Direct activation of the J774.1 Murine macrophage cell line by mycoplasma arthritidis.

Viable Mycoplasma arthritidis and supernatants from M. arthriditis cultures produced marked morphological changes in the J774.1 continuous macrophage line similar to those seen during activation of these cells by Mycobacterium bovis BCG cell walls. The mycoplasma-treated macrophages developed pronounced tumoricidal activity against syngenic 3T12-3 target cells and developed an enhanced capacity for the killing of intracellular listeriae, including both virulent and laboratory-maintained strains. Increased acid phosphatase levels and [14C]glucosamine uptake were also seen. We conclude that mycoplasmas can profoundly alter the functions of macrophages, an event which may not only have in vivo significance with regard to disease pathogenesis, but which may pose considerable problems for in vitro work when unsuspected mycoplasma contamination is present.

Elimination of Mycoplasma hyorhinis infections from four cell lines.

Four monolayer mammalian cell lines were cured of Mycoplasma hyorhinis infections by cloning in microtiter dishes in the presence of tetracycline and kanamycin. During cloning, cultures were refed with fresh antibiotic containing medium every 2 or 3 d for 14 day and were then cultured without effective antibiotics for at least 21 d. From the four lines we recovered 29 clones, none of which were infected after treatment as judged by the lack of extranuclear fluorescence after staining with the fluorochrome Hoechst 33258, and by normal autoradiographic labeling of the cells by tritiated nucleosides. One clone from each line was tested further by attempted culture of mycoplasmas and was also judged to be uninfected. Infection has not reappeared in any of the clones after extensive culture in the absence of the effective antibiotics.

Linkage analysis of Von Recklinghausen neurofibromatosis: chromosomes 4 and 19.

This report describes a study that examines the hypotheses of genetic linkage between the autosomal dominant disorder neurofibromatosis (NF) and loci on human chromosomes 4 and 19. Twelve Utah families were evaluated for evidence of possible linkage of NF to six known markers on chromosome 4 and five markers on chromosome 19. Due to previous reports suggesting tight linkage of NF to the GC locus on chromosome 4 and the C3 (linked to myotonic dystrophy) locus on chromosome 19, these two markers were of particular interest. For the Utah families the cumulative LOD score for GC was -4.81 (r = 0.05). Cumulative LOD scores were -0.90 (r = 0.05) and -1.01 (r = 0.05) for C3 serum determinations and a C3 DNA polymorphism respectively. Linkage data is also included on all individual informative families for the GC and C3 loci to specifically address the question of heterogeneity. Linkage data is consistent with, but does not strongly support, the existence of heterogeneity implicating both the GC locus on chromosome 4 and the C3 locus on chromosome 19. A compilation of cumulative LOD scores from this and other current linkage studies produces values that in the absence of heterogeneity refute previous reports for tight linkage of NF to GC and to C3.