Application | Comment | Organism |
---|---|---|
medicine | alveolar macrophages increase AOAH expression upon exposure to lipopolysaccharide and Aoah+/+ mice recover more rapidly than Aoah-/- mice from acute lung injury induced by nasally instilled lipopolysaccharide or Klebsiella pneumoniae. Aoah-/- mouse lungs have more prolonged leukocyte infiltration, greater pro- and anti-inflammatory cytokine expression, and longer lasting alveolar barrier damage. The persistently bioactive lipopolysaccharide in Aoah-/- alveoli can stimulate alveolar macrophages directly and epithelial cells indirectly to produce chemoattractants that recruit neutrophils to the lung and may prevent their clearance. Alveolar macrophages that lack AOAH maintain or increase their responses to bioactive lipopolysaccharides and sustained inflammation | Mus musculus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | O35298 | - |
- |
General Information | Comment | Organism |
---|---|---|
physiological function | alveolar macrophages increase Aoah expression upon exposure to lipopolysaccharide and Aoah+/+ mice recover more rapidly than Aoah-/- mice from acute lung injury induced by nasally instilled lipopolysaccharide or Klebsiella pneumoniae. Aoah-/- mouse lungs have more prolonged leukocyte infiltration, greater pro- and anti-inflammatory cytokine expression, and longer lasting alveolar barrier damage. The persistently bioactive lipopolysaccharide in Aoah-/- alveoli can stimulate alveolar macrophages directly and epithelial cells indirectly to produce chemoattractants that recruit neutrophils to the lung and may prevent their clearance. Alveolar macrophages that lack AOAH maintain or increase their responses to bioactive lipopolysaccharides and sustained inflammation | Mus musculus |