In a study appearing online on June 15 in advance of print publication in the July issue of the Journal of Clinical Investigation, Jamel El-Benna and colleagues from INSERM in Paris examine neutrophils from the joint fluid of rheumatoid arthritis patients and show that GM-CSF and TNF-alpha induce the phosphorylation of a serine residue at position 345 on a component of NADPH oxidase. This event, which occurs via ERK1/2 and MAPK signaling pathways, "primes" the enzyme for action at sites of inflammation. The authors suggest that using drugs that inhibit this phosphorylation step might prevent the exaggerated neutrophil response in inflammatory conditions like rheumatoid arthritis, yet still preserve the ability of neutrophils to fight infection.
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