| respiratory syncytial virus persisted longer in the lungs of infected TLR4-deficient mice ( | |
TLR4-defective mice subjected to sensitization and pulmonary challenge with a protein allergen had reductions in airway inflammation with eosinophils, allergen-specific IgE levels, and Th2 cytokine production ( |
|
TLR4 deficiency of bone marrow-derived mast cells in mice resulted in significantly higher mortality because of defective neutrophil recruitment and production of proinflammatory cytokines in the peritoneal cavity ( |
|
TLR4(+/+) mice receiving TLR4(-/-) bone marrow, 6 weeks after transplant TLR4 was absent in all circulating leukocytes and in resident macrophages , and these cells were completely nonresponsive to lipopolysaccharide |
|
TLR4(-/-) mice receiving TLR4(+/+) bone marrow, endothelial cells but not leukocytes were deficient in TLR4, numbers of circulating leukocytes decreased by 90%, and systemic LPS (0.5 mg/kg) induced a dramatic increase in neutrophil sequestration into the lungs ( |
|
Apolipoprotein E-deficient mice that also lacked TLR4 or MyD88 demonstrated reduced aortic atherosclerosis that was associated with reductions in circulating levels of proinflammatory cytokines IL-12 or monocyte chemoattractant protein 1, plaque lipid content, numbers of macrophage, and cyclooxygenase 2 immunoreactivity in their plaques ( |