Previous experiments showed that nutritionally induced hypercholesteremia in mice caused an increase in susceptibility to coxsackievirus B, with a marked suppression of cellular infiltrates in infected tissues and an increased mortality. The present studies demonstrated that a hypercholesteremic diet was associated with an inhibition in host resistance as measured by susceptibility to Listeria monocytogenes infection and the growth of two transplanted syngeneic murine tumors. Moreover, the ability of Corynebacterium parvum to induce regression of a transplanted methylcholanthrene-induced fibrosarcoma was inhibited in hypercholesteremic hosts, as was the histiocytic infiltration normally accompanying C. parvum inoculation. In contrast, the peritoneal macrophages from C. parvum-treated hypercholesteremic mice were indistinguishable from similarly treated macrophages from normal mice with respect to their in vitro tumoricidal activity and the presence of a cell surface antigen associated with activated macrophages. Hypercholesteremia was also associated with a decreased antibody response to sheep erythrocytes in vivo, but did not appear to exert a detrimental effect on Bor T-cell blastogenesis when tested in vitro. The findings that the hypercholesteremic diet was associated with an impairment in the host immune response and increased susceptibility to viral, bacterial, and tumor cell challenge are discussed with respect to virus-lipid interactions in the pathogenesis of atherogenesis and diabetes mellitus.Hyperlipemia, particularly hypercholesteremia, has long been recognized as one of the independent risk factors associated with atherosclerosis (35, 39) as well as being a complication of diabetes mellitus (5,27,28). Previous studies demonstrated that a hypercholesteremic (HCHOL) diet significantly augmented the susceptibility of outbred mice to coxsackievirus B infection and induced a more severe and divergent pathology than observed in coxsackievirus B-infected normal mice (6, 31). Histopathological examination of tissue sections from these animals revealed that the marked inflammatory infiltrate which normally occurred in coxsackievirus infection was conspicuously absent in HCHOL mice, suggesting a diet-mediated immunological impairment (31). Observation that resistance to coxsackievirus B3 is dependent on the function of the reticuloendothelial system (42,43), whereas lipids may act as modulators of this system's function, are consistent with these findings (8,12).Dietary fats have been shown to increase the t Present address: Division of Microbiology, School of Dentistry, Marquette University, Milwaukee, WI 53233. incidence of 7,12-dimethyl-benz-a-anthracene-(21) or diethylstilbesterol-induced (13) mammary tumors as well as increasing the number of eye, ear duct, and liver tumors in animals fed high-fat diets and treated with 2-acetylaminofluorene (14). Although the mechanism(s) by which high-fat diets promote tumor growth is unknown, suppression of the immune system may be in part related to this effect. Both...
Staining methods for determining fungal viability are usually assessed by comparisons with enumeration of colony-forming units (CFU) on solid media. The purpose of the present study was to compare viability as assessed by the acridine orange (AO) and M T T methods with the numbers of CFUs obtained for Candida albicans yeast cells undergoing prolonged incubation in distilled water. In initial assessments of the assays using various proportions of control and heat-killed C. albicans, the A 0 and M T T methods consistently indicated significantly higher values for viability than did CFU determinations. Experiments using organisms cultured overnight revealed that z 95 % of the cells were capable of dividing at least once in a microscopic proliferation assay, whereas only 69% were capable of forming colonies. Parallel assays comparing A 0 uptake and M T T reduction gave excellent agreement with the microscopic proliferation assay, but not with CFU determinations. Using organisms undergoing prolonged incubations in distilled water, much lower viabilities were obtained with the CFU method at 7 and 10 days than with the microscopic proliferation assay or the two staining methods. These results indicate that the A 0 and M T T assays correlate well with the ability of C. albicans to divide at
The minimal inhibitory concentrations of penicillin and six other antibiotics were determined for 66 oral black-pigmented Bacteroides isolates by using the National Committee for Clinical Laboratory Standards proposed standard agar dilution technique. These results plus iodometric determination of β-lactamase activity showed that oral isolates of black-pigmented Bacteroides are remaining relatively susceptible to commonly used antibiotics.
Suppression of aortic elastic tissue autofluorescence was achieved by employing a modification of Verhoeff's elastic tissue staining procedure. Consquently, coxsackievirus B antigen present in the aortic media was detected by conventional fluorescent antibody staining.
Mice fed a diet high in cholesterol, lard, and sucrose were shown to exhibit an impairment of specific immunity to Listeria monocytogenes. Whereas titers of L. monocytogenes in livers of normal mice decreased rapidly after 6 days of infection, L. monocytogenes persisted in livers of diet-fed mice. Adoptive transfer experiments indicated that L. monocytogenes-immune spleen cells are generated in diet-fed mice. However, the function of immune spleen cells from donors of either nutritional status was impaired in dietfed recipients. The results indicate that the site(s) of impairment of specific immunity to L. monocytogenes in diet-fed mice occurs at a stage beyond the generation of immune T-cells.
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