Effects of Bacterial Endotoxin on Metabolism

Berry, L. Joe; Smythe, Dorothy S.; Young, Leona G.

doi:10.1084/jem.110.3.389

Cited by 77 publications

(17 citation statements)

References 28 publications

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“…Damaged mitochondria due to endotoxin result in hydropic degeneration in hepatocytes. 28 Therefore, functional changes such as the depletion of hepatic glycogen could point to impending liver damage during H. pylori infection.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori promotes hepatic fibrosis in the animal model

Goo

Lee

et al. 2009

Laboratory Investigation

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Helicobacter pylori infection has been reported to be very common in patients with chronic liver diseases, including cirrhosis. To elucidate the pathological effect of H. pylori infection on the progression of hepatic fibrosis, C57BL/6 mice and Sprague-Dawley rats were orally inoculated with H. pylori, and hepatic fibrosis was induced with carbon tetrachloride (CCl 4 ) administration. We observed the histopathological changes and the presence of H. pylori genes by PCR in the liver. Significant increase in the fibrotic score as well as in serum alanine aminotransferase and aspartate aminotransferase levels was shown in the CCl 4 þ H. pylori group compared with that in the CCl 4 -treated group. Compared with the CCl 4 -treated group, a-smooth muscle actin and transforming growth factor-b1 were enhanced; however, senescence marker protein-30, a multifunctional protein protecting hepatocytes against oxidative stress and apoptosis, was suppressed in the CCl 4 þ H. pylori group. The 16S rRNA (400 bp) was demonstrated by PCR for H. pylori genes from genomic DNA extracted from the liver, and H. pylori-infected mice showed 93.8% (15 of 16) seropositivity by contrast with seronegativity in all H. pylori-noninfected mice. In addition, immunohistochemical study against H. pylori showed positive antigen fragments in the liver of the infected groups. Consequently, our data suggest that H. pylori infection could be an important contributing infectious factor to the development of liver cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori promotes hepatic fibrosis in the animal model

Goo

Lee

et al. 2009

Laboratory Investigation

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“…No compound alone nor in combination with glucose was effective nor did any appear to potentiate endotoxin in a manner similar to tryptophan. Glucose was added to the metabolite since previous work from this laboratory (12) and elsewhere (13,14) has established the fact that endotoxin rapidly depletes carbohydrate reserves in the mouse and in other laboratory animals. The possibility exists, therefore, that available metabolic energy in the poisoned animal would be increased by the addition of substrate.…”

Section: Protection Of Mice Against E Cotl I2popolysaccharide ~Ith Cmentioning

confidence: 99%

Effects of Bacterial Endotoxins on Metabolism

Berry

1963

The Journal of Experimental Medicine

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The ability of certain adrenocortical hormones to protect experimental animals against the lethal effects of lipopolysaccharides derived from Gramnegative bacteria is well established (14). The underlying basis for this protection has not been determined. Brooke et al. (5) recently reported for several adrenocorticoids a lack of correlation between their antllnflammatory properties and their ability to protect against endotoxins. It is perhaps a matter of faith that leads one to the view that all such hormonal capabilities (and of other substances with pharmacological actions as well) are ascribable to primary biochemical or metabolic effects. The problem becomes a matter of detecting the significant enzymic "needle" from among the mammalian "haystack" of enzymes. A number of enzymes may become altered by hormonal injections after a suflficient delay but most of these changes are probably secondary or adaptive rather than primary. A hopeful way out of this challenging situation is to find alternate ways of modifying an enzyme to see if by both methods a protective effect against endotoxins results.Such an approach to the problem of corticoid protection against endotoxin is made possible by the work of Knox and Auerbach (6) and Feigelson et al. (7). These investigators have shown that an injection of cortisone into rats is followed within about 4 hours by a significant increase in liver tryptophan pyrrolase. The enzyme also becomes more active following an injection of tryptophan, probably as a result of induced enzyme formation.Very briefly, tryptophan pyrrolase, with hematin as cofactor, oxidatively converts tryptophan into formyl kynurenine which, in turn, is further degradated into nicotinic acid. The ultimate metabolic fate of tryptophan v/a this pathway is the incorporation of nicotinamide into the di-and triphosphopyridine nucleotides (DPN and TPN), compounds of major significance in the energy release by organisms.

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“…This alone is undeniable proof that the adrenal contributes in a major way to an animal's response to endotoxin. Cortisone given concurrently with an LDg0+ dose of heat-killed S. typhimurium protects to the extent that only about 20 per cent die (14). A greater total body carbohydrate remains in the surviving animals and, according to the data of Tables II and V, the kidney remains capable of keeping blood NPN and carcass NPN within normal limits.…”

Section: Discussionmentioning

confidence: 86%

“…The total combined nitrogen is 9.1 mg greater than that in control mice. Since cortisone protects against endotoxin when the two are administered simultaneously (14) (see data of Table II), cortisone was injected 3 hours after endotoxin with the results given in row 7 of Table V. Carcass N P N is above normal by an amount almost equal to the elevation found in urine of mice injected with cortisone alone. The total combined nitrogen augmented by the 1.0 mg found in the intestine is about the same in the presence of endotoxin as it was in its absence (37.3-28.2 = 9.1 versus 37.5-29.3 = 8.3).…”

Section: The Effect Of Dihydroergocornlne (Hydergine) On Urinary Nitrmentioning

confidence: 99%

Effects of Bacterial Endotoxins on Metabolism

Berry

Smythe

1961

The Journal of Experimental Medicine

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An injection of either heat-killed Salmonella typMmurium or the lipopolysaccharide from any one of several different Gram-negative bacteria prevents or lowers, depending upon dosage, the increase in urinary nitrogen excreted by mice in response to an injection of adrenocorticotrophic hormone (ACTH) (1). All available evidence points to the fact that endotoxin is responsible for this effect and that the quantity required is inversely proportional to the toxicity of the specific preparation employed. The underlying physiological basis for this action of endotoxin, however, remains obscure.In order to place the problem in clearer perspective, the following facts have been established: (a) Fasted female mice weighing about 20 gm excrete in an overnight period (17 hours) between 13 and 14 mg urinary nitrogen. This quantity is depressed slightly but not by a statistically significant amount following intraperitoneally administered endotoxin at dosage levels sublethal but toxic for mice (2).(b) Fasted mice injected subcutaneously with 0.5 to 8 units of ACTH (Armour's acthar gel) excrete overnight about 29 mg urinary nitrogen (2).(c) Fasted mice injected subcutaneously with 5 mg cortisone acetate excrete overnight about 21 mg urinary nitrogen (2).(d) An LDa0 dose of endotoxin fails to alter the urinary nitrogen excreted after an injection of cortisone while a toxic but sublethal dose of endotoxin either prevents completely or lowers in proportion to dose the elevation in nitrogen excreted after an ACTH injection. It is the latter effect that serves as the previously described assay for endotoxin (1).It is reasonable to assume from reports in the literature (3) that the rise in urinary nitrogen excreted by normal mice given ACTH results, at least in

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Effects of Bacterial Endotoxin on Metabolism

Cited by 77 publications

References 28 publications

Helicobacter pylori promotes hepatic fibrosis in the animal model

Helicobacter pylori promotes hepatic fibrosis in the animal model

Effects of Bacterial Endotoxins on Metabolism

Effects of Bacterial Endotoxins on Metabolism

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