Title : Glutamine deficiency shifts the asthmatic state toward neutrophilic airway inflammation.

Pub. Date : 2022 Apr

PMID : 34601745






5 Functional Relationships(s)
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1 BACKGROUND: The administration of L-glutamine (Gln) suppresses allergic airway inflammation via the rapid upregulation of MAPK phosphatase (MKP)-1, which functions as a negative regulator of inflammation by deactivating p38 and JNK mitogen-activated protein kinases (MAPKs). Glutamine dual specificity phosphatase 1 Mus musculus
2 BACKGROUND: The administration of L-glutamine (Gln) suppresses allergic airway inflammation via the rapid upregulation of MAPK phosphatase (MKP)-1, which functions as a negative regulator of inflammation by deactivating p38 and JNK mitogen-activated protein kinases (MAPKs). Glutamine dual specificity phosphatase 1 Mus musculus
3 Therefore, we investigated the mechanism by which endogenous Gln regulates MKP-1 induction and allergic airway inflammation in an ovalbumin-based murine asthma model. Glutamine dual specificity phosphatase 1 Mus musculus
4 Importantly, homeostatic MKP-1 induction did not occur at all, which resulted in prolonged p38 MAPK and cytosolic phospholipase A2 (cPLA2 ) phosphorylation in Gln-deficient mice. Glutamine dual specificity phosphatase 1 Mus musculus
5 CONCLUSION: Gln deficiency leads to the impairment of MKP-1 induction and activation of p38 MAPK and cPLA2 , resulting in the augmentation of neutrophilic, more so than eosinophilic, airway inflammation. Glutamine dual specificity phosphatase 1 Mus musculus