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Inflammation is an adaptive response to infection or injury, which involves the orchestrated delivery of leukocytes to the initiating site. In addition to classic acute and chronic inflammatory responses, there is also a para-inflammatory response, which is induced by tissue stress. Classic inflammatory responses are triggered by pattern recognition receptors such as the Toll-like receptors (TLRs) and nucleotide-binding oligomerization-domain protein (NOD)-like receptors (NLRs). TLR/NLR signaling results in the secretion of potent inflammatory mediators, such as cytokines and chemokines. The underlying goal of this response is to facilitate neutrophil invasion of the extravascular site of infection or injury. Activated neutrophils release the toxic contents of their granules and eliminate the initiating trigger. If this cascade of events is successful, the acute inflammatory response ends, and is followed by phases of repair and recovery. However, if removal of the initiating factor is not complete, inflammation can persist prompting the replacement of neutrophils by macrophages and T cells. If this response fails, a chronic state of inflammation can develop. Thus, the inflammatory response comprises physiological pathways that must be tightly controlled to avoid evolution into the chronic inflammatory states that exist during disease conditions such as type-2 diabetes, Alzheimer's disease, and cardiovascular disease.