Abnormal neutrophil chemotactic activity in children with congenital insensitivity to pain with anhidrosis (CIPA) the role of nerve growth factor

Abnormal neutrophil chemotactic activity in children with congenital insensitivity to pain with anhidrosis (CIPA) : the role of nerve growth factor

A 1926-ins-T mutation in the TrkA gene encoding the tyrosine kinase receptor for nerve growth factor (NGF) was previously documented in patients with congenital insensitivity to pain with anhidrosis (CIPA). These patients suffer from skin lacerations which often evolve into deep tissue infections. A...

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Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 130(2009), 3 vom: 01. März, Seite 365-72
1. Verfasser: Beigelman, Avraham (VerfasserIn)
Weitere Verfasser: Levy, Jacov, Hadad, Nurit, Pinsk, Vered, Haim, Alon, Fruchtman, Yariv, Levy, Rachel
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2009
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Chemokines Nerve Growth Factor 9061-61-4 Mitogen-Activated Protein Kinase 3 EC 2.7.11.24 MAP Kinase Kinase 4 EC 2.7.12.2
Beschreibung
Zusammenfassung:A 1926-ins-T mutation in the TrkA gene encoding the tyrosine kinase receptor for nerve growth factor (NGF) was previously documented in patients with congenital insensitivity to pain with anhidrosis (CIPA). These patients suffer from skin lacerations which often evolve into deep tissue infections. Abnormality in neutrophil functions may explain this high rate of severe infections. In this study we show that chemotaxis was significantly (P<0.001) suppressed in patients' neutrophils, compared to healthy controls. Although NGF alone did not exert a chemotactic effect, its presence enhanced both migration toward fMLP and phosphorylation of MAP kinases (ERK and JNK) in neutrophils from healthy controls, but not in neutrophils from CIPA patients. The significantly impaired chemotactic activity of neutrophils from a CIPA patient, which has been attributed to the molecular defect in the TrkA receptor, may contribute to the high rate of infection
Beschreibung:Date Completed 03.03.2009
Date Revised 31.03.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2008.09.005