Model
Digital Document
Publisher
Florida Atlantic University
Description
Chitin Microparticles (CMPs, 1-10um), a special form of the ubiquitous and nontoxic
polysaccharide Chitin (GlcNAc), is capable of inducing a switch in macrophages
from the wound-healing M2 phenotype to the classically activated pro-inflammatory M1
phenotype; which has therapeutic implications in allergy and cancer. We hypothesized
that TLR2 forms a complex with CMPs and Chitin-Binding Proteins (CBPs) at the
surface of peritoneal macrophages and remains with that complex after internalization to
initiate downstream signaling events, leading to the production of the M1 cytokine, TNFalpha.
Our results from experiments performed in RAW 264.7 cells show that TLR2 and
TLR1, but not TLR6, are associated with the CMP binding fraction, and that both TLR1
and TLR2 might be important for M1 activation as a result of CMP phagocytosis. This
project sheds light on CMP as a potential therapeutic agent and provides more evidence
for a phagocytosis-dependent TLR2 signaling pathway.
polysaccharide Chitin (GlcNAc), is capable of inducing a switch in macrophages
from the wound-healing M2 phenotype to the classically activated pro-inflammatory M1
phenotype; which has therapeutic implications in allergy and cancer. We hypothesized
that TLR2 forms a complex with CMPs and Chitin-Binding Proteins (CBPs) at the
surface of peritoneal macrophages and remains with that complex after internalization to
initiate downstream signaling events, leading to the production of the M1 cytokine, TNFalpha.
Our results from experiments performed in RAW 264.7 cells show that TLR2 and
TLR1, but not TLR6, are associated with the CMP binding fraction, and that both TLR1
and TLR2 might be important for M1 activation as a result of CMP phagocytosis. This
project sheds light on CMP as a potential therapeutic agent and provides more evidence
for a phagocytosis-dependent TLR2 signaling pathway.
Member of