Considering the high occurrence of profilin as an allergen in many plant species, the assumption was made that profilin might be an allergen in Hevea brasiliensis, a member of the latex producing Euphorbiaceae family. Using IgE-binding inhibition by purified profilins we demonstrated that profilin is an IgE-binding component in the cytosolic fraction of natural latex and, to a lower extent, in the rubber fraction. Thirty-five out of 36 sera containing IgE to ragweed-profilin reacted with profilin from latex, indicating structural homologies between profilins from latex and ragweed. A large percentage (59%) of these sera were found to be positive in CAP latex assay. The preincubation of these sera with purified ragweed profilin greatly inhibited the CAP latex. Because profilin is also present in banana extract, it is likely to be involved in cross-sensitivity to banana and latex. In a group of 19 individuals allergic to latex only two had anti-profilin IgE antibodies. Profilin was barely detectable on glove extract immunoblots, whereas some sera from patients allergic to latex reacted with a 15 kDa allergen which was not profilin. Consequently, IgE antibodies to latex-profilin is a questionable factor for sensitization of occupationally-exposed patients; however, sensitization to profilin should be taken into account when interpreting the results of latex IgE antibody assays.

The in-vitro intraphagocytic uptake and retention of azithromycin in both human polymorphonuclear leucocytes (PMN) and alveolar macrophages was measured by an improved high-performance liquid chromatography (HPLC) method that was approximately three-fold more sensitive than previous methods. Azithromycin was accumulated in PMN and alveolar macrophages (about 300-fold), with maximum uptake being obtained after incubation for 60 min. Azithromycin was eliminated only partially from the cells during the washing process, and was released slowly during re-incubation of phagocytic cells in antibiotic-free medium. This intracellular retention distinguishes azithromycin from most of the macrolides and quinolones which, in spite of high I/E ratios, are released rapidly from cells.

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The in-vitro and in-vivo uptake of spiramycin by human and animal alveolar macrophages was studied. In-vitro penetration was studied in guinea pig and human alveolar macrophages incubated in medium 199 at 37 degrees C containing spiramycin at various concentrations. Results were expressed as the cellular/extracellular concentration ratio (C/E). The in-vivo study was performed in patients receiving 500 or 1000 mg spiramycin every 8 h as a 1-h infusion on day 1. A single infusion was given on day 2, 2 h before serum and bronchoalveolar lavage (BAL) sampling. Spiramycin was assayed by HPLC, and by a microbiological assay. In guinea pig alveolar macrophages, the C/E ratio of spiramycin after 60 min at 37 degrees C was 20.3 +/- 6.5 when the concentration was 10 mg/l. In human alveolar macrophages, the C/E ratio was 21.3 +/- 8.7 at 5 mg/l spiramycin and 23.8 +/- 8.7 at 50 mg/l. The accumulated spiramycin was slowly released when the cells (guinea pig alveolar macrophages) were washed and re-incubated in antibiotic free medium. Spiramycin was able to penetrate the alveolar space. In BAL supernatant, spiramycin levels were about 24-fold the serum level (n = 6 patients), when the BAL/serum glucose ratios were used as the dilution estimate. Alveolar macrophage levels ranged from 17 to 210 mg/l (n = 6 patients receiving 500 mg spiramycin infusion). These results are consistent with the in-vitro data.

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