Alterations in cytokine/chemokine expression during organ-to-organ communication established via acetaminophen-induced toxicity

Neff, Simona B; Neff, Thomas; Kunkel, Steven L.; Hogaboam, Cory M.

doi:10.1016/s0014-4800(03)00096-0

Cited by 27 publications

(18 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hepatic TNF-␣, interleukin (IL)-4, IFN-␥, and IL-12 levels were determined via ELISA as previously described 23,25 and results expressed pg/mg protein (Bio-Rad, Mississaugua, ON, Canada).…”

Section: Methodsmentioning

confidence: 99%

CD154-CD40 interactions drive hepatocyte apoptosis in murine fulminant hepatitis

Zhou¹,

Ajuebor²,

Beck³

et al. 2005

Hepatology

View full text Add to dashboard Cite

The CD154 -CD40 interaction is a critical costimulatory pathway modulating the cellular immune response. Moreover, fulminant hepatitis of various etiologies is characterized by a hepatic influx of CD154-expressing T cells and an upregulation of CD40 expression on Kupffer cells and hepatocytes, implicating this pathway in the pathogenesis of fulminant hepatitis. In this study, we used a murine model of fulminant hepatitis induced by concanavalin A (con A) and documented a significant influx of CD154-expressing T cells into the livers of mice treated with con A, in association with markedly increased expression of CD40 restricted mainly to hepatocytes in damaged areas of the liver. Furthermore, con A hepatitis in CD154-deficient mice was significantly attenuated compared with that in wildtype controls and was associated with a decrease in hepatic tumor necrosis factor ␣ (TNF-␣) levels and hepatocyte death.

show abstract

Section: Methodsmentioning

confidence: 99%

CD154-CD40 interactions drive hepatocyte apoptosis in murine fulminant hepatitis

Zhou¹,

Ajuebor²,

Beck³

et al. 2005

Hepatology

View full text Add to dashboard Cite

show abstract

“…For peripheral TNF␣ blocking studies, BDR mice were injected intraperitoneally with 0.5 ml of either normal rabbit serum or anti-TNF␣ serum (kindly provided by Dr. C. Hogoboam, University of Michigan, Ann Arbor, MI) on days 2 and 4 postsurgery (Huffnagle et al, 1996;McCullough et al, 2000;Neff et al, 2003). MCP-1/CCL2 expression in microglia was examined (as above) on day 5 postsurgery (see Results).…”

Section: Model Of Peripheral Organ-specific Inflammatory Injurymentioning

confidence: 99%

Cerebral Microglia Recruit Monocytes into the Brain in Response to Tumor Necrosis Factorα Signaling during Peripheral Organ Inflammation

D’Mello¹,

Le²,

Swain³

2009

J. Neurosci.

563

505

View full text Add to dashboard Cite

In inflammatory diseases occurring outside the CNS, communication between the periphery and the brain via humoral and/or neural routes results in central neural changes and associated behavioral alterations. We have recently identified another immune-to-CNS communication pathway in the setting of organ-centered peripheral inflammation: namely, the entrance of immune cells into the brain. In our current study, using a mouse model of inflammatory liver injury, we have confirmed the significant infiltration of activated monocytes into the brain in mice with hepatic inflammation and have defined the mechanism that mediates this trafficking of monocytes. Specifically, we show that in the presence of hepatic inflammation, mice demonstrate elevated cerebral monocyte chemoattractant protein (MCP)-1 levels, as well as increased numbers of circulating CCR2-expressing monocytes. Cerebral recruitment of monocytes was abolished in inflamed mice that lacked MCP-1/CCL2 or CCR2. Furthermore, in mice with hepatic inflammation, microglia were activated and produced MCP-1/CCL2 before cerebral monocyte infiltration. Moreover, peripheral tumor necrosis factor (TNF)␣ signaling was required to stimulate microglia to produce MCP-1/CCL2. TNF␣ signaling via TNF receptor 1 (TNFR1) is required for these observed effects since in TNFR1 deficient mice with hepatic inflammation, microglial expression of MCP-1/CCL2 and cerebral monocyte recruitment were both markedly inhibited, whereas there was no inhibition in TNFR2 deficient mice. Our results identify the existence of a novel immune-to-CNS communication pathway occurring in the setting of peripheral organ-centered inflammation which may have specific implications for the development of alterations in cerebral neurotransmission commonly encountered in numerous inflammatory diseases occurring outside the CNS.

show abstract

“…All mice were deprived of food for approximately 18 h prior to APAP administration to reduce hepatic stores of glutathione (Neff et al, 2003). Female CB6F1 mice undergoing CR received a single intraperitoneal injection of APAP (Sigma) at 250 mg/kg body weight (20 ml/kg) in warm (37 °C) sterile PBS.…”

Section: Assessment Of Acetaminophen Resistancementioning

confidence: 99%

Stress resistance and aging: Influence of genes and nutrition

Harper

Salmon

Chang

et al. 2006

Mechanisms of Ageing and Development

View full text Add to dashboard Cite

Previous studies have shown that dermal fibroblast cell lines derived from young adult mice of the long-lived Snell dwarf (dw/dw), Ames dwarf (df/df) and growth hormone receptor knockout (GHR-KO) mouse stocks are resistant, in vitro, to the cytotoxic effects of hydrogen peroxide, cadmium, ultraviolet light, paraquat, and heat. Here we show that, in contrast, fibroblasts from mice on low-calorie (CR) or low methionine (Meth-R) diets are not stress resistant in culture, despite the longevity induced by both dietary regimes. A second approach, involving induction of liver cell death in live animals using acetaminophen (APAP), documented hepatotoxin resistance in the CR and Meth-R mice, but dw/dw and GHR-KO mutant mice were not resistant to this agent, and were in fact more susceptible than littermate controls to the toxic effects of APAP. These data thus suggest that while resistance to stress is a common characteristic of experimental life span extension in mice, the cell types showing resistance may differ among the various models of delayed or decelerated aging.

show abstract

Alterations in cytokine/chemokine expression during organ-to-organ communication established via acetaminophen-induced toxicity

Cited by 27 publications

References 18 publications

CD154-CD40 interactions drive hepatocyte apoptosis in murine fulminant hepatitis

CD154-CD40 interactions drive hepatocyte apoptosis in murine fulminant hepatitis

Cerebral Microglia Recruit Monocytes into the Brain in Response to Tumor Necrosis Factorα Signaling during Peripheral Organ Inflammation

Stress resistance and aging: Influence of genes and nutrition

Contact Info

Product

Resources

About