22.214.171.124: acyloxyacyl hydrolase
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neutrophil acyloxyacyl hydrolase, AOAH, acyloxyacyl hydrolase
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General Information on EC 126.96.36.199 - acyloxyacyl hydrolase
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acyloxyacyl hydrolase acts as one of the diverse antimicrobial peptides and proteins expressed in the placenta
bacterial lipopolysaccharide, from Escherichia coli strain O14, induce hepatomegaly in mice, a recovery requires the murine enzyme, acyloxyacyl hydrolase, that inactivates bacterial lipopolysaccharide, overview
acyloxyacyl hydrolase is a mammalian enzyme expressed by antigen-presenting cells that deacylates and thereby inactivates lipopolysaccharide in host tissues. Deacylated lipopolysaccharide does not activate TLR4 and competitively inhibits signaling by biologically active lipopolysaccharide. The enzyme shows ability to modulate microbial signals that influence mucosal T cell immunity. Colonic dendritic cell subset (CD103+CD11beta+ALDH-) display a unique capacity to both express the enzyme and polarize interleukin 17-secreting CD4+ helper T cells, Th17 cells
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
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. Aoah-deficient mice have significantly higher levels of bladder vascular endothelial growth factor
transgenic mice overexpressing AOAH in dendritic cells and macrophages deacylate lipopolysaccharide more rapidly than wildtype controls. Transgenic mice are also protected from lipopolysaccharide-induced hepatosplenomegaly, recover more quickly from lipopolysaccharide-induced weight loss, and are more likely to survive when challenged with live Escherichia coli
Aoah-/- mice with low doses of bacterial lipopolysaccharide, from from Escherichia coli strain O14, or Gram-negative bacteria have livers remaining enlarged, as much as 80% above normal, many weeks longer than do the livers of Aoah+/+ animals. When compared with livers from bacterial lipopolysaccharide-primed Aoah+/+ mice, bacterial lipopolysaccharide-primed Aoah-/- livers have more numerous and larger Kupffer cells, intrasinusoidal leukocyte aggregates and activated sinusoidal endothelial cells, and sustained production of interleukin-10 and mRNAs for tumor necrosis factor, interleukin-10, and IRAKM, phenotype, overview
acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 polarization and immunity due to altered inactivation of commensal lipopolysaccharides. Lipopolysaccharide-containing Gram-negative microbiota augment the differentiation of antigen-specific Th17 cells