Abstract
Abnormalities of polymorphonuclear leukocyte (PMN) chemotaxis and phagocytosis have been described. In each instance the combined chemotactic and phagocytic defects were a consequence of an abnormality in humoral, not cellular, function. We now describe a 3½ year-old white male with recurrent pneumonia and skin infections associated with a cellular defect of PMN chemotaxis and phagocytosis, as well as a sex-linked form of congential agammaglobulinemia. He had normal delayed hypersensitivity and normal levels of hemolytically active whole complement and Cl thru C5. The impairments of PMN function were demonstrated in vitro by an inability of his PMNS to respond to chemotactic factors, to phagocytize S. aureus, and by abnormal MBT dye tests. These abnormalities were not corrected by the addition of normal serum to the patient's PMNs. Mo evidence was obtained for a humoral inhibitor of PMN function since normal PMNs were capable of normal chemotaxis and phagocytosis in the presence of his serum. In addition to the intrinsic granulocytic defect, the patient's serum was deficient in generating chemotactic activity for normal PMNs. The parent's PMNs were capable of normal chemotaxis and phagocytosis. It is not certain whether the patient's PMN abnormalities are the result of an acquired or an inherited defect. These studies demonstrate a previously unrecognized abnormality of PMN function, namely, an intrinsic defect of the PMN resulting in impaired chemotaxis and phagocytosis.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Steerman, R., Snyderman, R., Leikin, S. et al. Intrinsic defect of the polymorphonuclear leukocyte resulting in impaired chemotaxis and phagocytosis. Pediatr Res 5, 404 (1971). https://doi.org/10.1203/00006450-197108000-00139
Issue Date:
DOI: https://doi.org/10.1203/00006450-197108000-00139