Intravenous administration
of mesenchymal stem cells (MSCs) has
served as a clinical intervention for inflammatory diseases. Once
entered to blood circulation, MSCs are exposed to a harsh environment
which sharply decreases cell viability due to the fact that injected
cells, being susceptible to shear stress, are subjected to the high
velocities of the bloodstream and lack of proper mechanical support
that keeping them in an attachment-deprived state. Here, we coated the nanofilm onto viable
MSCs by depositing poly-l-lysine and hyaluronic acid molecules
along with arginine-glycine-aspartic acid (RGD peptide) as building
blocks to protect cells from shear stress and stabilize them in a
single cell, suspension state. In this article, we found that nanofilm-coated
cells showed significantly increased cell survival in vitro and in vivo, which was also supported by the activation
of survival-related protein, Akt. The coated nanofilm did not interfere
with the stemness of MSCs which was determined based on the colony
forming unit-fibroblast (CFU-F) assay and in vitro differentiation potential. Because of the characteristics of films
showing light molecular deposition density, flexibility, and looseness,
application of nanofilms did not block cell migration. When the cells
were administrated intravenously, the nanofilm coated MSCs not only
prolonged blood circulation lifetime but also showed increased stem
cell recruitment to injured tissues in the muscle injury in
vivo model, due to prolonged survival. Surface modification
of MSCs using nanofilms successfully modulated cell activity enabling
them to survive the anoikis-inducing state, and this can provide a
valuable tool to potentiate the efficacy of MSCs for in vivo cell therapy.
Staphylococcus aureus (S. aureus) is one of the well-known agents causing atopic dermatitis (AD) in susceptible individuals, and Staphylococcus epidermidis (S. epidermidis) produces class I thermostable bacteriocins that can selectively kill S. aureus, suggesting protective roles against AD. There is a large need for developing precise therapies only to target S. aureus and not to harm the beneficial microbiome. On the agar well diffusion assay, live planktonic S. epidermidis showed clear zones of inhibition of S. aureus growth, but heat-killed cells and cell-free supernatants did not show this. These results would lead us to hypothesize that cytoplasmic bacteriocin from S. epidermidis will be a promising agent to inhibit S. aureus growth. Therefore, we have extracted a novel thermolabile cytoplasmic bacteriocin from S. epidermidis using trichloroactic acid (TCA)/acetone precipitation method after cell lysis with a SDS-containing buffer. These bacteriocin selectively exhibited antimicrobial activity against S. aureus and methicillin-resistance Staphylococcus aureus (MRSA), presenting no active actions against S. epidermidis, E. coli, and Salmonella Typhimurium. The extracted cytoplasmic bacteriocin compounds revealed several diffuse bands of approximately 40–70 kDa by SDS-PAGE. These findings suggest that these cytoplasmic bacteriocin compounds would be a great potential means for S. aureus growth inhibition and topical AD treatment.
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