and a functional adaptive immune system, and that the soluble protease sensor IL-33 was necessary for eosinophil tissue invasion whereas the membrane-bound protease sensor PAR2 was not, leading the authors to propose a third mechanism in which S. aureus releases allergens such as SplB that sensitize individuals and lead to asthma.