A; KRP, Krebs-Ringer phosphate buffer; MEM, minimal essential medium; MEM-S, 15% heat inactivated guinea pig serum; MIF, migration inhibitory factor; OCB-BGG, orthochlorobenzoyl bovine gamma globulin; PEC, peritoneal exudate ceils; PPD, purified protein derivative.
We conducted a case-control study to evaluate the effectiveness of BCG vaccination in preventing childhood tuberculosis (TB) in Cali, Colombia. We ascertained 178 cases aged 0 to 14 years from the respiratory clinics with cough or fever for at least three weeks and a positive chest X-ray for TB, as well as 320 controls who were from the same households but had no symptoms and negative X-rays. Using matched set multiple logistic regression analysis, we found the age- and sex-adjusted relative risk (RR) of TB among vaccinees compared with non-vaccinees to be 0.84 with 95% confidence limits (CL) from 0.43 to 1.62. There was, however, a significantly lowered relative risk of TB with increasing time since vaccination (RR = 0.83 per year since time of vaccination with 95% CL from 0.74 to 0.94.)
Sera from guinea pigs given niridazole, an anti-schistosomal compound, have been shown to reversibly block the production of antigen-induced migration inhibitory factor by sensitized guinea pig lymph node cells. Since niridazole itself has no effect in vitro, the blockade of production of migration inhibitory factor is probably due to drug metabolites in the serum. We report here further studies on the mechanism of this drug-induced suppression of cellular hypersensitivity; the data show that niridazole active serum does not block the production of migration inhibitory factor once it has been initiated. Indeed, if niridazole active serum is added as little as 60 sec after the addition of antigen, the lymphocytes will produce migration inhibitory factor. These results suggest the presence of at least two stages in production of migration inhibitory factor after the addition of antigen to lymphocytes. The first, lasting less than 60 sec, is susceptible to lockade by niridazole active serum; the second is not. The elucidation of the mechanism of this blockade should lead to further understanding of the early events after antigen triggering of sensitized lymphocytes. In recent studies, it has been shown that niridazole, an antischistosomal compound, will markedly suppress a number of manifestations of cellular hypersensitivity. These include granuloma formation, delayed footpad swelling, and graft rejection in mice (1, 2), as well as delayed hypersensitivity skin reactions in man (3) and guinea pigs (4). On the other hand, niridazole only suppresses antibody responses minimally (5).In studying the mechanism of the suppression of cellular hypersensitivity, we found that sera obtained from guinea pigs given a single dose of niridazole would block the production of migration inhibitory factor (MIF) by sensitized lymph node cells in vitro (4). This blockade was reversible. Since niridazole itself had no effect in vitro, the blockade of MIF production is probably due to drug metabolites in the serum. For the sake of simplicity, the sera from niridazoletreated animals is referred to as "niridazole active serum" or NAS.The studies reported here were undertaken to further analyze the mechanism of this drug-induced suppression of cellular hypersensitivity; the data indicate that NAS will not block the production of MIF once it has been initiated. Indeed, it was surprising to find that if NAS was added to cells as little as 60 sec after the addition of antigen, the lymphocytes produced MIF. The results reveal the presence of at least two stages in MIF production after the addition of antigen to lymphocytes. The first, lasting less than 60 sec. is susceptible to blockade by NAS; the second is not susceptible. The elucidaAbbreviations: MIF, migration inhibitory factor; NAS, niridazole active serum; NGPS, normal guinea pig serum; OCB-BGG, orthochloro-benzoyl chloride-bovine gamma globulin.
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