Some of the immediate sequelae of injury are uncomfortably familiar: Soon after an injury occurs, the affected site and its surrounding tissues become reddened, warm, swollen, and painful. These four signs which are probably the most useful and ubiquitous diagnostic clues in all of clinical medicine are hallmarks of acute inflammation, the body’s initial physiologic reaction to tissue distress. In its simplest form, inflammation is a response carried out by blood vessels and by the endothelial cells that line them. It serves an important protective function by setting in motion the processes of defense, healing, and repair. Inflammation is not considered an immune reaction, because it can be triggered not only by microbial infection but also by blunt trauma, thermal or chemical burns, lacerations, radiation injury (eg, sunburn), vascular obstruction, or myriad other causes. Nevertheless, immune and inflammatory reactions are closely linked, and they often promote and enhance one another. In particular, many types of innate or acquired immune reactions (eg, those that lead to complement activation) trigger inflammation in nearby blood vessels, so that the involved tissues become red, warm, swollen, and painful. On the other hand, as we shall see, the changes that take place in inflamed blood vessels are key to attracting cells of the immune system into an injured or infected tissue. Before discussing the cells of innate immunity, we begin with a brief overview of the vascular events of inflammation that set the stage for their arrival.
The spectrum of events that occur during inflammation varies according to the tissue and type of injury involved. The most fundamental are changes in the diameter and permeability of local blood vessels, and in the surface molecules expressed on their lining endothelial cells. But a given response may also involve an influx of particular types of leukocytes from the bloodstream, activation of the clotting or coagulation systems, fever, or a host of other phenomena. Individual aspects of the response are controlled by diffusible signaling molecules known as inflammatory mediators, a class that encompasses many unrelated proteins, peptides, and small organic compounds, each with unique biologic effects. Some, called vasoactive mediators, act principally on the vasculature, whereas others mediate pain, fever, coagulation, or leukocyte chemotaxis assay. We lists the mediators believed to be most important for certain key aspects of inflammation.
In general, these inflammation mediators come from three main sources. Some are secreted by injured or distressed host cells; others are byproducts either of tissue injury per se (eg, fragments of collagen) or of the host’s reaction to it (eg, activation of the clotting or complement cascades); and still others are unique microbial macromolecules (eg, LPS) that may also serve as targets for innate immunity system. Thus, as a rule, the inflammatory response is triggered by molecules that broadly signify tissue damage, infection, or distress, regardless of its specific cause.
