The Impact of Hypoxia on Neutrophil Signaling and Function

Dear Colleagues,

Molecular oxygen is essential for the development and growth of multicellular organisms. Tissue oxygen tensions reflect a balance between oxygen delivery mechanisms and oxygen consumption, with each tissue compartment having a set-point which may be perturbed by a range of pathological processes (e.g., interruption of blood supply, infection, inflammation, malignancy).

Neutrophils are highly mobile and accumulate rapidly in response to such pathological insults, hence they must operate within a wide and rapidly changing range of oxygen tensions.  They are therefore highly adapted to function in the setting of limited oxygen availability, swiftly modifying their cellular signaling pathways and functional properties. Such adaptations may profoundly affect the interaction of these professional phagocytes with their environment, altering outcomes in a range of inflammatory scenarios. Hypoxia inducible factors (HIFs) are transcription factors which function as key molecular regulators of hypoxic responses, but it is increasingly recognized that HIF regulation of neutrophil function integrates other micro-environmental cues alongside hypoxia and that HIF-independent pathways may also influence the neutrophil’s response to hypoxia. 

This Special Issue focuses on the recent advances in our understanding of the biology of hypoxia signaling and its impact on neutrophil function and interactions with the inflammatory microenvironment, in particular in the setting of infection and malignancy.

Prof. Dr. Alison Condliffe
Dr. Philip Elks
Dr. Roger Thompson
Dr. Pranvera Sadiku
Guest Editors

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