![]() ![]() If microbes are introduced, they can stimulate potent inflammation. We now know that there are several mechanisms by which injury can cause inflammation. Of course the discovery of infection as the other important trigger of inflammation occurred much later, not in small part because it had to await the discovery of germs and their connection to disease by Pasteur and Koch in the late 1800s. ![]() ![]() Waller (1846) and Cohnheim (1867) first described that injury caused vessels to dilate and leak fluid and stimulated the recruitment of leukocytes. Study of the response to injury also played a key role in the elucidation of the underlying pathophysiologal mechanisms that account for the signs and symptoms recorded by Celsus. It is perhaps not surprising, therefore, that the fact that injury causes inflammation (phlogosis) was recorded in the medical literature at the start of the first millennium AD by Galen. For example, a burn rapidly becomes red, hot, swollen and painful, a constellation of the four cardinal signs of inflammation that were described over 2,000 years ago by Celsus. Here we review what is presently known about the sterile inflammatory response and its underlying mechanisms.Įveryone has experienced injuries and knows from common observation that the injured site becomes inflamed. Many of the specific molecules and mechanisms involved in these various processes are still poorly understood. In addition to stimulating inflammation, dead cells also release danger signals that activate dendritic cells and promote the generation of immune responses to antigens in and around the dying cells. The resulting mediators then orchestrate the inflammatory response, eliciting its various vascular and cellular components. Other molecules released by dead cells stimulate the generation of mediators from extracellular sources. Some of these molecules are recognized by cellular receptors that stimulate the generation of proinflammatory mediators. Injured cells release “danger signals” that alert the host to cell death. The broad outline of this pathway is understood. Given the key role of inflammation in these processes it is important to understand the underlying mechanisms that drive this response. However, this response can also cause tissue damage and in so doing contributes to the pathogenesis of a number of diseases. The ensuing hyperemia, leak of plasma proteins, and recruitment of leukocytes subserve a number of useful functions in host defense and tissue repair. When cells die in vivo they trigger an inflammatory response. ![]()
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