Paradoxical Synergistic Effects of Tumour Necrosis Factor and Interleukin 1 in Murine Gut-Derived Sepsis With Pseudomonas Aeruginosa

Matsumoto, Tetsuya; Tateda, Kazuhiro; Miyazaki, Shunichi; Furuya, Nobuhiko; Ohno, Akira; Ishii, Yoshikazu; Hirakata, Yoichi; Yamaguchi, Keizo

doi:10.1006/cyto.1998.0434

Cited by 12 publications

(13 citation statements)

References 34 publications

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“…12) This might explain the relative importance of bacterial loads in our complex model system, despite suppressive effects of FOF or even FOF ϩ on key cytokines for shock development in in vitro and in vivo studies solely relying on LPS. 12,15) Our conclusion is also in agreement with a very recent study of Giacometti et al where several cecropins and IPM provided significant protection against i.p. infection-mediated shock by equally reducing bacterial loads, even though IPM caused significantly higher release of endotoxin.…”

Section: Resultssupporting

confidence: 93%

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Time- and Dose-Dependent Effect of Fosfomycin on Suppression of Infection-Induced Endotoxin Shock in Mice.

Kawaguchi

Hasunuma

Kikuchi

et al. 2002

Biological & Pharmaceutical Bulletin

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Septic shock, systemic inflammatory response syndrome and multiple organ failure caused by infections correlate with high mortality. In infections with gram-negative bacteria, these systemic inflammatory responses are caused by lipopolysaccharide (LPS), the major component of the outer membrane. LPS triggers the production of various cytokines (TNF-a, IL-1b and IL-6 etc.), chemokines (IL-8 and monocyte chemoattractant protein 1 etc.), and biologically active components implicated in inflammation (tissue factor, platelet activating factor, prostaglandins, thromboxanes, leukotrienes and nitric oxide etc.) via toll-like receptor 4 (TLR4)-dependent or -independent pathways. 1-3) These substances play a pivotal role for triggering septic shock.Although several animal models for LPS-induced lethal shock have been developed, 4-6) they are not always satisfactory in terms of rapid clearance of LPS from the circulation and necessity of large quantity of LPS for causing lethal shock. Since these aspects are different from clinical cases, infection-induced shock models are necessary for analyzing the protective effect of antibiotics in vivo. When D-galactosamine (GalN)-sensitized mice were infected intraperitoneally (i.p.) with Escherichia coli or Pseudomonas aeruginosa and then treated with antibiotics, mice showed septic shock with differences in outcome, depending on different amounts of LPS released from bacilli by treatment with imipenem (IPM) and ceftazidime (CAZ). 7)b-Lactam antibiotics such as IPM block the final step of peptidoglycan biosynthesis in the outer membrane and preferentially bind to penicillin-binding protein-2 (PBP-2).8) As result, they cause rapid killing and spheroplast formation of gram-negative bacteria with relatively little release of LPS. 9)In contrast, fosfomycin (FOF) binds to UDP-N-acetyl-glucosamine enolpyruvate transferase and irreversibly inactivates this enzyme which catalyzes the first step of peptidoglycan biosynthesis in the bacterial cytoplasm. 10) Recently, interesting studies showed that FOF suppressed TNF-a production by human monocytes and murine macrophages stimulated with LPS. 11,12) We recently established a new endotoxin shock model based on infection with high numbers (10 8 colony forming units (CFU)) of attenuated Salmonella typhimurium. In this model severe thrombosis and liver dysfunction following lethal shock is observed in LPS-responder but not in LPSnonresponder mice, suggesting that this shock is potentially mediated by host responses to LPS released during infection. The result about suppression of TNF-a production by FOF and its enantiomer FOF ϩ encouraged us to investigate beneficial effects of FOF in infection-induced lethal models. We demonstrated in this study that the therapeutic effects of FOF and IPM were time-and dose-dependent using a novel endotoxin shock model. MATERIALS AND METHODSChemicals, Glassware and Plastics Heparin (1000 units/ml, Novo Nordisk A/S, Denmark), Endospecy ® (Seikagaku Corp., Tokyo), an endotoxin-free alkaline reagent consisting of 0....

