ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2011
E. coli lipopolysaccharide attenuates adenosine A(1) receptor-mediated increase in plasma exudation from the hamster cheek pouch.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 2 citations in OpenAlex.
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2 authors at 2 institutions in 1 country.
Funding
Abstract
OBJECTIVE AND
designTo determine whether exposure to E. coli lipopolysaccharide (LPS) modulates adenosine A(1) receptor-induced increase in plasma exudation from the intact hamster cheek pouch microcirculation. METHODS AND
resultsUsing intravital microscopy, we found that suffusion of R(-)-N(6)-(2-phenylisopropyl)-adenosine (R(-)-PIA) (1.0 and 10.0 nM), a selective adenosine A(1) receptor agonist, onto the intact cheek pouch elicited significant, concentration-dependent leaky site formation and increase in clearance of fluorescein thioisocyanate-dextran (mol mass, 70 kDa) from post-capillary venules (p < 0.05). These responses were significantly attenuated by pre-treatment of hamsters with LPS (p < 0.05). By contrast, LPS had no significant effects on CGS-21680-, a selective adenosine A(2A) receptor agonist, bradykinin- and substance P-induced increases in plasma exudation from the cheek pouch.
conclusionThese data indicate that LPS attenuates adenosine A(1) receptor-induced increase in plasma exudation in vivo in a specific fashion. We suggest that this phenomenon represents an endogenous anti-inflammatory cue to avoid excessive inflammation during Gram-negative bacterial infections.
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Registered trials
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