NDLI: Glutamate induces neutrophil cell migration by activating class I metabotropic glutamate receptors

Content Provider	Springer Nature Link
Author	Gupta, Rahul Palchaudhuri, Santanu Chattopadhyay, Dhrubajyoti
Copyright Year	2012
Abstract	Leukocytes are recruited at the site of infection or injury as a part of the innate immune system, and play a very critical role in fighting the invading microorganisms and/or healing wounds. Neutrophils are the most abundant leukocytes in healthy humans and are the principal cell types that arrive at the target site in the initial phase of this process. Previous studies from our laboratory have shown that the amino acid glutamate is a novel chemotaxis-inducing factor for human neutrophils. In this report, we provide evidences that clearly demonstrate that the glutamate-induced neutrophil cell migration activity is mediated by the class I metabotropic glutamate receptors. Our results further show that a specific integrin β2 (ITG β2) receptor, namely LFA1 (αLβ2) is activated upon glutamate treatment and is required for further downstream signaling events leading to increased migration of human neutrophil cells. Following glutamate stimulation, LFA1 is phosphorylated by the Src Kinase Lck at the Y735 residue, which triggers a downstream signaling cascade leading to activation of PI3K, Syk, Vav and finally the Rho family GTPase, Rac2. Interestingly, glutamate was previously found to be present in elevated levels in wound fluid. Furthermore, glutamate level was also found to go up following inflammation. Taken together, our study suggests a novel mode of neutrophil recruitment to the target site following an infection or injury.
Starting Page	757
Ending Page	767
Page Count	11
File Format	PDF
ISSN	09394451
Journal	Amino Acids
Volume Number	44
Issue Number	2
e-ISSN	14382199
Language	English
Publisher	Springer Vienna
Publisher Date	2012-09-19
Publisher Place	Vienna
Access Restriction	Subscribed
Subject Keyword	Neutrophil recruitment Chemotaxis Glutamate receptor Integrin Biochemistry Analytical Chemistry Biochemical Engineering Life Sciences Proteomics Neurobiology
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Biochemistry Clinical Biochemistry

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