Pathophysiology of Sepsis Inflammatory Response Essay
Pathophysiology of Sepsis
Sepsis begins with a systemic inflammatory response to a perceived threat to the immune system (Powers & Burchell, 2010). Tissue injury or invading pathogens stimulate production of phagocytes, such as monocytes and macrophages, which act as the first line of defence against infection. These phagocytes release pro-inflammatory mediators called cytokines, in order to attract neutrophils to the site of infection. The release of cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumour necrosis factor alpha (TNFα), results in release of further chemical agents, such as complement, histamine and prostaglandin. These agents cause localised vasodilation and release of cytotoxic chemicals, in an effort to destroy the invading pathogen. (Daniels, 2009) A rise in inflammatory markers (such as an elevated CRP) demonstrates this inflammatory response (due to release of IL-6).
In a certain sub-group of people with a host predisposition, such as those possessing a genetic variant of a receptor known as a