Role of the hepatic function in the development of the pyrogenic tolerance to muramyl dipeptide

Ferreira, Márcia E. S.; Coelho, Márcio M.; Pelá, Irene Rosemir

doi:10.1152/ajpregu.2001.281.1.r162

Cited by 10 publications

(5 citation statements)

References 38 publications

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“…Those stimuli include peptidoglycan, 25-hydroxy-cholesterol, tissue ischemia, and surgical stress [27][28][29][30]. In this study, we demonstrated that portal congestion and subsequent visceral congestion also induced LPS tolerance in rats following PTO.…”

Section: Discussionmentioning

confidence: 50%

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

Unno

Uchiyama

Yamamoto

et al. 2006

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 50%

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

Unno

Uchiyama

Yamamoto

et al. 2006

Journal of Surgical Research

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“…At least some TLR2 agonists from Gram-positive bacteria are known to cause fever when injected in rats (6,14), guinea pigs (17,35), rabbits (3), and cats (2). Neither does the present study rule out the possibility that LPS causes some of its thermoregulatory effects by acting on receptors other than TLR4.…”

Section: Discussionmentioning

confidence: 63%

Thermoregulatory responses of rats to conventional preparations of lipopolysaccharide are caused by lipopolysaccharide per se— not by lipoprotein contaminants

Steiner¹,

Chakravarty²,

Robbins³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Several TLR2-dependent responses of immunocytes to cLPS in vitro are triggered by endotoxin proteins and not by LPS itself. We tested whether any Tb response to cLPS from Escherichia coli 055:B5 is triggered by non-TLR4-signaling contaminants. A decontaminated (d) LPS preparation (free of endotoxin proteins) was produced by subjecting cLPS to phenol-water reextraction. The presence of non-TLR4-signaling contaminants in cLPS (and their absence in dLPS) was confirmed by showing that cLPS (but not dLPS) induced IL-1␤ expression in the spleen and increased serum levels of TNF-␣ and IL-1␤ of C3H/HeJ mice; these mice bear a nonfunctional TLR4. Yet, both cLPS and dLPS caused cytokine responses in C3H/HeOuJ mice; these mice bear a fully functional TLR4. We then studied the Tb responses to cLPS and dLPS in Wistar rats preimplanted with jugular catheters. At a neutral ambient temperature (30°C), a low (0.1 g/kg iv) dose of cLPS caused a monophasic fever, whereas a moderate (10 g/kg iv) dose produced a polyphasic fever. In the cold (20°C), a high (500 g/kg iv) dose of cLPS caused hypothermia. All Tb responses to dLPS were identical to those of cLPS. We conclude that all known Tb responses to LPS preparations are triggered by LPS per se and not by non-TLR4-signaling contaminants of such preparations. body temperature; fever; hypothermia; inflammation; Toll-like receptors; TLR2; TLR4; LPS INTRAVENOUS ADMINISTRATION of bacterial LPS preparations to laboratory animals is widely used to induce thermoregulatory responses associated with systemic inflammation. These responses are dependent on both the dose of LPS preparation and ambient temperature (T a ); for a review, see Ref. 27. For example, rats respond to LPS in a thermoneutral or supraneutral environment with fever, either monophasic (a single rise in deep body temperature caused by low, near-threshold doses) or polyphasic (several sequential rises in body temperature caused by higher doses) (29,30,32,33,37). At a subneutral T a , rats respond to LPS with either fever, hypothermia, or a combination of the two: a fever response is elicited by low doses; a mild hypothermic response followed by fever is elicited by intermediary doses; and pronounced hypothermia is elicited by high, shock-inducing doses (30,31,33,37).In vitro, conventional preparations of LPS activate immunocytes via signaling through both Toll-like receptor (TLR) 4 and TLR2 (5,15,43). However, these preparations contain highly active lipoprotein contaminants (so-called endotoxin proteins) that signal through TLR2 (16). Elimination of endotoxin proteins by phenol-water reextraction abolishes the ability of LPS preparations to produce TLR2-mediated effects (9,40) or to activate cells with a nonfunctional TLR4 (4,9,18,19,38). These observations indicate that endotoxin protein-free LPS preparations signal largely through TLR4 and not through TLR2. They also show that many effects of conventional LPS preparations are caused, in part, by TLR2-activating endotoxin protein contaminants; these effects include the acti...

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“…4 This refractory state of the host is not solely induced by LPS (endotoxin) but also by various other PAMPs. 5,6 Although the molecular mechanisms are not fully understood, 4 PAMP-mediated tolerance is characterized by a transient inactivation of TLR-mediated induction of distinct inflammatory genes (e.g. TNF-α).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide pretreatment of the udder protects against experimental Escherichia coli mastitis

Petzl¹,

Günther

Pfister³

et al. 2011

Innate Immun

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Exposure to pathogen-associated molecular patterns such as LPS can cause an immune refractory state in mammals known as endotoxin tolerance (ET), resulting in a decreased inflammatory response after pathogen contact. This ET concept was used to reduce the severity of an experimentally-induced clinical mastitis. Cows were pretreated with 1 µg LPS per udder quarter and challenged 72 h (group L72EC) or 240 h (group L240EC) later with 500 CFU Escherichia coli. Pretreated animals showed no leukopenia after challenge, no (L72EC), or only slightly (L240EC), elevated body temperature and significantly reduced systemic and local clinical scores compared with cows that were not pretreated. Whereas an increase of milk somatic cell count after the E. coli challenge was abrogated in L72EC animals, it was significantly delayed in the L240EC group. In both pretreated groups the bacterial load in milk was markedly reduced. Based on the expression of inflammation-related genes in lobulo-alveolar mammary tissue, the tolerizing effect of LPS pretreatment is based on the inhibited up-regulation of inflammatory (TNF-α, IL-6, CXCL8, CCL20) and anti-inflammatory genes (IL-10, IRAK-M). These findings indicate that the concept of ET may be usefully applied as mastitis prophylaxis facilitating a rapid response to microbial infection and avoiding dysregulated inflammation.

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Role of the hepatic function in the development of the pyrogenic tolerance to muramyl dipeptide

Cited by 10 publications

References 38 publications

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

Thermoregulatory responses of rats to conventional preparations of lipopolysaccharide are caused by lipopolysaccharide per se— not by lipoprotein contaminants

Lipopolysaccharide pretreatment of the udder protects against experimental Escherichia coli mastitis

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