Effects of Acute Infection on Cholesterogenesis in the Rhesus Monkey

Rh, Fiser; Jc, Denniston; Rb, Rindsic; Wr, Beisel

doi:10.3181/00379727-138-35951

Cited by 19 publications

(5 citation statements)

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“…This possible relationship between cholesterol and immune functions might also explain altered depressed responses to vaccines during a viral illness. We previously reported enhanced cholesterol utilization in both man and rhesus monkey during experimental viral and bacterial infections (8,9,12). Although at present it is highly speculative, increased cholesterol utilization and degradation possibly mediated through the RES (4) might alter ability of the host to take up and process antigens.…”

Section: Discussionmentioning

confidence: 99%

Altered Immune Functions in Hypercholesterolemic Monkeys

et al. 1973

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Humoral and cellular immune responses to several antigens were compared in control and hypercholesterolemic groups of monkeys. Chronic hypercholesterolemia, with concomitant hyperphospholipidemia and hypotriglyceridemia, was produced experimentally by feeding monkeys a high-fat, high-cholesterol diet. When studied prior to infection, hypercholesterolemic monkeys exhibited impaired development of precipitating antibodies against ovalbumin, enhanced sensitivity to tuberculin antigen (stimulated apparently by mycobacterial components in complete Freund adjuvant), and an increased rate of clearance of colloidal carbon from blood. During pneumococcal infection the ability of neutrophiles from hypercholesterolemic monkeys to reduce nitroblue tetrazolium dye showed an increase greater than that of control monkeys; both groups exhibited increased but comparable final clearance rates of colloidal carbon, although the increment of increase was smaller in hypercholesterolemic monkeys.

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Section: Discussionmentioning

confidence: 99%

Altered Immune Functions in Hypercholesterolemic Monkeys

et al. 1973

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“…Gram positive infections induce cytokine cascades similar to those of LPS and can also lead to septic shock (34)(35)(36)(37)(38)(39). Although less well studied than gram-negative infections, there is evidence that gram positive infection leads to similar disturbances in lipid metabolism (40)(41)(42)(43)(44)(45). Gram-positive organisms can affect both lipoprotein production and lipoprotein clearance (43)(44)(45).…”

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confidence: 99%

Lipoproteins inhibit macrophage activation by lipoteichoic acid

Grünfeld

Marshall

Shigenaga

et al. 1999

Journal of Lipid Research

121

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Regulation of lipid metabolism during infection is thought to be part of host defense, as lipoproteins neutralize endotoxin (LPS) and viruses. Gram-positive infections also induce disturbances in lipid metabolism. Therefore, we investigated whether lipoproteins could inhibit the toxic effects of lipoteichoic acid (LTA), a fragment of grampositive bacteria. LTA activated RAW264.7 macrophage cells, stimulating production of tumor necrosis factor (TNF) in a dose-dependent matter, but produced less TNF than that seen after LPS activation. High density (HDL) or low density lipoprotein (LDL) alone inhibited the ability of LPS to stimulate TNF production, but had little effect on the activation by LTA. When a maximally effective dose of LTA was mixed with lipoproteins and 10% lipoprotein-depleted plasma (LPDP), the ability of LTA to stimulate macrophage production of TNF was inhibited. HDL, LDL, and the synthetic particle, Soyacal, when mixed with LPDP, were able to inhibit the ability of LTA to activate macrophages. Lipopolysaccharide-binding protein (LBP) substituted for LPDP in catalyzing lipoprotein neutralization of LTA by HDL. Antibody to LBP inhibited the ability of LPDP to induce LTA neutralization by HDL. Thus, lipoproteins can prevent macrophage activation by fragments from both gram-positive and gram-negative microorganisms.-Grunfeld, C., M.

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“…Unchanged plasma cholesterol values after endotoxin ( Fig. 1) do not preclude the possibility that cholesterol turnover increased; studies in the rhesus monkey during gram-positive and gram-negative infections have documented markedly increased rates of cholesterol turnover [8] with unchanged plasma concentrations.…”

Section: Resultsmentioning

confidence: 96%

Endotoxemia in the Rhesus Monkey: Alterations in Host Lipid and Carbohydrate Metabolism

1974

Pediatr Res

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ExtractExperimentally induced endotoxemia in the rhesus monkey produced a two-to fourfold increase in plasma triglyceride concentration; glucose administration partially prevented this rise. Plasma free fatty acid and phospholipid values were depressed 40-50y0 of control values whereas cholesterol values were unchanged. Endotoxin-treated monkeys displayed slowed glucose disap~earance (K values, 2.2 versus 1.1) and higher levels of sugar in blood when given glucose (72 =t 8 mg/ 100 ml versus 15 1 + 1 1 mg/ 100 ml). These studies indicate that endotoxin has a marked effect on the pattern of substrate utilization by the host. SpeculationAlterations in lipid and carbohydrate metabolism affecting substrate utilization of the host may account for many of the clinicopathologic events associated with endotoxemia. Therapeutic measures designed to increase the availability of metabolic fuels for efficient cellular fuel utilization might be of value to patients during endotoxemia.

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Effects of Acute Infection on Cholesterogenesis in the Rhesus Monkey

Cited by 19 publications

References 1 publication

Altered Immune Functions in Hypercholesterolemic Monkeys

Altered Immune Functions in Hypercholesterolemic Monkeys

Lipoproteins inhibit macrophage activation by lipoteichoic acid

Endotoxemia in the Rhesus Monkey: Alterations in Host Lipid and Carbohydrate Metabolism

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