scholarly journals Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

2003 ◽  
Vol 171 (2) ◽  
pp. 1001-1008 ◽  
Author(s):  
Dunia Rodríguez ◽  
Alexandre C. Keller ◽  
Eliana L. Faquim-Mauro ◽  
Mahasti S. de Macedo ◽  
Fernando Q. Cunha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Bacterial Lipopolysaccharide ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals Expression of nitric oxide synthase isoforms in the mouse kidney: cellular localization and influence by lipopolysaccharide and Toll-like receptor 4

2006 ◽  
Vol 36 (8-9) ◽  
pp. 499-516 ◽  
Author(s):  
Bo Holmqvist ◽  
Christina Falk Olsson ◽  
Maj-Lis Svensson ◽  
Catharina Svanborg ◽  
Johan Forsell ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cellular Localization ◽  
Mouse Kidney ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Oxide Synthase

Toll-like receptor 4 mediates ozone-induced murine lung hyperpermeability via inducible nitric oxide synthase

2001 ◽  
Vol 280 (2) ◽  
pp. L326-L333 ◽  
Author(s):  
Steven R. Kleeberger ◽  
Sekhar P. M. Reddy ◽  
Liu-Yi Zhang ◽  
Hye-Youn Cho ◽  
Anne E. Jedlicka
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Specific Inhibitor ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tlr4 Mrna ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

We tested the hypotheses that 1) inducible nitric oxide synthase (iNOS) mediates ozone (O3)-induced lung hyperpermeability and 2) mRNA levels of the gene for iNOS ( Nos2) are modulated by Toll-like receptor 4 ( Tlr4) during O3exposure. Pretreatment of O3-susceptible C57BL/6J mice with a specific inhibitor of total NOS ( NG-monomethyl-l-arginine) significantly decreased the mean lavageable protein concentration (a marker of lung permeability) induced by O3(0.3 parts/million for 72 h) compared with vehicle control mice. Furthermore, lavageable protein in C57BL/B6 mice with targeted disruption of Nos2 [ Nos2(−/−)] was 50% less than the protein in wild-type [ Nos2(+/+)] mice after O3. To determine whether Tlr4 modulates Nos2 mRNA levels, we studied C3H/HeJ (HeJ) and C3H/HeOuJ mice that differ only at a missense mutation in Tlr4 that confers resistance to O3-induced lung hyperpermeability in the HeJ strain. Nos2 and Tlr4 mRNA levels were significantly reduced and correlated in resistant HeJ mice after O3relative to those in susceptible C3H/HeOuJ mice. Together, the results are consistent with an important role for iNOS in O3-induced lung hyperpermeability and suggest that Nos2 mRNA levels are mediated through Tlr4.

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