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An infant had recurrent bacterial infections but failed to produce pus. His neutrophils migrated slowly and ingested particles at 15 per cent of the rate of normal. The secretion of granule contents into phagosomes was 2.5 times greater than the control when corrected for the impaired ingestion. Because of the neutrophil abnormalities the role of actin was studied. As compared with normal, fewer microfilament-rich pseudopodia were visible in the patient's neutrophils. Heavy meromyosin bound to microfilaments in both normal and the patient's glycerinated neutrophils, indicating that the filaments were actin polymers. The patient's and normal neutrophils contained equal quantities (13.8 and 14.3 per cent) of actin protein. However, seven times less of the patient's actin sedimented after polymerizing treatment with potassium chloride. The association of a poorly polymerizable actin in extracts of neutrophils exhibiting abnormal locomotion, ingestion and degranulation is evidence for the participation of this protein in these functions. (N Engl J Med 291: 1093–1099, 1974)
Boxer et al. (Thu,) studied this question.