RGD Reference Report - Down-regulation of the non-neuronal acetylcholine synthesis and release machinery in acute allergic airway inflammation of rat and mouse. - Rat Genome Database

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Down-regulation of the non-neuronal acetylcholine synthesis and release machinery in acute allergic airway inflammation of rat and mouse.

Authors: Lips, KS  Luhrmann, A  Tschernig, T  Stoeger, T  Alessandrini, F  Grau, V  Haberberger, RV  Koepsell, H  Pabst, R  Kummer, W 
Citation: Lips KS, etal., Life Sci. 2007 May 30;80(24-25):2263-9. Epub 2007 Jan 23.
RGD ID: 5686690
Pubmed: PMID:17328924   (View Abstract at PubMed)
DOI: DOI:10.1016/j.lfs.2007.01.026   (Journal Full-text)

Acetylcholine (ACh), derived both from nerve fibres and from non-neuronal sources such as epithelial cells, is a major regulator of airway function. There is evidence that dysfunction of the neuronal cholinergic system is involved in the pathogenesis of asthma. Here, we asked whether the pulmonary non-neuronal ACh-synthesis and release machinery is altered in a rat and a mouse model of allergic airway disease. Animals were sensitized against ovalbumin, challenged by allergen inhalation, and sacrificed 24 or 48 h later. Targets of investigation were the high-affinity choline transporter-1 (CHT1), that mediates cellular uptake of choline, the ACh-synthesizing enzyme choline acetyltransferase (ChAT), the vesicular ACh transporter (VAChT), and the polyspecific organic cation transporters (OCT1-3), which are able to translocate choline and ACh across the plasma membrane. With cell-type specific distribution patterns, immunohistochemistry identified these proteins in airway epithelial cells and alveolar macrophages. Real-time RT-PCR revealed significant decreases in ChAT-, CHT1-, VAChT-, OCT-mRNA in the lung of sensitized and allergen challenged animals. These data were supported by immunohistochemistry, demonstrating reduced labeling intensity of airway epithelial cells. ChAT-, CHT1-, VAChT-, and OCT1-mRNA were also significantly reduced in cells recovered by bronchoalveolar lavage from sensitized and challenged rats. In conclusion, the pulmonary non-neuronal cholinergic system is down-regulated in acute allergic airway inflammation. In view of the role of ACh in maintenance of cell-cell-contacts, stimulation of fluid-secretion and of ciliary beat frequency, this down-regulation may contribute to epithelial shedding and ciliated cell dysfunction that occur in this pathological condition.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CHATHumanasthma  ISOChat (Rattus norvegicus)Protein:decreased expression:lung epitheliumRGD 
ChatRatasthma  IEP Protein:decreased expression:lung epitheliumRGD 
ChatMouseasthma  ISOChat (Rattus norvegicus)Protein:decreased expression:lung epitheliumRGD 
SLC18A3Humanasthma  ISOSlc18a3 (Rattus norvegicus) RGD 
SLC22A1Humanasthma  ISOSlc22a1 (Rattus norvegicus) RGD 
SLC5A7Humanasthma  ISOSlc5a7 (Rattus norvegicus)mRNA:decreased expression:lungRGD 
Slc18a3Ratasthma  IEP  RGD 
Slc18a3Mouseasthma  ISOSlc18a3 (Rattus norvegicus) RGD 
Slc22a1Ratasthma  IEP  RGD 
Slc22a1Mouseasthma  ISOSlc22a1 (Rattus norvegicus) RGD 
Slc5a7Ratasthma  IEP mRNA:decreased expression:lungRGD 
Slc5a7Mouseasthma  ISOSlc5a7 (Rattus norvegicus)mRNA:decreased expression:lungRGD 

Objects Annotated

Genes (Rattus norvegicus)
Chat  (choline O-acetyltransferase)
Slc18a3  (solute carrier family 18 member A3)
Slc22a1  (solute carrier family 22 member 1)
Slc5a7  (solute carrier family 5 member 7)

Genes (Mus musculus)
Chat  (choline O-acetyltransferase)
Slc18a3  (solute carrier family 18 (vesicular monoamine), member 3)
Slc22a1  (solute carrier family 22 (organic cation transporter), member 1)
Slc5a7  (solute carrier family 5 (choline transporter), member 7)

Genes (Homo sapiens)
CHAT  (choline O-acetyltransferase)
SLC18A3  (solute carrier family 18 member A3)
SLC22A1  (solute carrier family 22 member 1)
SLC5A7  (solute carrier family 5 member 7)


Additional Information