Use of TLR9 and TLR7/8 agonists in combination with d-galactosamine in exploring models for distinct severities of systemic inflammation relative to liver injury
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
33210934
PubMed Central
PMC8549874
DOI
10.33549/physiolres.934455
PII: 934455
Knihovny.cz E-zdroje
- MeSH
- galaktosamin toxicita MeSH
- imidazoly toxicita MeSH
- lékové postižení jater etiologie metabolismus patologie MeSH
- lipopolysacharidy toxicita MeSH
- membránové glykoproteiny agonisté MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- stupeň závažnosti nemoci MeSH
- toll-like receptor 7 agonisté MeSH
- toll-like receptor 8 agonisté MeSH
- toll-like receptor 9 agonisté MeSH
- zánět chemicky indukované metabolismus patologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- galaktosamin MeSH
- imidazoly MeSH
- lipopolysacharidy MeSH
- membránové glykoproteiny MeSH
- resiquimod MeSH Prohlížeč
- Tlr7 protein, mouse MeSH Prohlížeč
- TLR8 protein, mouse MeSH Prohlížeč
- Tlr9 protein, mouse MeSH Prohlížeč
- toll-like receptor 7 MeSH
- toll-like receptor 8 MeSH
- toll-like receptor 9 MeSH
Challenges with various TLR ligands (TLRLs)in combination with D-galactosamine (GalN) in rodents may mimic diverse conditions of acute inflammation and organ failure. Here, we report that CpG (ODN1826, TLR9 agonist)/GalN induced a liver-specific injury with modest systemic effects, whereas R848 (resiquimod, TLR7/8 agonist)/GalN exhibited systemic and liver toxicity. We also observed the protective effect of Gr-1+ cells (the population containing neutrophils) against liver injury in both the R848/GalN and CpG/GalN models. In cytokine measurements, the intraperitoneal administration of antibodies showed a non-specific tolerance induction effect, which was more pronounced in the CpG/GalN than in the R848/GalN model. Cytokine analyses also suggested that the TLR9 agonist/GalN induced a limited degree of systemic inflammation compared to TLR7/8 agonist/GalN models. The relevance of this finding to the TLR9-mediated induction of stress tolerance (protective effect) in non-immune cells is discussed.
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