Corrigendum: An Exploration of Charge Compensating Ion Channels across the Phagocytic Vacuole of Neutrophils

Foote, Juliet R.; Béhé, Philippe; Frampton, Mathew; Levine, Adam P.; Segal, Anthony W.

doi:10.3389/fphar.2017.00728

Cited by 2 publications

(1 citation statement)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neutrophil migration, adhesion, neutrophil extracellular trap formation, bacterial killing, and production of reactive oxygen species (ROS) require coordinated ion fluxes (1)(2)(3)(4)(5)(6). Ca 2+ is among the best studied ions in this context (7,8).…”

Section: Introductionmentioning

confidence: 99%

Role of the Intracellular Sodium Homeostasis in Chemotaxis of Activated Murine Neutrophils

et al. 2020

View full text Add to dashboard Cite

The importance of the intracellular Ca 2+ concentration ([Ca 2+ ] i) in neutrophil function has been intensely studied. However, the role of the intracellular Na + concentration ([Na + ] i) which is closely linked to the intracellular Ca 2+ regulation has been largely overlooked. The [Na + ] i is regulated by Na + transport proteins such as the Na + /Ca 2+-exchanger (NCX1), Na + /K +-ATPase, and Na +-permeable, transient receptor potential melastatin 2 (TRPM2) channel. Stimulating with either N-formylmethionine-leucyl-phenylalanine (fMLF) or complement protein C5a causes distinct changes of the [Na + ] i. fMLF induces a sustained increase of [Na + ] i , surprisingly, reaching higher values in TRPM2 −/− neutrophils. This outcome is unexpected and remains unexplained. In both genotypes, C5a elicits only a transient rise of the [Na + ] i. The difference in [Na + ] i measured at t = 10 min after stimulation is inversely related to neutrophil chemotaxis. Neutrophil chemotaxis is more efficient in C5a than in an fMLF gradient. Moreover, lowering the extracellular Na + concentration from 140 to 72 mM improves chemotaxis of WT but not of TRPM2 −/− neutrophils. Increasing the [Na + ] i by inhibiting the Na + /K +-ATPase results in disrupted chemotaxis. This is most likely due to the impact of the altered Na + homeostasis and presumably NCX1 function whose expression was shown by means of qPCR and which critically relies on proper extra-to intracellular Na + concentration gradients. Increasing the [Na + ] i by a few mmol/l may suffice to switch its transport mode from forward (Ca 2+-efflux) to reverse (Ca 2+-influx) mode. The role of NCX1 in neutrophil chemotaxis is corroborated by its blocker, which also causes a complete inhibition of chemotaxis.

show abstract