EC Number   |
Application |
Reference |
|---|
   3.1.1.77 | analysis |
potential use in studies of LPS structure and bioactivity |
246545 |
| 3.1.1.77 | 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 |
751999 |
| 3.1.1.77 | medicine |
constitutive overexpression of AOAH in vivo hasten recovery from lipopolysaccharide exposure without interfering with the normal acute inflammatory response |
704964 |
| 3.1.1.77 | medicine |
in a murine neurogenic cystitis model, the gene encoding acyloxyacyl hydrolase is induced in the sacral spinal cord of pseudorabies virus-infected mice. Aoah-deficient mice exhibit increased vesicomotor reflex in response to bladder distension, consistent with spontaneous bladder hypersensitivity, and increased pelvic allodynia in neurogenic cystitis and postbacterial chronic pain models. Aoah deficiency results in greater bladder pathology and tumor necrosis factor production in pseudorabies virus neurogenic cystitis |
749541 |
