Inflammation contributes to skin aging.
Once one inflammatory pathway gets activated, others become activated and inflammation is difficult to stop.
Legalization of cannabis has led to research about the anti-inflammatory effects of cannabinoids.
Diet, exercise, and lifestyle habits are being studied to learn how they affect inflammation.
Several botanical ingredients have been shown to block various inflammatory pathways but formulations that can deliver the ingredients into the skin need to be improved to ensure penetration and stability.
More knowledge about the microbiome and its effects on inflammation is anticipated.
Inflammation, from the Latin word inflammatio (“to set on fire”), is a dynamic vascular and cellular reflexive response of living tissue to injury; such injury may present in the form of infection, chemical damage (e.g., toxins, irritants), physical damage (e.g., heat, cold, radiation, mechanical trauma), and the binding of antibodies to antigens within the body.1 Inflammation is therefore a protective mechanism of the organism intended to remove such injurious stimuli as well as to initiate the healing process of the damaged tissue.
Localized vasodilation, increased vascular permeability, extravasation of plasmatic proteins, and migration of leukocytes into the affected tissue produce what Cornelius Celsius defined in the first century as the “cardinal signs” of acute inflammation: calor (heat), dolor (pain), rubor (redness), and tumor (swelling).2 Functio laesa (loss of function) was later added to the definition of inflammation by Rudolf Virchow in the 19th century.3
A basic sequence of events characterizes virtually all types of inflammatory responses regardless of the provocative stimuli.4 The initial reaction is vasodilation followed by transient vasoconstriction. The microvascular endothelium then becomes more permeable to plasma proteins that leak out into the extravascular compartment, establishing an inflammatory exudate. Inflammatory mediators released in the area induce the expression of selectin-type adhesion molecules on the endothelial cells. Recruited leukocytes then interact with such adhesion molecules, bind to the inflamed endothelium and extravasate into the tissue where they respond to the insult through phagocytosis and degranulation. Finally, the inflammatory response must be actively terminated when no longer essential to prevent unnecessary damage to tissue.
The process of inflammation, both vascular and cellular, is orchestrated by a large array of inflammatory mediators, which will be reviewed in this chapter. These mediators include: (1) cellular-derived products, such as vasoactive amines (e.g., histamine), cytokines, eicosanoids (e.g., prostaglandins, thromboxanes, and leukotrienes), enzymes, and oxygen radicals; and (2) plasma-derived mediators, which include complement cascade components, kinins, and fibrinopeptides.
CELL-DERIVED INFLAMMATORY MEDIATORS AND THEIR ROLES IN THE INFLAMMATORY PROCESS
In reaction to inflammatory stimuli, molecular signaling, or cell destruction, phospholipids contained in the cellular membrane are hydrolyzed by phospholipase A2 (PLA2), releasing free arachidonic acid (AA). This fatty acid is ...