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Section: Resultssupporting

confidence: 93%

“…For further experiments the oral route, although less effective, was chosen as the one later more suitable for patients. To base our results not only on inbred mice but also on more robust outbred strains and ensure compatibility to other studies, 12,15) ddY mice were used, which were found to die from LPS shock within 48 h (Fig. 1B).…”

Section: Resultsmentioning

confidence: 99%

Time- and Dose-Dependent Effect of Fosfomycin on Suppression of Infection-Induced Endotoxin Shock in Mice.

Kawaguchi

Hasunuma

Kikuchi

et al. 2002

Biological & Pharmaceutical Bulletin

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“…The increased IL-1b levels observed in the current study might suggest that Traumeel beneficially affects the septic process in a manner shown in prior studies. [25][26][27][28][29][30][31][32][33] …”

Section: Discussionmentioning

confidence: 99%

Effect of Traumeel S on Cytokine Profile in a Cecal Ligation and Puncture (CLP) Sepsis Model in Rats

Oberbaum

Spira²,

Lukasiewicz³

et al. 2011

The Journal of Alternative and Complementary Medicine

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“…Quinolones and macrolides have been reported to suppress the production of IL-1 or TNF from LPS-stimulated human monocytes (5,12). Furthermore, the administration of fosfomycin (FOF) led to a reduction in serum TNF alpha (TNF-␣) and IL-1␤ concentrations in LPS-stimulated mice (9). Clindamycin (CLI), which is effective against gram-positive and anaerobic bacteria, has been demonstrated to induce neutrophil phagocytosis in the host at subMIC levels (18,19).…”

mentioning

confidence: 99%

“…Morikawa et al (10) demonstrated that treatment with FOF in vitro resulted in the suppression of TNF and IL-1 release from LPS-stimulated human monocytes but an increase in IL-6 release. Furthermore, Matsumoto et al (9) reported that administration of FOF to LPS-stimulated mice resulted in reductions in TNF-␣ and IL-1␤ concentrations in serum and slight increases in IL-6 and IFN-␥ levels in serum. These results with FOF resembled our experimental results following the administration of CLI.…”

mentioning

confidence: 99%

Pretreatment of Mice with Clindamycin Improves Survival of Endotoxic Shock by Modulating the Release of Inflammatory Cytokines

Hirata

Hiramatsu

Kishi

et al. 2001

Antimicrob Agents Chemother

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Suppression of endotoxin release and subsequent production of inflammatory cytokines is crucial in the treatment of septic shock. We investigated the effect of clindamycin (CLI) on endotoxic shock induced in mice by Escherichia coli lipopolysaccharide (LPS). Mice were treated with CLI (160 to 600 mg/kg) or saline and then injected with E. coli LPS and D-(؉)-galactosamine intraperitoneally 0.5 h after CLI administration. Pretreatment with CLI significantly improved survival in a dose-dependent manner (CLI, at 160, 300, and 440 mg/kg) and significantly lowered the peak concentrations of tumor necrosis factor alpha and interleukin-1␤ (IL-1␤) in serum. However, the peak concentrations of IL-6 in the sera of CLI-treated mice were higher than in control mice. Our findings suggest that CLI alters LPS-induced inflammatory cytokine production and suppresses endotoxin-induced mortality in this murine model.

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Paradoxical Synergistic Effects of Tumour Necrosis Factor and Interleukin 1 in Murine Gut-Derived Sepsis With Pseudomonas Aeruginosa

Cited by 12 publications

References 34 publications

Time- and Dose-Dependent Effect of Fosfomycin on Suppression of Infection-Induced Endotoxin Shock in Mice.

Time- and Dose-Dependent Effect of Fosfomycin on Suppression of Infection-Induced Endotoxin Shock in Mice.

Effect of Traumeel S on Cytokine Profile in a Cecal Ligation and Puncture (CLP) Sepsis Model in Rats

Pretreatment of Mice with Clindamycin Improves Survival of Endotoxic Shock by Modulating the Release of Inflammatory Cytokines

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