Monomeric human IgE evokes a transient calcium rise in individual human neutrophils

• Published in: Journal of leukocyte biology 1995-10, Vol.58 (4), p.459-467
• Main Authors: Collison, Kate S, Kvvaasi, Aaron A A, Parhar, Ranjit S, Al-Sedairy, Sultan T, Al-Mohanna, Futwan A A
• Format: Article
• Language: English
• Subjects: [Ca2+]i; Amino Acid Sequence; Calcium - blood; calcium imaging; Extracellular Space - chemistry; Extracellular Space - drug effects; Extracellular Space - metabolism; Fcγ receptors; Fluorescence; Homeostasis - drug effects; Humans; Image Processing, Computer-Assisted; Immunoglobulin E - pharmacology; Intracellular Fluid - chemistry; Intracellular Fluid - drug effects; Intracellular Fluid - metabolism; Molecular Sequence Data; N-Formylmethionine Leucyl-Phenylalanine - pharmacology; Neutrophils - drug effects; Neutrophils - metabolism; Neutrophils - ultrastructure; receptor ligation; Receptors, IgG - physiology
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.58.4.459

Digital fluorescence calcium imaging was used to investigate and identify the primary biological responses of human neutrophils to monomeric immunoglobulin E (IgE). Treatment of neutrophils with IgE caused a transient rise in the level of intracellular calcium that was inhibited by pertussis toxin. The calcium rise was due mainly to release from an intracellular membrane‐enclosed store that is also sensitive to the chemotactic peptide formyl‐Met‐Leu‐Phe. The IgE‐induced calcium transient was independent of Fcγ receptors and of Fc receptor ligation. Our data suggest that the mere binding of IgE to neutrophils is sufficient to evoke a biological response without the need for IgE/receptor cross‐linking.