{'fraction_non_alphanumeric': 0.009900990099009901, 'fraction_numerical': 0.009075907590759076, 'mean_word_length': 5.738888888888889, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Relation between serum opsonic activity for Streptococcus pneumoniae and complement function in sickle cell disease.

Opsonic activity for Streptococcus pneumoniae mediated by the alternative and classic complement pathways and concomitant binding of activated C3 to the bacteria were measured in sera from children with sickle cell disease and normal siblings of similar age. Uptake of radiolabeled serotypes 7F, 10A, 15B, and 24F by normal human polymorphonuclear leukocytes and intracellular killing were the parameters used to assess opsonization. C3 fixation was quantitated by radioimmunoassay under conditions identical to those used for opsonic measurements. Both classic and alternative pathway-mediated opsonic activities were significantly reduced in a subset of patients. These alterations were associated with reduction in C3 fixation by way of the classic pathway and normal C3 fixation by way of the alternative pathway. The data implicate auxiliary serum factors rather than an intrinsic defect in the complement system in the opsonic alterations. Retrospective data were suggestive of an increased incidence of pneumococcal bacteremia occurring in association with reduction in opsonic activity.