The increased potential for the production of inflammatory cytokines by Kupffer cells and splenic macrophages eight days after thermal injury

Wu, Jun-Zheng; Ogle, Cora K.; Mao, J.-X.; Szczur, Kathy; Fischer, Josef E.; Ogle, James D.

doi:10.1007/bf01539133

Cited by 35 publications

(12 citation statements)

References 30 publications

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“…This is consistent with the report of Wu et al that the plasma levels of TNF-α were undetectable in rats on day 8 following burn injury. 19 However, the plasma TNF-α concentrations were higher than the detection limit of the kit in 75% of the TPN-fed animals. Previous animal studies have shown that the plasma TNF-α concentration is significantly increased in rats infused with TPN than that in rats fed with TEN after endotoxin injection and bacterial intraperitoneal challenge.…”

Section: Discussionmentioning

confidence: 98%

Route of Feeding Influences the Production and Expression of Tumor Necrosis Factor α in Burned Rats

Cui¹,

Iwasa²,

Kuge

et al. 2001

Surgery Today

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The effect of nutritional route on tumor necrosis factor alpha (TNF-alpha) production in burned rats was examined. Scald burns covering about 30% of the whole body surface area were inflicted on 43 male Wistar rats weighing about 200g. The animals were divided into three groups: CHOW (n = 10), total parenteral nutrition (TPN) (n = 22), and total enteral nutrition (TEN) (n = 11), continuously given a chow diet, TPN solution, or an enteral diet, respectively, for 7 days after the burn injury. The rate of detection of TNF-alpha in plasma on day 7 was significantly higher in the TPN group than in the CHOW or TEN groups. The messenger RNA (mRNA) expression of TNF-alpha was significantly increased in the spleen, lungs, liver, and ileum of the rats receiving TPN compared with the CHOW and TEN rats. On the other hand, the expression of TNF-alpha mRNA was markedly decreased in the thymus of the TPN group compared with the CHOW group. The mortality rate in the TPN group (63.6%) was higher than that in the CHOW (0.0%) or TEN (27.3%) groups on day 7 after burn injury. These data suggest that TPN increases the expression of TNF-alpha mRNA in organ tissues and systemic TNF-alpha production, and reduces the survival rate of rats after thermal injury, but TEN does not.

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Section: Discussionmentioning

confidence: 98%

Route of Feeding Influences the Production and Expression of Tumor Necrosis Factor α in Burned Rats

Cui¹,

Iwasa²,

Kuge

et al. 2001

Surgery Today

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“…As [18,22,30,31]. Thus, we were interested in determining if changes in TLR4 responses could contribute to the development of severe SIRS and MOF in a mouse injury model.…”

Section: Discussionmentioning

confidence: 99%

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

Murphy

Paterson

Kriynovich

et al. 2004

Journal of Leukocyte Biology

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Severe injury can initiate an exaggerated systemic inflammatory response and multiple organ failure (MOF) if a subsequent immune stimulus, "second hit", occurs. Using a mouse thermal injury model, we tested whether changes in innate immune cell reactivity following injury can contribute to the development of heightened inflammation and MOF. Using high-purity Escherichia coli lipopolysaccharide (LPS) to selectively stimulate Tolllike receptor 4 (TLR4), we demonstrate augmented interleukin (IL)-1␤, tumor necrosis factor ␣ (TNF-␣), and IL-6 production by 1 day but particularly, at 7 days after injury. The in vivo significance of enhanced TLR4 responsiveness was explored by challenging sham or burn mice with LPS at 1 or 7 days after injury and determining mortality along with in vivo cytokine and chemokine levels. Mortality was high (75%) in LPS-challenged burn but not sham mice at 7 days, although not at 1 day, after injury. Death was associated with leukocyte sequestration in the lungs and livers along with increased proinflammatory cytokine and chemokine levels in these organs. Blocking TNF-␣ activity prevented this mortality, suggesting that excessive TNF-␣ production contributes to this lethal response. These findings demonstrate the potential lethality of excessive TLR4 reactivity after injury and provide an explanation for the exaggerated inflammatory response to a second hit, which can occur following severe injury. J. Leukoc. Biol. 77: 16 -23; 2005.

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“…Acting via cytokine-receptor interactions, intracellular signaling pathways, and ultimately influencing transcription factors, these cytokines are able to modulate the promoter regions of multiple acute phase proteins. [5][6][7] Although the effects that individual and small combinations of cytokines have on acute phase protein production have been well described, the temporal sequence by which this occurs after burn injury has been poorly examined. Kataranovski 4 found a correlation between an increase in alpha 2 -microglobin and haptoglobin 12 hours after injury, a concominant increase in serum IL-6 activity at 6 and 12 hours after injury, and an increase in TNF-␣ activity at 12 hours after injury.…”

mentioning

confidence: 99%

The Early Acute Phase Response After Burn Injury in Mice

Plackett

Colantoni²,

Heinrich

et al. 2007

Journal of Burn Care & Research

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In the hours immediately after burn injury, the body enters into an acute phase reaction characterized, in part, by the augmentation of cytokine and acute phase protein production. This reaction has been poorly characterized in the 24 hours immediately after injury. To better understand the early acute phase response, 8- to 10-week-old BALB/C female mice were subjected to a 15% total body surface area (TBSA). Hepatic levels of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were monitored. In addition, the circulating level of serum amyloid A, an acute phase protein, also was measured at the same time points. Tumor necrosis factor-alpha levels peaked 2 hours after burn injury, whereas interleukin-1beta had a biphasic response, increasing 2 hours after injury and again at 12 hours. Interleukin-6 and serum amyloid A were not increased until 12 hours after injury and began to decline at 24 hours. These results demonstrate that within the liver, the acute phase response after burn injury initially involves tumor necrosis factor-alpha and interleukin-1beta, whereas interleukin-6 is not involved until later and that systemic serum amyloid A levels are not increased until interleukin-6 is also increased.

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The increased potential for the production of inflammatory cytokines by Kupffer cells and splenic macrophages eight days after thermal injury

Cited by 35 publications

References 30 publications

Route of Feeding Influences the Production and Expression of Tumor Necrosis Factor α in Burned Rats

Route of Feeding Influences the Production and Expression of Tumor Necrosis Factor α in Burned Rats

Linking the “two-hit” response following injury to enhanced TLR4 reactivity

The Early Acute Phase Response After Burn Injury in Mice

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