Liver-lung interactions during E. coli endotoxemia. TNF-alpha:leukotriene axis.

Matuschak, George M.; Mattingly, Matthew; Tredway, T. L.; Lechner, Andrew J.

doi:10.1164/ajrccm.149.1.8111596

Cited by 45 publications

(59 citation statements)

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“…Kupffer cells in the liver detoxify and subsequently clear endotoxin from the portal circulation (58) and protect the lung in experimental models of sepsis and adult respiratory distress syndrome (59,60). However, if the capacity of the liver to clear an endotoxin challenge is exceeded, both inflammatory cytokines and unprocessed LPS can traverse into the systemic circulation and cause acute end organ damage (61)(62)(63). Support for this hypothesis is provided by clinical reports of acute noninfectious pulmonary toxicity associated with severe GVHD and venoocclusive disease (VOD) (2,64) and by our previous work demonstrating that exogenous LPS challenge of animals with extensive GVHD overwhelmed the capacity of the liver to detoxify the endotoxin surge and resulted in extensive hepatocellular damage and enhanced lung inflammation via a TNF-␣-mediated mechanism (16).…”

Section: Discussionmentioning

confidence: 99%

Hyporesponsiveness of Donor Cells to Lipopolysaccharide Stimulation Reduces the Severity of Experimental Idiopathic Pneumonia Syndrome: Potential Role for a Gut-Lung Axis of Inflammation

Cooke

Hill

Gerbitz

et al. 2000

The Journal of Immunology

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Idiopathic pneumonia syndrome (IPS) is a major complication of allogeneic bone marrow transplantation (BMT). We have shown that experimental IPS is associated with increased levels of LPS and TNF-α in the bronchoalveolar lavage (BAL) fluid. We hypothesized that the deleterious effects of these inflammatory mediators in the lung may be linked to gut injury that develops after BMT. To test this hypothesis, we used mouse strains that differ in their sensitivity to LPS as donors in an experimental BMT model. Lethally irradiated C3FeB6F1 hosts received BMT from either LPS-sensitive or LPS-resistant donors. Five weeks after BMT, LPS-resistant BMT recipients had significantly less lung injury compared with recipients of LPS-sensitive BMT. This effect was associated with reductions in TNF-α secretion (both in vitro and in vivo), BAL fluid LPS levels, and intestinal injury. The relationship between TNF-α, gut toxicity, and lung injury was examined further by direct cytokine blockade in vivo; systemic neutralization of TNF-α resulted in a significant reduction in gut histopathology, BAL fluid LPS levels, and pulmonary dysfunction compared with control-treated animals. We conclude that donor resistance to endotoxin reduces IPS in this model by decreasing the translocation of LPS across the intestinal border and systemic and pulmonary TNF-α production. These data demonstrate a potential etiologic link between gut and lung damage after BMT and suggest that methods that reduce inflammatory responses to LPS, and specifically, those that protect the integrity of the gut mucosa, may be effective in reducing IPS after BMT.

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Section: Discussionmentioning

confidence: 99%

Hyporesponsiveness of Donor Cells to Lipopolysaccharide Stimulation Reduces the Severity of Experimental Idiopathic Pneumonia Syndrome: Potential Role for a Gut-Lung Axis of Inflammation

Cooke

Hill

Gerbitz

et al. 2000

The Journal of Immunology

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“…Studies in sheep suggest that lipoxygenase inhibition can modify the inflammatory response to endotoxin [22], and in rat models, DEC has been shown to improve red cell deformability and survival [10,23]. Furthermore, this modulation appears to be dependent on baseline hepatocyte function [8] and liver blood flow [24]. As IL-6 appears to function primarily as a metabolic cytokine, and because the liver is one of its primary targets, we further wished to define the effect of DEC pretreatment on TNF-· and IL-6 kinetics in a dog model of endotoxic shock.…”

Section: Introductionmentioning

confidence: 99%

Effect of Ibuprofen and Diethylcarbamazine on the Hemodynamic and Inflammatory Response to Endotoxin in the Dog

Pinsky

Roman²,

Buurman³

et al. 2000

Eur Surg Res

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We studied the effects of pretreatment with either ibuprofen (15 mg/kg), diethylcarbamazine (DEC, 15 mg/kg), or vehicle, on the hemodynamic, hematologic, and serum tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 responses to a bolus Escherichia coli endotoxin infusion (2 mg/kg) in 21 pentobarbital-anesthetized dogs (n = 7 each group). Hematologic and cytokine data were collected before and 0.5, 1, and 3 h after endotoxin infusion. Endotoxin decreased arterial pressure (P_a), cardiac output (CO), total leukocyte (WBC) and platelet counts, and increased lactate, TNF-α, and IL-6. TNF-α levels peaked at 1 h and decreased by 3 h, whereas IL-6 remained elevated. Ibuprofen abolished the endotoxin-induced changes in P_a and lactate, but did not alter the initial decrease in CO, WBC, and platelets or the increase in TNF-α and IL-6. DEC did not alter the response to endotoxin, although the DEC group had higher TNF-α and IL-6 levels before endotoxin infusion compared to controls. We conclude that the cardiovascular effects of ibuprofen in the canine model of acute endotoxemia are not due to suppression of the systemic inflammatory response.

