Enhancing The Resolution of Inflammation: A Therapeutic Target?

Abstract

Over-recruitment, uncontrolled activation and defective removal of inflammatory

Cells (especially neutrophil and eosinophil granulocytes) from inflammatory loci

Likely play a prominent role in the development of chronic inflammatory conditions

Such as rheumatoid arthritis and asthma. During resolution of inflammation

Granulocytes undergo apoptosis thereby allowing their recognition and clearance by

Phagocytes using mechanisms that down-modulate the inflammatory response.

Although there is little doubt that apoptosis plays a critical role in embryological

Morphogenesis and tissue remodeling, it’s precise role in inflammatory disease is

Still unclear, Evidence will be presented showing that inflammatory mediators and

Pharmacological agents can differentially modulate neutrophil and eosinophil

Apoptosis and alter macrophage phagocytosis of apoptotic cells. For example, we

Believe that the powerful anti-inflammatory glucocorticoids may be using the above

Processes to selectively induce eosinophil (as well as lymphocyte) apoptosis and

Importantly enhance the clearance of the apoptotic cells. Thus the hypothesis that

Selective induction of neutrophil or eosinophil apoptosis and augmented non-

Phlogistic removal of apoptotic granulocytes by phagocytes as a potential therapeutic

Target will be discussed.