Inflammation

Inflammation works as a controlled emergency response: damaged or infected tissue releases signalling molecules that widen nearby blood vessels, make them leaky, and draw immune cells out of the bloodstream to clear debris and pathogens before repair begins. The four classical signs — redness, heat, swelling, and pain — are direct consequences of that vascular change rather than of the injury itself.

How it works

Detection. Resident cells (mast cells, macrophages) recognise either damage-associated molecules released by broken cells or pathogen-associated molecules on microbes.

Vascular phase. Histamine, prostaglandins, and nitric oxide dilate arterioles and loosen the junctions between endothelial cells. Plasma and its proteins leak into the tissue, which is the swelling.

Cellular phase. Neutrophils arrive first, within hours, and destroy pathogens. Monocytes follow and mature into macrophages, which clear dead neutrophils and debris.

Resolution. Macrophages switch from a destructive profile to a reparative one, specialised lipid mediators shut off recruitment, and lymphatic drainage clears the fluid. Failure at this last step is what turns acute inflammation into the chronic kind.

Cytokines

Cytokines are the small proteins that carry the instructions. Interleukin-1β, interleukin-6, and tumour necrosis factor alpha (TNF-α) amplify the response; interleukin-10 and transforming growth factor beta damp it down. A compound described as “anti-inflammatory” usually means it shifts this balance — lowering the first group, raising the second — rather than switching inflammation off.

Acute versus chronic

Acute inflammation is short, local, and necessary; blocking it entirely slows healing. Chronic inflammation is a low-grade version that never resolves and is implicated in atherosclerosis, insulin resistance, arthritis, and neurodegeneration. The two are the same machinery running on different timescales, which is why “reduce inflammation” is a far more ambiguous goal than it sounds.

Why peptides care

• BPC-157 is reported in animal models to lower pro-inflammatory cytokines while supporting repair in gut and musculoskeletal tissue.
• GHK-Cu is described as having antioxidant and anti-inflammatory activity alongside its effects on skin remodelling.
• TB-500 is described as reducing pro-inflammatory cytokines while promoting anti-inflammatory mediators.

As with most compounds catalogued here, the anti-inflammatory findings rest mainly on preclinical work. Each article grades its own evidence.

Related concepts

Inflammation opens the repair programme that tissue repair and wound healing complete, and it both produces and responds to oxidative stress.