No drawback to the incorporation of dexamethasone in the standard therapy plan for CAP was found with respect to the pneumococcal immune response. Footnotes Published ahead of printing 29 February 2012 REFERENCES 1. damping of the systemic inflammatory response (10). Although these providers suppress primarily cell-mediated immunity, they can also impact humoral immunity (1, 3, 6, 7). In this study, we investigated the potential negative effect of dexamethasone on the formation of pneumococcal antibodies during CAP. Patients participated inside a double-blind, placebo-controlled trial investigating the effect of dexamethasone therapy on the space of hospitalization for CAP (8). All individuals were above 18 years of age and nonimmunocompromised. Individuals were randomized to receive 5 mg dexamethasone or a placebo once a day time for the 1st 4 days after hospital admission. In the present study, only individuals in whom was diagnosed as the causative agent were included. They were individuals having a positive blood or sputum tradition with or having a positive urine antigen test (BinaxNOW). Pneumococcal strains were serotyped from the Quellung reaction. Serum samples for antibody measurements were obtained from day time 0 to day time 3 (baseline samples) and from day time 11 to day time 100 (convalescent-phase samples) after hospital admission. Excluded were individuals with a period of symptoms of more than 10 days before admission, because in these cases, a possible immune response in the onset of disease would remain undetected. The concentrations of IgG against 14 pneumococcal serotypes were measured using the Luminex XMAP Pneumococcal Immunity Panel (Luminex Corporation, Austin, TX). The serotypes included in this panel are 1, 3, 4, 6B, 7F, 8, 9N, 9V, 12F, 14, 18C, 19A, 19F, and 23F (Danish nomenclature). A positive immune response was defined as at least a 2-collapse antibody concentration increase between the baseline and convalescent-phase serum samples with an end concentration of at least 0.35 g/ml (16). If the increase in antibody against a certain serotype was at least 2-collapse higher than the increase in antibody against some other serotype, it was determined to become the infecting serotype (16). Statistical significance of the difference between the immune response rates of the dexamethasone- and placebo-treated organizations was determined by using the 2 2 test. In individuals in whom the infecting serotype could be identified, the mean concentrations of antibody against the infecting serotype in both the baseline and convalescent-phase samples were compared between the treatment organizations from the College student test. A value of 0.05 SARP2 was considered to represent a statistically significant difference. In the original trial, 304 individuals were enrolled, GRI 977143 of which 151 were randomized to receive dexamethasone and 153 were randomized to receive a placebo (Fig. 1). The baseline characteristics of the individuals in the two treatment organizations were comparable. was identified as the causative agent of CAP in 64 individuals, 35 in the dexamethasone group and 29 in the placebo group. Three and two individuals in both organizations, respectively, were excluded due to a period of symptoms of more than 10 days before admission. Representative baseline and convalescent-phase serum samples for antibody measurements were available for 48 individuals, 25 individuals in the dexamethasone group and 23 GRI 977143 individuals in the placebo group, the total quantity of individuals included in this study. Pneumococcal strains isolated from 22 of the 48 pneumococcal pneumonia individuals were serotyped; in 18 instances, the etiological analysis was centered solely on a positive urine antigen test, which made serotyping impossible, and in 8 instances, the isolate was not available for serotyping. The most frequently recognized serotype was serotype 1 (= 6), followed by 7F (= 3), 4, 8, 14, and 9V (all = 2). A pneumococcal immune response was elicited in a total of 31 individuals (2-collapse increase in antibody concentrations in time and an end concentration of 0.35 g/ml), 18 (72%) of 25 individuals in the dexamethasone group compared to 13 (57%) of 23 individuals in the placebo group (difference nonsignificant [NS]). In 19 of these individuals (11 in the dexamethasone group and 8 in the placebo group), the infecting pneumococcal serotype could be determined because the increase in the concentrations of antibody against this serotype was at least 2-collapse higher than the increase in the concentrations of antibody against some other serotype. All but one serotype-specific antibody reactions corresponded to the type of the isolated strain identified with the Quellung reaction; in one patient infected with serotype 6A, serotype 6B was identified to become the infecting serotype by a positive immune response. The mean baseline GRI 977143 concentration of antibody against the infecting serotype was 0.45 (range, 0.03 to 1 1.90; standard error [SE], 0.16) g/ml in the dexamethasone group compared to 0.39 (range, 0.01 to 0.87; SE, 0.12) g/ml in the placebo group (NS) (Fig. 2). The end concentrations were 6.00.