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The concept of inflammation has a long history. Although an inflammatory response to injury or another trigger is necessary, chronic diseases, such as coronary heart disease and diabetes, may develop because of unchecked inflammatory responses that have maladapted over decades. For example, the earliest changes in atherosclerosis occur in the endothelium, leading to a cascade of inflammatory responses, such as accumulation of monocytes and T cells, migration of leukocytes into the intima, monocyte differentiation and proliferation, and lesion and fibrous cap development. Inflammatory markers, such as C-reactive protein, may allow clinical insight into these decades-long processes, adding value to predictive measures of disease outcomes. Anti-inflammatory factors, such as adiponectin, may provide further understanding of the inflammatory pathways involved. Greater understanding of the complex pathways involved in inflammation may provide alternative therapeutic strategies to combat inflammation and chronic diseases potentially arising from it.
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Dyke et al. (2008) studied this question.
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