Altered Immune Functions in Hypercholesterolemic Monkeys

Fiser, Robert H.; Denniston, Joseph C.; McGann, Virginia G.; Kaplan, J. M.; Adler, William H.; Kastello, Michael D.; Beisel, William R.

doi:10.1128/iai.8.1.105-109.1973

Cited by 16 publications

(1 citation statement)

References 13 publications

(18 reference statements)

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“…Finally, increased susceptibility to coxsackievirus B5 has recently been detected in HCHOL animals with normal body weights (A. E. Campbell, R. M. Loria, G. E. Madge, and A. M. Kaplan, unpublished data). These results are also in good agreement with the observations of Fiser et al (16) which showed that monkeys fed a high-fat, high-cholesterol diet had impaired development of precipitating antibodies to ovalbumin-enhanced susceptibility to tuberculin antigen and an increased rate of clearance of colloidal carbon from blood. These observations strongly suggest that the data presented in this communication are not due to the lack of sufficient nutrition in the HCHOL mice but rather related to the lipid abnormalities induced by the diet.…”

Section: Discussionsupporting

confidence: 92%

Inhibition of host resistance by nutritional hypercholesteremia

Kos¹,

Loria²,

Snodgrass³

et al. 1979

Infect Immun

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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...

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Section: Discussionsupporting

confidence: 92%