Skip to main content
. Author manuscript; available in PMC: 2012 Oct 15.
Published in final edited form as: Eur J Pharmacol. 2011 Mar 31;668(3):435–442. doi: 10.1016/j.ejphar.2011.02.045

FIG. 10. Potential Effects of the isomers of NAc-PGP on neutrophilic inflammation.

FIG. 10

Fig. 10A

Upon injury or insult the airway epithelium releases CXCL8. CXCL8 draws neutrophils in from the periphery at which point they either actively release MMP8 and/or 9 and PE or release it upon apoptosis. The MMPs perform an initial cleavage of collagen creating an optimum substrate for the final catalysis by PE to release PGP. PGP, acting via the same CXCR1 and CXCR2 receptors that CXCL8 utilizes, can cause further neutrophil influx and activation.

Fig. 10B

DD-NAc-PGP binds at CXCR1 and 2 on neutrophils but prevents the activation. This blocks the downstream release of proteases resulting in less collagen cleavage and epithelial damage, ultimately blocking the chronic neutrophil influx.