A year-long prospective study of 152 Bangladeshi children with mild to moderate protein-calorie malnutrition related nutritional status and cellular immune defects to morbidity due to diarrheal, respiratory, and febrile diseases. In children older than 36 mo, wasting correlated with skin test anergy to three recall antigens and with inability to initiate hypersensitivity to dinitrochlorobenzene. In this older age group, anergy was associated with a 58% increased attack rate and an 83% increased duration of diarrheal diseases but not with febrile or respiratory infections. In stepwise regression analysis, this anergy effect was independent of the small negative impact of poorer nutritional status on morbidity. Ninety-three percent of diarrheal illnesses lasting at least 14 d were among anergic children. Cellular immune incompetence, indicated by anergy of unknown etiology, is associated with increased diarrheal morbidity and may promote the vicious cycle of repeated infections and deteriorating nutritional status.
The results from this study suggest that the large nul cell lymphocyte population seen in patients with Shigella dysentery, does contain a sub-population of cells that will respond in vitro to thymopoietin, a bovine thymic extract, by increased E-rosette formation. It is felt that this sub-population is in fact immature T-cells. A previous study has shown that an unusual leukaemoid reaction develops in a substantial number of patients with Shigella dysentery. The leukaemoid response was primarily granulocytic in nature but there was also a substantial increase in the mean number of lymphocytes. The proportion of the various populations of lymphocytes from leukaemoid and non-leukaemoid subjects were altered, B-cells remained constant, while the T-cells were depressed with a corresponding rise in the proportion of nul cells. The cumulative results of this and other studies demonstrate that the T-cell arm of immunity is compromised in shigellosis. Indeed the degree of compromise may ultimately be the decisive factor in determining the severity of this disease.
We describe, for the measurement of 6-keto prostaglandin F1 alpha in biological media, a solid-phase immunoassay with immobilized antibodies that requires a total processing time of less than 2 h with hands-on time less than 30 min for 40 samples. The method combines the convenience of the microplate format with the sensitivity of radiolabeled prostaglandin derivatives as tracers in a competitive immunoassay. The intra- and interassay variations at 50% displacement of the radiolabeled prostaglandin derivative as tracer were 9.0% and 11.8%, respectively. At 50% displacement of the radiolabeled tracer, the sensitivity is about 20 pg per well. Optimal incubation time is between 60 and 90 min. Nonspecific binding was less than 1% if about 8 pg of tracer (approximately 25,000 counts/min per well) was used. Inhibition curves of samples in different dilutions were parallel to standard curves. The variation of bound radiolabeled prostaglandin derivative within the wells of one microplate (n = 96) was less than 3%. Human plasma samples and medium from tissue culture assayed for 6-keto prostaglandin F1 alpha correlated well with results obtained with a solid-phase assay based on use of magnetic particles (r = 0.99, n = 24 for culture-medium samples; r = 0.99; n = 26 for plasma samples.
Fifty Bangladeshi children with severe protein-calorie malnutrition were randomly allocated at admission to four groups and sensitized to dinitrochlorobenzene either immediately or after 1, 2, or 3 wk of protein-calorie replacement therapy. Ability to initiate cutaneous hypersensitivity to dinitrochlorobenzene on admission was impaired when the total serum proteins was less than 5.5 g/dl, but uniformly recovered after 1 wk of feeding. Three severely malnourished children with total serum proteins less than 4.5 g/dl in whom sensitization was attempted before refeeding failed to respond despite repeated challenge, suggesting immunological tolerance to dinitrochlorobenzene. The data support the concept of a threshold serum protein level, at least as an indicator, below which cellular immunity may be temporarily, or even permanently, impaired.
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