Abstract
Perhaps the most important feature of neutrophils is their ability to rapidly change shape. In the bloodstream, the neutrophils circulate as almost spherical cells, with the ability to deform in order to pass along narrower capillaries. Upon receiving the signal to extravasate, they are able to transform their morphology and flatten onto the endothelium surface. This transition, from a spherical to a flattened morphology, is the first key step which neutrophils undergo before moving out of the blood and into the extravascular tissue space. Once they have migrated through tissues towards sites of infection, neutrophils carry out their primary role—killing infecting microbes by performing phagocytosis and producing toxic reactive oxygen species within the microbe-containing phagosome. Phagocytosis involves the second key morphology change that neutrophils undergo, with the formation of pseudopodia which capture the microbe within an internal vesicle. Both the spherical to flattened stage and the phagocytic capture stage are rapid, each being completed within 100 s. Knowing how these rapid cell shape changes occur in neutrophils is thus fundamental to understanding neutrophil behaviour. This article will discuss advances in our current knowledge of this process, and also identify an important regulated molecular event which may represent an important target for anti-inflammatory therapy.
Highlights
IntroductionWhen neutrophils undergo spreading on the endothelium (or experimentally, on other surfaces) or phagocytosis, there is an apparent expansion of the plasma membrane by nearly 200% [1,2]
When neutrophils undergo spreading on the endothelium or phagocytosis, there is an apparent expansion of the plasma membrane by nearly 200% [1,2]
We have focused on (i) the signalling from an elevation of cytosolic Ca2+ to (ii) μ-calpain activation, leading to (iii) the cleavage of ezrin and (iv) the release of cell surface wrinkles and microridges which (iv) permit actin polymerisation at the cell cortex to push the unfolding plasma membrane and (v) result in a rapid transition into the spread morphology or the localised formation of pseudopodia required for phagocytosis (Figure 1)
Summary
When neutrophils undergo spreading on the endothelium (or experimentally, on other surfaces) or phagocytosis, there is an apparent expansion of the plasma membrane by nearly 200% [1,2]. Sci. 2019, 1383ER [5] and none near the plasma membrane [6] It is unlikely 2that of 15 in case, very, little localised exocytosis at the forming phagocytic cup may provide the additional membrane. Explaining the area of each granule would provide less than 0.1% of the membrane required for cell spreading, origin of the additional membrane may be simpler when the geometry of the neutrophil surface and this would consume all of the granular membrane content [1,2]. Neutrophil spreading, these surface wrinkles these membrane microridges could contribute 100% additional cell surface area [9], these in the membrane are reduced.
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