Celsus named four fiery signs of acute inflammation
Inflammation is tissue defence triggered by trauma, infection, toxins, and more—an innate, not adaptive, immune pattern involving cells, vessels, and mediators. Acute bursts recruit plasma and leukocytes within minutes; chronic forms linger. Classical Latin still labels the five cardinal signs of the acute stage.
Celsus, writing around 30 BC–38 AD, listed the first four: pain, heat, redness, and swelling. Loss of function came later, credited variously to Galen, Thomas Sydenham or Rudolf Virchow, and covers things like a dulled sense of smell during a cold or laboured breathing with bronchitis. Bradykinin and histamine sting nerves; core-temperature blood floods the site for heat and flush; fluid leakage swells tissue.
The acute response unfolds in two stages, vascular first and cellular second. Resident sentinels such as macrophages, dendritic cells, Kupffer cells and mast cells carry pattern-recognition receptors that spot molecular signatures of microbes or of damaged tissue. Once triggered they release histamine, serotonin, prostaglandin E2 and leukotriene B4, widening arterioles and making vessels leaky. Plasma protein cascades join in: complement tags and punches holes in bacteria, the kinin system prolongs vessel widening, clotting throws a protein mesh over the wound, and fibrinolysis keeps that clotting in check. White cells, above all neutrophils, then squeeze out of the bloodstream to engulf microbes and debris.
Because these signalling molecules break down quickly, the acute flare needs constant fuel and fades once the trigger is gone, usually within days. Chronic inflammation, by contrast, lasts months or years and is dominated by macrophages, lymphocytes and plasma cells. It underlies diabetes, cardiovascular disease, allergies and chronic obstructive pulmonary disease, and obesity, smoking, stress and poor diet all encourage it; gut problems such as reflux or diarrhoea can be among its signs. Type 1 and Type 2 labels track cytokine and T-helper profiles.
Calling inflammation purely villainous misses the point: without the flare, wounds would not seal. The art is knowing when the fire should cool.
Source: Inflammation
