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• They make cell and vessel walls leaky (which helps transport the important immune cells and chemicals to where they're needed most). So far, so good—all of these inflammatory functions are healthy, normal, and needed. In most cases, the immune system's anti-inflammatory and resolution- triggering mechanisms come to bear, winding down these acute inflammatory reactions. Tissue healing progresses, sensation normalizes, and function returns. THE CYTOKINE STORM But, for reasons we don't entirely understand, in about 15 percent of people battling any serious infection, 1 the immune cycle seems to get stuck in a raging release of more and more cytokines, leading to more cell death, and even more cytokines. Perhaps related to underlying genetic defects, 2 this phenomenon (first described in 1993) has been long studied in related forms such as systemic inflammatory response syndrome, cytokine release syndrome, macrophage activation syndrome, hemophagocytic lymphohistiocytosis, or cytokine storm syndrome (CSS). 3 In the 1918 Spanish flu epidemic, differences in cytokine storm reactions between old and young, and between that virus and COVID-19, are thought to explain why that epidemic killed so many young people. CSS doesn't just occur in influenza, but in other respiratory diseases caused by coronaviruses, as well, such as SARS and MERS. They are also associated with noninfectious diseases such as multiple sclerosis and pancreatitis. But whenever cytokine orchestration has turned into a cytokine storm, their normally helpful functions contribute to an escalating spiral of worsening symptoms: • The pain, sensitivity, and fatigue from influenza's cytokines can make the host inhibit breathing and movement, so much that the concentrated and by- now toxic inflammatory soup collects in the lungs' alveoli (Image 2). • The cytokine-summoned first-responder cells are aggressive and indiscriminate in their destruction. Flooding into the tissues on the wash of leaked interstitial fluids, they use powerful enzymatic and oxidative processes to demolish both friend and foe alike (Image 3). Other cells, such as fibroblasts, simultaneously try to repair this ongoing damage, but when the cytokine-induced destruction continues, N e w ! A B M P P o c k e t P a t h o l o g y a t w w w. a b m p . c o m / a b m p - p o c k e t - p a t h o l o g y - a p p . 81 the resulting excess collagen makes tissues denser and more fibrous, further inhibiting normal perfusion and drainage. 4 • In musculoskeletal tissues, the plasma leakage of acute inflammation causes its characteristic swelling and redness. In lung tissue, this fluid buildup causes coughing; and if excessive or prolonged, can lead to breathing difficulties and pneumonia. What's more, capillaries damaged by the inflammatory riot can let the cytokine-rich fluids spill over into the bloodstream, resulting in systemic inflammation and multi-organ failure. 5 Microdamage to the lungs' alveoli from virus replication can, in some cases, trigger a self-escalating "cytokine storm" of hyperinflammatory cytokine overproduction and further tissue damage. 2