Optimal assessment of the ability of children with recurrent respiratory tract infections to produce anti-polysaccharide antibodies.

Specific anti-polysaccharide antibody deficiency (SPAD) is an immune disorder. Diagnostic criteria have not yet been defined clearly. One hundred and seventy-six children evaluated for recurrent respiratory tract infections were analysed retrospectively. For each subject, specific anti-pneumococcal antibodies had been measured with two enzyme-linked immunosorbent assays (ELISAs), one overall assay (OA) using the 23-valent pneumococcal polysaccharide vaccine (23-PPSV) as detecting antigen and the other purified pneumococcal polysaccharide serotypes (serotype-specific assay, SSA) (serotypes 14, 19F and 23F). Antibody levels were measured before (n = 176) and after (n = 93) immunization with the 23-PPSV. Before immunization, low titres were found for 138 of 176 patients (78%) with OA, compared to 20 of 176 patients (11%) with the SSA. We found a significant correlation between OA and SSA results. After immunization, 88% (71 of 81) of the patients considered as responders in the OA test were also responders in the SSA; 93% (71 of 76) of the patients classified as responders according to the SSA were also responders in the OA. SPAD was diagnosed in 8% (seven of 93) of patients on the basis of the absence of response in both tests. Thus, we propose to use OA as a screening test for SPAD before 23-PPSV immunization. After immunization, SSA should be used only in case of a low response in OA. Only the absence of or a very low antibody response detected by both tests should be used as a diagnostic criterion for SPAD.

Effect of cytochalasin B on 3-O-[(14)C]-methyl-D-glucose or D-[U-(14)C]glucose handling by BRIN-BD11 cells.

The present study aimed to investigate the effects of cytochalasin B (20 μM) on the uptake of 3-O-[(14)C]-methyl-D-glucose or D-[U-(14)C]glucose (8.3 mM each) by BRIN-BD11 cells. Taking into account the distribution space of tritiated water ((3)HOH), which was unexpectedly increased shortly after exposure of the cells to cytochalasin B and then progressively returned to its control values, and that of L-[1-(14)C]glucose, used as an extracellular marker, it was demonstrated that cytochalasin B caused a modest, but significant inhibition of the uptake of D-glucose and its non-metabolized analog by the BRIN-BD11 cells. These findings resemble those observed in acinar or ductal cells of the rat submaxillary gland and displayed a relative magnitude comparable to that found for the inhibition of D-glucose metabolism by cytochalasin B in purified pancreatic islet B cells. These findings reinforce the view that the primary site of action of cytochalasin B is located at the level of the plasma membrane.