Asset Details
Do you wish to reserve the book?
Streptococcus Suis Serotype 2 Stimulates Neutrophil Extracellular Traps Formation via Activation of p38 MAPK and ERK1/2
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?
Streptococcus Suis Serotype 2 Stimulates Neutrophil Extracellular Traps Formation via Activation of p38 MAPK and ERK1/2
Do you wish to request the book?
Streptococcus Suis Serotype 2 Stimulates Neutrophil Extracellular Traps Formation via Activation of p38 MAPK and ERK1/2
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
Streptococcus Suis Serotype 2 Stimulates Neutrophil Extracellular Traps Formation via Activation of p38 MAPK and ERK1/2
2018
Overview
serotype 2 is a major pathogen of swine streptococcicosis, which result in serious economic loss worldwide. SS2 is an important zoonosis causing meningitis and even death in humans. Neutrophil extracellular traps (NETs) constitute a significant bactericidal strategy of innate immune. The battle between SS2 and NETs may account for the pathogenicity of SS2. However, the molecular mechanism underlying release of SS2-induced NETs remains unclear. In this study, SS2 was found to induce NETs within 2-4 h, and was dependent on reactive oxygen species (ROS) from NADPH oxidase. Moreover, SS2 could activate neutrophil p38 MAPK and ERK1/2. Blockage of p38 MAPK or ERK1/2 activation decreased SS2-induced NETs formation by 65 and 85%, respectively. In addition, NADPH oxidase derived ROS inhibition negatively affected phosphorylation of p38 MAPK and ERK1/2 in SS2 induced neutrophils. Both TLR2 and TLR4 were significantly up-regulated by SS2 infection in blood cells
and neutrophils
, which indicates these two receptors are involved in SS2 recognition. Blocking TLR4 signaling could further inhibit the activation of ERK1/2, but not p38 MAPK; however, TLR4 signaling inhibition reduced NETs formation induced by SS2. In conclusion, SS2 could be recognized by TLR2 and/or TLR4, initiating NETs formation signaling pathways in a NADPH oxidase derived ROS dependent manner. ROS will activate p38 MAPK and ERK1/2, which ultimately induces NETs formation.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Animals
/ Bacteria
/ Biofilms
/ ERK1/2
/ Extracellular signal-regulated kinase
/ Extracellular Traps - immunology
/ Extracellular Traps - metabolism
/ Female
/ Hogs
/ Humans
/ Kinases
/ MAP Kinase Signaling System - immunology
/ Mice
/ Mitogen-Activated Protein Kinase 1 - metabolism
/ Mitogen-Activated Protein Kinase 3 - metabolism
/ neutrophil extracellular traps
/ p38 MAPK
/ p38 Mitogen-Activated Protein Kinases - metabolism
/ Reactive Oxygen Species - metabolism
/ Streptococcal Infections - immunology
/ Streptococcal Infections - microbiology
/ Streptococcus suis - immunology
/ Streptococcus suis serotype 2
/ Toll-Like Receptor 2 - metabolism
/ Toll-Like Receptor 4 - genetics
