Does cyclosporine-inhibitable blood-brain barrier drug transport influence clinical morphine pharmacodynamics?
Morphine is a transporter substrate at the human blood-brain barrier. Results suggest a role for P-glycoprotein or other efflux transporters in brain morphine access, although the magnitude of the effect is small, and unlikely to be a major determinant of morphine clinical effects. Efflux may explain some variability in clinical morphine effects.
Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.