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| 2. |
- Kaca, W, et al.
(författare)
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Complement activation by Proteus mirabilis negatively charged lipopolysaccharides
- 2000
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Ingår i: Journal of endotoxin research. - : SAGE Publications. - 0968-0519. ; 6:3, s. 223-234
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Tidskriftsartikel (refereegranskat)abstract
- Proteus mirabilis strains are human pathogens responsible for urinary tract infections and bacteremias and may be involved in rheumatoid arthritis. Lipopolysaccharide (LPS, bacterial endotoxin), the major component of the cell wall, is one of the virulence factors of Proteus. In the presented studies, we have investigated complement activation by LPSs isolated from P. mirabilis O10, O23, O30, and O43 strains, which differ in the number of negative COO— groups on their polysaccharide components. Four P. mirabilis strains studied were sensitive to complement-mediated killing, despite complement binding by their LPSs. The optimal complement binding by LPSs was detected in serum with functional assays for both the classical and alternative pathways. Complement activation in 80% serum by the smooth, uronic acid, and hexosamine containing P. mirabilis LPSs was not critically determined by the structure of their O-chain polysaccharides. One of four LPSs used as a model, P. mirabilis O10 LPS, fragmented C3 in an LPS dose- and time-dependent manner. It was detected by crossed-immunoelectrophoresis and capture ELISA with anti-C3c antibodies. The lower complement activation by O23 LPS correlates with its reduced C3 fragmentation, compared with three other Proteus LPSs studied. Rabbit anti-O antibodies enhanced the complement binding and factor C3 fragmentation by O10, O23, O30, and O43 P. mirabilis LPSs.
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| 3. |
- Lakio, L, et al.
(författare)
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Pro-atherogenic properties of lipopolysaccharide from the periodontal pathogen Actinobacillus actinomycetemcomitans.
- 2006
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Ingår i: Journal of Endotoxin Research. - 0968-0519 .- 1743-2839. ; 12:1, s. 57-64
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Tidskriftsartikel (refereegranskat)abstract
- An association between cardiovascular and periodontal disease may be due to lipopolysaccharide (LPS)-promoted release of inflammatory mediators, adverse alterations of the lipoprotein profile, and an imbalance in cholesterol homeostasis. Since periodontopathogenic potential differs between serotypes of a major periodontal pathogen, Actinobacillus actinomycetemcomitans, we studied the pro-atherogenic properties of LPS preparations from serotypes b and d strains on macrophages (RAW 264.7). A. actinomycetemcomitans LPS preparations induced a time-dependent release of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). LPS induced foam cell formation and cholesteryl ester accumulation from native low density lipoprotein in the following order: A. actinomycetemcomitans strains JP2 (serotype b) > Y4 (serotype b) > IDH781 (serotype d). mRNA expression levels of scavenger receptor class B, type-I, and ATP-binding cassette transporter-1, receptors mediating cholesterol efflux from macrophages, were decreased by LPS preparations. The results suggest that the pro-atherogenic potential of A. actinomycetemcomitans LPS may depend on the infecting strain and correlate with the periodontopathogenic potential of the pathogen.
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| 4. |
- Lipcsey, Miklós, et al.
(författare)
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Inflammatory, coagulatory and circulatory responses to logarithmic increases in the endotoxin dose in the anaesthetised pig
- 2006
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Ingår i: Journal of Endotoxin Research. - : SAGE Publications. - 0968-0519 .- 1743-2839. ; 12:2, s. 99-112
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Although porcine intravenous endotoxin shock models are widely employed in experimental sepsis, endotoxin dose-effect studies are scarce. Our primary aim was to establish the dose response to increasing endotoxin doses in inflammatory, coagulatory and haemodynamic effect variables, as well as to determine the optimal time point for assessment in a pig model. A secondary aim was to study pathophysiological covariations between the different responses. Twenty anaesthetised piglets received endotoxin intravenously in doses of 0.063 (n = 3), 0.25 (n = 3), 1.0 (n = 3), 4.0 (n = 3), 8 (n = 3) and 16 microg/kg/h (n = 2). In addition, non-endotoxin piglets constituted a control group (n = 3). Physiological variables were registered and blood samples analysed for TNF-alpha, IL-6, leukocyte, platelet and haemoglobin concentrations hourly for 6 h. Increases in the endotoxin dose induced significant log-log cytokine responses as well as log-linear leukocyte and platelet responses. Significant log-linear responses were observed for circulatory parameters, plasma leakage, hypoperfusion and pulmonary compliance. Significant covariations in the responses were noted. In conclusion, there were log-log or log-linear responses to endotoxin suggesting a greater effect of a given dose at lower pre-existing endotoxin concentrations and lower doses of < or = 1 microg/kg/h may be of advantage in experiments designed to study potential anti-endotoxin effects of experimental drugs or measures.
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| 6. |
- O'Neill, Luke A. J., et al.
(författare)
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Mal and MyD88 : adapter proteins involved in signal transduction by Toll-like receptors
- 2003
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Ingår i: Journal of Endotoxin Research. - : Maney Publishing. - 0968-0519 .- 1743-2839. ; 9:1, s. 55-59
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Tidskriftsartikel (refereegranskat)abstract
- Signal transduction processes activated by Toll-like receptors (TLRs) include the important transcription factor NF-kappaB and 2 MAP kinases, p38 and Jun N-terminal kinase. These signals ultimately give rise to increased expression of a multitude of pro-inflammatory proteins. Receptor-proximal proteins involved in signalling by all TLRs include the adapter MyD88, 3 IRAKs (IRAK-4, IRAK and IRAK-2), Tollip, Traf-6 and TAK-1. Differences between signals generated by TLRs are emerging, with both TLR4 and TLR2 signalling requiring an additional adapter termed MyD88-adapter-like (Mal; also known as TIRAP). MyD88 and Mal both have a homologous Toll/IL-1 receptor (TIR) domain although they differ in their N-termini, with MyD88 possessing a death domain. In addition, structural models reveal marked differences in surface charges which, when taken with surface charge differences between TLR2 and TLR4 TIR domains, may indicate that TLR4 but not TLR2 recruits Mal directly. Another difference is that Mal can become phosphorylated. Future studies on Mal will reveal specificities in signal transduction by different TLRs, which may ultimately provide molecular explanations for specificities in the innate immune response to infection.
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| 7. |
- Svensen, C, et al.
(författare)
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Volume kinetics of Ringer solution during endotoxinemia in conscious rabbits
- 1997
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Ingår i: JOURNAL OF ENDOTOXIN RESEARCH. - : SAGE Publications. - 0968-0519. ; 4:6, s. 425-430
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The volume effect of Ringer solution was studied in normal and endotoxinemic rabbits to find out whether endotoxin alters the body's handling of crystalloid fluid. Ten rabbits (mean body weight 4.4 kg) were given 25 ml/kg of Ringer solution over 30 min with and without receiving 20 μg/kg of endotoxin 1 h before the infusion. The hemodilution, as measured every 10 min during 2 h, was used to calculate the size of the fluid space expanded by the fluid (V) and the elimination rate constant (kr). Apart from fever and leukopenia, the injection of endotoxin reduced V from 473 (37) ml to 327 (54) ml (mean (SEM); P < 0.04) and kr increased from 2.9 (0.5) ml/min to 5.9 (2.8) ml/min (not significant). Computer-based simulations using the derived kinetic data indicated that endotoxin increases the volume effect of infused fluid when it is infused very fast but reduces it when the fluid is infused more slowly.
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