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Acute inflammation is a coordinated, adaptive response that is triggered by a number of noxious stimuli and conditions, the most prominent being microbial infection and tissue injury.1 The major function of acute inflammation is to provide protection against infection and/or to repair tissue damage. Thus, the process must be carefully regulated in order to be beneficial. A successful acute inflammatory response leads to the elimination of the invading organisms followed by a period of resolution and repair. In certain cases, such as septic shock, acute inflammation becomes dysregulated and can result in extensive tissue damage. Considerable progress has been made in elucidating the molecular mechanisms involved in the acute inflammatory response to microbial pathogens and, to a somewhat lesser extent, to tissue injury. Although there are other triggers to inflammation, much less is known about them and they will not be discussed here. Regardless of the trigger, one key fact is that the hallmarks of inflammation that are commonly associated with microbial infection (ie, redness [rubor], heat [calor], pain [dolor], and swelling [tumor]) are initiated by the innate immune response. Although the cells of the adaptive immune response can contribute to and amplify these effects, the primary signals that initiate and ultimately resolve acute inflammation are linked to innate immune recognition. Of the two branches of the immune system, innate and adaptive, innate immunity is the most ancient and exists, in some form, in all metazoans. Cells of the innate immune system utilize a collection of genomically encoded invariant receptors to recognize the presence of microbial pathogens and signal their presence.2 The role of these mechanisms is becoming increasingly recognized in a large variety of disease conditions and therefore the pediatric clinician benefits from a summary understanding of their biological basis. This chapter is intended to provide this basis through a discussion of the signals that are involved in the initiation of the inflammatory response, the mediators and effectors of the inflammatory response, as well as the factors involved in the transition from inflammation to resolution and tissue remodeling. For a further discussion of the development of the immune system see Chapter 186, and for a discussion of bacterial pathogenesis, bacteremia and septic shock see Chapters 222 and 223.


As stated previously, the predominant trigger of acute inflammation is the recognition of microbes by the receptors of the innate immune system. In contrast to the adaptive immune system, which uses the vast repertoire of B- and T-cell antigen receptors to potentially recognize almost any target, the specificities of the innate immune system are “hardwired,” meaning that their microbial targets are selected evolutionarily over time and are, therefore, much more limited in their scope.3 Thus, the innate immune system has evolved a strategy of “pattern recognition” that involves targeting highly conserved features of microbes for detection, enabling receptors of the innate system to detect the wide range of microbial diversity.4,5 The innate receptors that are involved in ...

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