Characterization of the febrile response induced by fibroblast-stimulating lipopeptide-1 in guinea pigs

Greis, Andrea; Murgott, Jolanta; Rafalzik, Sandra; Gerstberger, Rüdiger; Hübschle, Thomas; Roth, Joachim

doi:10.1152/ajpregu.00182.2007

Cited by 17 publications

(15 citation statements)

References 52 publications

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“…This relationship was confirmed by the use of TNF binding protein. TNFbp blocked the pyrogenic effect of FSL-1 and its ability to induce IL-6 expression (Greis et al, 2007). Zymosan, a yeast particulate, given to rats induced a fever and diminished a motivated behavior: decreased consumption of sweetened cereal (Cremeans-Smith and Newberry, 2003).…”

Section: Tlr2 Heterodimers and Tlr4: Membrane Lipidsmentioning

confidence: 99%

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

McCusker

Kelley

2013

Journal of Experimental Biology

358

259

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Sickness and depressionOver the past 30years, it has become clear that the immune system plays a critical role in animal behavior. This role is tightly linked to the obvious role that immune cell activation plays in the clearance of pathogenic organisms. Systemic or central infections elicit a group of symptoms that are necessary for the organism to conserve resources, reorganize priorities and limit the spread of the infection to other members of the community. This sickness behavior is a motivational state that is common to most pathogeninduced infections ranging from viruses to multicellular parasites, but, because of its ubiquitous nature, is frequently accepted as an unavoidable and non-specific consequence of infection. However, considering the broad spectrum of symptoms -fever, nausea, decreased appetite, malaise, fatigue and achiness -it seems clear that a highly organized, although not pathogen-specific, response is being manifested to aid in the fight against infection (Dantzer, 2001;Ericsson et al., 1995).We are all familiar with the human symptoms of sickness but, to investigate changes in behavior associated with sickness, it is critical to have reliable animal measurements that relate to changes in the affective state. Using preclinical animal models, sickness behavior is best evaluated when the test involves a means to assess motivation. Sickness behavior is frequently assessed as social exploration/investigation (in rodent models, this response is frequently reported as a decrease in time actively seeking interaction with a novel animal as a result of diminished motivation for social exploration or neophobia). Social exploration is a naturalistic behavior and all animals have a strong motivation, whether driven by curiosity or sexual desire. With this strong motivational stimulus, infections cause a strong differential between time of exploration of healthy and sick animals, with less time of exploration being observed with sick animals. Another simpler but effective model is exploration of the environment [often referred to as locomotor activity (LMA), representing some level of physical movement in a novel environment such as rearing, quadrant entry, line crossings or total distance traveled; all of which are highly correlated]. LMA is best conducted in a novel environment, as the motivation to explore is stronger in this

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Section: Tlr2 Heterodimers and Tlr4: Membrane Lipidsmentioning

confidence: 99%

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

McCusker

Kelley

2013

Journal of Experimental Biology

358

259

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“…Importantly, several studies (including in our laboratory) showed that TLR2, TLR5, and TLR9 agonists up-regulated PGE 2 in vivo [14], [16], [17]. While TLR2 and TLR9 agonists signal exclusively through adaptor molecule MyD88, TLR4 signaling may proceed via either MyD88 or through TRIF resulting in activation of interferon regulatory factor (IRF)-3 and a subsequent induction of the type 1 interferon (IFN-β) [18].…”

Section: Introductionmentioning

confidence: 96%

“…In addition to LPS, other TLR agonists have been shown to induce fever in animal models: the TLR2 agonists, macrophage-activating lipopeptide-2 (MALP-2) from Mycoplasma fermentans ( M. fermentans ), and a synthetic analogue of fibroblast-stimulating lipopetide-1 (FSL-1) spanning the NH 2 -termial sequence of a lipoprotein from M. salivarium , as well as TLR9 agonists synthetic oligonucleotide (ODN) of bacterial DNA CpG [15]–[17]. Importantly, several studies (including in our laboratory) showed that TLR2, TLR5, and TLR9 agonists up-regulated PGE 2 in vivo [14], [16], [17].…”