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“…Shock is usually difficulty to treat, because it is a systemic response involving not only changes in immunological parameters but inducing dysfunction of circulation, coagulation and fibrinolysis. 1) There have been many studies establishing and analyzing animal models of shock. We have also long been analyzing septic and endotoxic shock from various points of view such as, the detoxification of endotoxin by lysozyme, modulation of antibiotic action by lysozyme, 2,3) development of a monoclonal anti-CD14 antibody and its application, 4,5) and establishing an endogenous septic shock model using non-steroidal anti-inflammatory drugs.…”

mentioning

confidence: 99%

“…[24][25][26][27][28] The lethal toxicity of CAWS 8) and O9 LPS [29][30][31] is similar with respect to the following. 1) Lethal toxicity occurs 15-60 min after intravenous injection.…”

mentioning

confidence: 99%

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

Tada

Nagi-Miura

Adachi

et al. 2006

Biological & Pharmaceutical Bulletin

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Shock is a serious clinical problem because of high mortality. There are many mechanisms inducing shock and major mechanisms related to immune dysfunction are anaphylaxis, septic shock, and endotoxin shock. Shock is usually difficulty to treat, because it is a systemic response involving not only changes in immunological parameters but inducing dysfunction of circulation, coagulation and fibrinolysis. 1) There have been many studies establishing and analyzing animal models of shock. We have also long been analyzing septic and endotoxic shock from various points of view such as, the detoxification of endotoxin by lysozyme, modulation of antibiotic action by lysozyme, 2,3) development of a monoclonal anti-CD14 antibody and its application, 4,5) and establishing an endogenous septic shock model using non-steroidal anti-inflammatory drugs. 6,7) In the course of studying early diagnosis of deep seated fungal infection we have found a limulus factor G activating activity in a water soluble polysaccharide fraction rich in mannan, named Candida albicans water soluble fraction (CAWS), released from Candida albicans, and it strongly caused acute anaphylaxis-like shock in mice. 8)The pathogenic yeast Candida albicans, a commensal of the human digestive tract and vaginal mucosa, is now one of the most common microbes of bloodstream infections in immunocompromised or intensive-care patients.9) The invasive mycoses including candidiasis, aspergillosis and cryptococcosis are increasingly becoming associated with immunosuppressive therapies and immunodeficiency associated with infections of the human immunodeficiency virus. The associated crude mortality is extensively high (38 to 75%), despite appropriate treatment with anti-fungal drugs.10-13) Sepsis, which is caused by a Gram-negative bacterial infection, has also increased for the reasons described above and the associated mortality is markedly high. 14)We previously obtained a water-soluble fraction (CAWS), prepared from the culture supernatants of Candida albicans grown in a completely synthetic medium. CAWS is mainly composed of a complex of mannoprotein and b-1,3-, b-1,6-glucans.15,16) CAWS exhibits various potential biological activities, such as cytokine synthesis by leukocytes, platelet aggregation, lethal toxicity like anaphylactoid shock, induction of coronary arteritis in various strains of mice, and so on. [17][18][19][20] However, the detailed mechanisms of these biological activities are unclear.It is reported that the intravenous injection of lipopolysaccharide from Escherichia coli O9, which possesses the mannose homopolysaccharide (MHP) as the O-antigen region, induced anaphylactoid shock within 15-60 min, but not lipopolysaccharide (LPS) from Escherichia coli O111, which possesses a heterosaccharide (not containing mannose). 21,22) The characteristics of this shock differ from those of the well-known endotoxic shock with respect to time until shock occurs and can be evoked in LPS-hyposensitive mice, like C3H/HeJ strain, 23) with a defect in Toll-like recept...

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Liver-lung interactions during E. coli endotoxemia. TNF-alpha:leukotriene axis.

Cited by 45 publications

References 0 publications

Hyporesponsiveness of Donor Cells to Lipopolysaccharide Stimulation Reduces the Severity of Experimental Idiopathic Pneumonia Syndrome: Potential Role for a Gut-Lung Axis of Inflammation

Hyporesponsiveness of Donor Cells to Lipopolysaccharide Stimulation Reduces the Severity of Experimental Idiopathic Pneumonia Syndrome: Potential Role for a Gut-Lung Axis of Inflammation

Effect of Ibuprofen and Diethylcarbamazine on the Hemodynamic and Inflammatory Response to Endotoxin in the Dog

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

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