Effect of Cytokines and Colony-Stimulating Factors on Passive Polymorphonuclear Leukocyte Deformability in Vitro

Skoutelis, Athanasios; Kaleridis, Vassilios E; Gogos, Charalambos; Athanassiou, G.; Missirlis, Yannis F.; Bassaris, Harry P.

doi:10.1006/cyto.2000.0761

Cited by 11 publications

(10 citation statements)

References 15 publications

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“…A major finding, that soluble agonist-activated or primed neutrophils are stiffer than resting neutrophils (14,42,73,118,119) and that such stiffening is a necessary and sufficient condition for sequestration in capillaries (42) has been challenged recently (47,81). Gossett et al imposed very high strains on the cells in their version of the deformability cytometer (81) (DC) and found agonist-activated PMNs to be more deformable than resting PMNs.…”

Section: Morphometric and Rheological Controversiesmentioning

confidence: 99%

Mechanotransduction in neutrophil activation and deactivation

Ekpenyong

Toepfner

Chilvers

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Mechanotransduction refers to the processes through which cells sense mechanical stimuli by converting them to biochemical signals and, thus, eliciting specific cellular responses. Cells sense mechanical stimuli from their 3D environment, including the extracellular matrix, neighboring cells and other mechanical forces. Incidentally, the emerging concept of mechanical homeostasis,long term or chronic regulation of mechanical properties, seems to apply to neutrophils in a peculiar manner, owing to neutrophils' ability to dynamically switch between the activated/primed and deactivated/deprimed states. While neutrophil activation has been known for over a century, its deactivation is a relatively recent discovery. Even more intriguing is the reversibility of neutrophil activation and deactivation. We review and critically evaluate recent findings that suggest physiological roles for neutrophil activation and deactivation and discuss possible mechanisms by which mechanical stimuli can drive the oscillation of neutrophils between the activated and resting states. We highlight several molecules that have been identified in neutrophil mechanotransduction, including cell adhesion and transmembrane receptors, cytoskeletal and ion channel molecules. The physiological and pathophysiological implications of such mechanically induced signal transduction in neutrophils are highlighted as a basis for future work. This article is part of a Special Issue entitled: Mechanobiology.

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Section: Morphometric and Rheological Controversiesmentioning

confidence: 99%

Mechanotransduction in neutrophil activation and deactivation

Ekpenyong

Toepfner

Chilvers

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Several biochemical agents, such as chemokines ( 1 , 2 ) and bacterial chemoattractants ( 3 , 4 ), induce the rapid transition of neutrophils from a resting state to a polarized and primed or fully activated state ( 5 – 7 ), leading to their transendothelial migration out of blood and recruitment to sites of infection and sterile injury in surrounding tissues ( 8 ). Activated neutrophils are implicated in a very broad spectrum of pathologies, especially infectious and pulmonary diseases, such as acute respiratory distress syndrome (ARDS).…”

Section: Introductionmentioning

confidence: 99%

Mechanical deformation induces depolarization of neutrophils

et al. 2017

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“…However, the roles of leukocyte adhesion and stiffness remain unclear. Microcirculation impairments have been associated with abnormal concentrations of cytokines and endotoxins in various inflammatory diseases [ 8 – 19 ], but the case of ARDS has rarely been studied. Moreover, consensus conclusions have been difficult to draw due to the diversity of experimental conditions and models.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, consensus conclusions have been difficult to draw due to the diversity of experimental conditions and models. For instance, some studies have failed to show any effect of interleukin (IL)-8 on leukocyte stiffness [ 12 , 19 ], whereas others have found a pronounced effect [ 16 ]. Additionally, IL-8 and tumor necrosis factor (TNF)-α have been reported to promote adherence in some conditions [ 12 ], whereas no effects have been detected in other studies [ 8 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

The leukocyte-stiffening property of plasma in early acute respiratory distress syndrome (ARDS) revealed by a microfluidic single-cell study: the role of cytokines and protection with antibodies

Preira¹,

Forel²,

Robert³

et al. 2016

Crit Care

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BackgroundLeukocyte-mediated pulmonary inflammation is a key pathophysiological mechanism involved in acute respiratory distress syndrome (ARDS). Massive sequestration of leukocytes in the pulmonary microvasculature is a major triggering event of the syndrome. We therefore investigated the potential role of leukocyte stiffness and adhesiveness in the sequestration of leukocytes in microvessels. MethodsThis study was based on in vitro microfluidic assays using patient sera. Cell stiffness was assessed by measuring the entry time (ET) of a single cell into a microchannel with a 6 × 9–μm cross-section under a constant pressure drop (ΔP = 160 Pa). Primary neutrophils and monocytes, as well as the monocytic THP-1 cell line, were used. Cellular adhesiveness to human umbilical vein endothelial cells was examined using the laminar flow chamber method. We compared the properties of cells incubated with the sera of healthy volunteers (n = 5), patients presenting with acute cardiogenic pulmonary edema (ACPE; n = 6), and patients with ARDS (n = 22), of whom 13 were classified as having moderate to severe disease and the remaining 9 as having mild disease. ResultsRapid and strong stiffening of primary neutrophils and monocytes was induced within 30 minutes (mean ET >50 seconds) by sera from the ARDS group compared with both the healthy subjects and the ACPE groups (mean ET <1 second) (p < 0.05). Systematic measurements with the THP-1 cell line allowed for the establishment of a strong correlation between stiffening and the severity of respiratory status (mean ET 0.82 ± 0.08 seconds for healthy subjects, 1.6 ± 1.0 seconds for ACPE groups, 10.5 ± 6.1 seconds for mild ARDS, and 20.0 ± 8.1 seconds for moderate to severe ARDS; p < 0.05). Stiffening correlated with the cytokines interleukin IL-1β, IL-8, tumor necrosis factor TNF-α, and IL-10 but not with interferon-γ, transforming growth factor-β, IL-6, or IL-17. Strong stiffening was induced by IL-1β, IL-8, and TNF-α but not by IL-10, and incubations with sera and blocking antibodies against IL-1β, IL-8, or TNF-α significantly diminished the stiffening effect of serum. In contrast, the measurements of integrin expression (CD11b, CD11a, CD18, CD49d) and leukocyte–endothelium adhesion showed a weak and slow response after incubation with the sera of patients with ARDS (several hours), suggesting a lesser role of leukocyte adhesiveness compared with leukocyte stiffness in early ARDS. ConclusionsThe leukocyte stiffening induced by cytokines in the sera of patients might play a role in the sequestration of leukocytes in the lung capillary beds during early ARDS. The inhibition of leukocyte stiffening with blocking antibodies might inspire future therapeutic strategies.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-1157-5) contains supplementary material, which is available to authorized users.

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Effect of Cytokines and Colony-Stimulating Factors on Passive Polymorphonuclear Leukocyte Deformability in Vitro

Cited by 11 publications

References 15 publications

Mechanotransduction in neutrophil activation and deactivation

Mechanotransduction in neutrophil activation and deactivation

Mechanical deformation induces depolarization of neutrophils

The leukocyte-stiffening property of plasma in early acute respiratory distress syndrome (ARDS) revealed by a microfluidic single-cell study: the role of cytokines and protection with antibodies

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