Section: Introductionmentioning

confidence: 99%

Differences in PGE2 Production between Primary Human Monocytes and Differentiated Macrophages: Role of IL-1β and TRIF/IRF3

et al. 2014

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Prostaglandin E2 (PGE2) is induced in vivo by bacterial products including TLR agonists. To determine whether PGE2 is induced directly or via IL-1β, human monocytes and macrophages were cultured with LPS or with Pam3CSK4 in presence of caspase-1 inhibitor, ZVAD, or IL-1R antagonist, Kineret. TLR agonists induced PGE2 in macrophages exclusively via IL-1β-independent mechanisms. In contrast, ZVAD and Kineret reduced PGE2 production in LPS-treated (but not in Pam3CSK4-treated) monocytes, by 30–60%. Recombinant human IL-1β augmented COX-2 and mPGES-1 mRNA and PGE2 production in LPS-pretreated monocytes but not in un-primed or Pam3CSK4-primed monocytes. This difference was explained by the finding that LPS but not Pam3CSK4 induced phosphorylation of IRF3 in monocytes suggesting activation of the TRIF signaling pathway. Knocking down TRIF, TRAM, or IRF3 genes by siRNA inhibited IL-1β-induced COX-2 and mPGES-1 mRNA. Blocking of TLR4 endocytosis during LPS priming prevented the increase in PGE2 production by exogenous IL-1β. Our data showed that TLR2 agonists induce PGE2 in monocytes independently from IL-1β. In the case of TLR4, IL-1β augments PGE2 production in LPS-primed monocytes (but not in macrophages) through a mechanism that requires TLR4 internalization and activation of the TRIF/IRF3 pathway. These findings suggest a key role for blood monocytes in the rapid onset of fever in animals and humans exposed to bacterial products and some novel adjuvants.

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“…Similarly, other investigators noted that circulating IL-6 levels remained unaffected after intra-arterial or peritoneal injection of diclofenac [26]. Moreover, investigating the modulatory effects of diclofenac on IL-6 and prostaglandin (PG) levels showed that diclofenac significantly decreased PGE2 production but had no significant effect on IL-6 levels [27].…”

Section: Discussionmentioning

confidence: 96%

Possible Potentiation by Certain Antioxidants of the Anti-Inflammatory Effects of Diclofenac in Rats

Abbas

Schaalan

Bahgat

et al. 2014

The Scientific World Journal

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In the present study, we investigated the potential beneficial impact of the addition of antioxidant supplements to diclofenac regimen in a model of carrageenan-induced paw. Rats were treated daily with antioxidants, that is, a-lipoic acid (50 mg/kg), selenium (2.5 mg/kg), vitamin C (1 g/kg), vitamin E (300 mg/kg), or zinc (25 mg/kg) on seven successive days and then received a single treatment with diclofenac or saline before carrageenan was injected to induce paw inflammation. The results indicated that these combinations did not significantly affect the percentage inhibition of paw edema caused by diclofenac alone; however, some combination treatments ameliorated signs of concomitant oxidative stress (such as alterations in plasma malondialdehyde (MDA) levels, hemolysate reduced glutathione levels, and erythrocytic superoxide dismutase enzyme activities) imparted by diclofenac alone. In some cases, few tested antioxidants in combination with diclofenac resulted in increased plasma levels of interleukin- (IL-) 6 and C-reactive protein (CRP). In conclusion, the results of these studies suggested to us that the added presence of natural antioxidants could be beneficial as standard anti-inflammatory therapeutics for a patient under diclofenac treatment, albeit that these effects do not appear to significantly build upon those that could be obtained from this common anti-inflammatory agent per se.

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Characterization of the febrile response induced by fibroblast-stimulating lipopeptide-1 in guinea pigs

Cited by 17 publications

References 52 publications

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

Differences in PGE2 Production between Primary Human Monocytes and Differentiated Macrophages: Role of IL-1β and TRIF/IRF3

Possible Potentiation by Certain Antioxidants of the Anti-Inflammatory Effects of Diclofenac in Rats

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