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Rather than indiscriminately blocking macrophage activity (which would impair the early inflammatory debridement phase of wound healing), GHK-Cu research documents a shift in macrophage phenotype from pro-inflammatory M1 toward the anti-inflammatory, pro-healing M2 profile at later stages of the inflammatory response

Stine, Z

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What the primary literature consistently supports is a directional decline in GHK-related plasma activity across adult life

Pyocyanin also initiates neutrophil extracellular trap (NET) formation (Rada et al., 2013) and aberrant NET release triggered by pyocyanin-mediated intracellular ROS production directly damages host tissues and has been linked to the severity of many diseases including CF (Rada et al., 2013)