Asset Details
Do you wish to reserve the book?
Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and β-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing Is Dependent Only on CR3
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and β-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing Is Dependent Only on CR3
Do you wish to request the book?
Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and β-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing Is Dependent Only on CR3
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Protein Deiminase 4 and CR3 Regulate Aspergillus fumigatus and β-Glucan-Induced Neutrophil Extracellular Trap Formation, but Hyphal Killing Is Dependent Only on CR3
2018
Overview
Neutrophil extracellular trap (NET) formation requires chromatin decondensation before nuclear swelling and eventual extracellular release of DNA, which occurs together with nuclear and cytoplasmic antimicrobial proteins. A key mediator of chromatin decondensation is protein deiminase 4 (PAD4), which catalyzes histone citrullination. In the current study, we examined the role of PAD4 and NETosis following activation of neutrophils by
hyphal extract or cell wall β-glucan (curdlan) and found that both induced NET release by human and murine neutrophils. Also, using blocking antibodies to CR3 and Dectin-1 together with CR3-deficient CD18
and Dectin-1
murine neutrophils, we found that the β-glucan receptor CR3, but not Dectin-1, was required for NET formation. NETosis was also dependent on NADPH oxidase production of reactive oxygen species (ROS). Using an antibody to citrullinated histone 3 (H3Cit) as an indicator of PAD4 activity, we show that β-glucan stimulated NETosis occurs in neutrophils from C57BL/6, but not PAD4
mice. Similarly, a small molecule PAD4 inhibitor (GSK484) blocked NET formation by human neutrophils. Despite these observations, the ability of PAD4
neutrophils to release calprotectin and kill
hyphae was not significantly different from C57BL/6 neutrophils, whereas CD18
neutrophils exhibited an impaired ability to perform both functions. We also detected H3Cit in
infected C57BL/6, but not PAD4
corneas; however, we found no difference between C57BL/6 and PAD4
mice in either corneal disease or hyphal killing. Taken together, these findings lead us to conclude that although PAD4 together with CR3-mediated ROS production is required for NET formation in response to
, PAD4-dependent NETosis is not required for
killing either
or during infection.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Adult
/ Aged
/ Animals
/ Aspergillus fumigatus - immunology
/ Cornea
/ CR3
/ Extracellular Traps - genetics
/ Extracellular Traps - immunology
/ Female
/ Fungal Polysaccharides - genetics
/ Fungal Polysaccharides - immunology
/ Histones
/ Humans
/ Hyphae
/ Kinases
/ Lectins
/ Macrophage-1 Antigen - genetics
/ Macrophage-1 Antigen - immunology
/ Male
/ Mice
/ neutrophil extracellular trap
/ Peptides
/ Protein-Arginine Deiminase Type 4
/ Protein-Arginine Deiminases - genetics
/ Protein-Arginine Deiminases - immunology
/ Proteins
/ β-Glucan
