scholarly journals Escherichia coli Lipopolysaccharide Modulates Biological Activities of Human-β-Defensin Analogues but Not Non-Ribosomally Synthesized Peptides

ACS Omega ◽  
2020 ◽  
Vol 5 (12) ◽  
pp. 6366-6375 ◽  
Author(s):  
Viswanatha Krishnakumari ◽  
Taniya Mary Binny ◽  
Harikrishna Adicherla ◽  
Ramakrishnan Nagaraj
Keyword(s):  
Escherichia Coli ◽  
Biological Activities ◽  
Escherichia Coli Lipopolysaccharide

Escherichia coli lipopolysaccharide induces alveolar epithelial cell stiffening

2019 ◽  
Vol 83 ◽  
pp. 315-318 ◽  
Author(s):  
Vinícius Rosa Oliveira ◽  
Juan José Uriarte ◽  
Bryan Falcones ◽  
Walter Araujo Zin ◽  
Daniel Navajas ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial ◽  
Escherichia Coli Lipopolysaccharide

A time-dependent balance between endothelins and nitric oxide regulating portal resistance after endotoxin

1996 ◽  
Vol 271 (5) ◽  
pp. H1953-H1961 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
M. G. Clemens
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Portal Pressure ◽  
Time Dependent ◽  
Epifluorescence Microscopy ◽  
Synthesis Inhibitor ◽  
Before And After ◽  
Etb Receptor ◽  
Escherichia Coli Lipopolysaccharide ◽  
Zero Flow

To test whether endothelins are involved in the regulation of portal resistance after endotoxin pretreatment and whether their effects are modulated by nitric oxide (NO), rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline. Six and twenty-four hours later, livers were isolated and perfused. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence microscopy were performed before and after administration of 1) the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10(-3) M), followed by L-arginine (2 x 10(-3) M), or 2) the endothelin ETA/ETB-receptor antagonist bosentan (2 x 10(-4) M), followed by L-NAME (10(-3) M). LPS pretreatment increased all measures of resistance, which included total portal resistance, zero flow, incremental resistance (slopes of P-Q relationship), and sinusoid resistance. L-NAME had no effect in sham controls but increased all measures of resistance at 6 h after LPS and increased total and incremental resistance 24 h after LPS. L-Arginine reversed these changes. Bosentan reduced total and sinusoid resistance slightly in control livers and caused substantial reductions in all measures of resistance at 6 and 24 h after LPS; these were partially reversed after L-NAME at 6 but not at 24 h. Our data support the hypothesis that a critical balance between endothelin-mediated vasoconstrictor influences and NO-mediated vasodilator influences controls portal resistance after endotoxin pretreatment.

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