nanonug
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(This could be an explanation for Post-exertional Malaise seen from the perspective of Mast Cell Activation)
1. PLoS One. 2012;7(11):e48934. doi: 10.1371/journal.pone.0048934. Epub 2012 Nov 14.
Neurotensin and CRH Interactions Augment Human Mast Cell Activation.
Alysandratos KD, Asadi S, Angelidou A, Zhang B, Sismanopoulos N, Yang H,
Critchfield A, Theoharides TC.
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of
Molecular Physiology and Pharmacology, Tufts University School of Medicine,
Boston, Massachusetts, United States of America ; Allergy Clinical Research
Center, Allergy Section, Attikon General Hospital, University of Athens Medical
School, Athens, Greece ; Sackler School of Graduate Biomedical Sciences, Tufts
University, Boston, Massachusetts, United States of America.
Stress affects immunity, but the mechanism is not known. Neurotensin (NT) and
corticotropin-releasing hormone (CRH) are secreted under stress in various
tissues, and have immunomodulatory actions. We had previously shown that NT
augments the ability of CRH to increase mast cell-dependent skin vascular
permeability in rodents. Here we show that NT triggered human mast cell
degranulation and significantly augmented CRH-induced vascular endothelial growth
factor (VEGF) release. Investigation of various signaling molecules indicated
that only NF-κB activation was involved. These effects were blocked by
pretreatment with the NTR antagonist SR48692. NT induced expression of CRH
receptor-1 (CRHR-1), as shown by Western blot and FACS analysis. Interestingly,
CRH also induced NTR gene and protein expression. These results indicate unique
interactions among NT, CRH, and mast cells that may contribute to auto-immune and
inflammatory diseases that worsen with stress.
PMID: 23155429
1. PLoS One. 2012;7(11):e48934. doi: 10.1371/journal.pone.0048934. Epub 2012 Nov 14.
Neurotensin and CRH Interactions Augment Human Mast Cell Activation.
Alysandratos KD, Asadi S, Angelidou A, Zhang B, Sismanopoulos N, Yang H,
Critchfield A, Theoharides TC.
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of
Molecular Physiology and Pharmacology, Tufts University School of Medicine,
Boston, Massachusetts, United States of America ; Allergy Clinical Research
Center, Allergy Section, Attikon General Hospital, University of Athens Medical
School, Athens, Greece ; Sackler School of Graduate Biomedical Sciences, Tufts
University, Boston, Massachusetts, United States of America.
Stress affects immunity, but the mechanism is not known. Neurotensin (NT) and
corticotropin-releasing hormone (CRH) are secreted under stress in various
tissues, and have immunomodulatory actions. We had previously shown that NT
augments the ability of CRH to increase mast cell-dependent skin vascular
permeability in rodents. Here we show that NT triggered human mast cell
degranulation and significantly augmented CRH-induced vascular endothelial growth
factor (VEGF) release. Investigation of various signaling molecules indicated
that only NF-κB activation was involved. These effects were blocked by
pretreatment with the NTR antagonist SR48692. NT induced expression of CRH
receptor-1 (CRHR-1), as shown by Western blot and FACS analysis. Interestingly,
CRH also induced NTR gene and protein expression. These results indicate unique
interactions among NT, CRH, and mast cells that may contribute to auto-immune and
inflammatory diseases that worsen with stress.
PMID: 23155429