Neutrophil deformability in patients with sepsis, septic shock, and adult respiratory distress syndrome

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

doi:10.1097/00003246-200007000-00029

Cited by 77 publications

(59 citation statements)

References 19 publications

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“…I t has been reported that neutrophils are activated in patients with systemic inflammatory response syndrome (SIRS) 1,2 that is associated with sepsis, [3][4][5] severe trauma, 6 and acute lung injury (ALI). 5,7,8 Under these conditions, activated neutrophils are sequestered, 9 produce inflammatory products 10 -12 such as neutrophil elastase (NE), 13 and show decreased deformability.…”

mentioning

confidence: 99%

A Neutrophil Elastase Inhibitor, Sivelestat, Improves Leukocyte Deformability in Patients With Acute Lung Injury

Inoue

Tanaka²,

Ogura³

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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mentioning

confidence: 99%

A Neutrophil Elastase Inhibitor, Sivelestat, Improves Leukocyte Deformability in Patients With Acute Lung Injury

Inoue

Tanaka²,

Ogura³

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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“…When neutrophils are activated, the increase of intracellular free calcium level and activation of F-actin make the neutrophils stiff. Skoutelis et al [15] have demonstrated that neutrophil deformability was significantly decreased in patients with ARDS. There are several studies reporting that selectins might be involved in cell activation [16].…”

Section: Discussionmentioning

confidence: 98%

P-selectin blockade fails to improve acute lung injury in sheep

et al. 2003

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Accumulation of neutrophils in the lung contributes to the endothelial damage in the tissue associated with acute respiratory distress syndrome. This initial recruitment of neutrophils within the pulmonary microvasculature may involve P-selectin. Thus we hypothesized that an antibody against P-selectin would reduce pulmonary damage. Sheep were chronically instrumented and prepared. The first group received 40% body surface area third-degree burns with 48 breaths of cotton smoke and 1 mg/kg of anti-(P-selectin) antibody (termed 3D4) 1 h post injury (n = 5). The second group (non-treated) received the same injury but no antibody treatment (n = 6). The third group comprised of sham animals without any injury or antibody treatment (n = 6). Sheep were studied for 48 h during which they were uniformly resuscitated with Ringer's lactate solution by following the Parkland formula. All the animals were mechanically ventilated. In the non-treated injured group, the arterial partial pressure of O(2) ('PaO(2)')/inspired fraction of O(2) ('F(i)O(2)') ratio dropped to 168+/-30 at 48 h, whereas the lung lymph flow increased to an average of 46+/-9 ml/h (10-fold of baseline). These changes were not prevented by an anti-(P-selectin) antibody. The plasma and lymph nitrate/nitrite levels were lower in the antibody-treated group than in the non-treated group. The lymph conjugated dienes were significantly lower in the treated animals. However, lung myeloperoxidase activity and lung tissue conjugated dienes were significantly increased in the treated animals compared with the non-treated injured controls. In conclusion, although the anti-(P-selectin) antibody did not protect against lung injury during the initial 48 h of burn and smoke, it decreased some aspects of injury in the peripheral microcirculation.

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“…The smaller increase in cell volume of activated PMNs observed in our study may be explained by exclusion of activated PMNs with irregular shapes from the volume analysis. Skoutelis et al [31] showed that deformability of passive PMNs of patients with septicemia was decreased compared with passive PMNs of healthy controls. They used micropipettes with internal diameters of 5 mm for aspiration of the whole cell.…”

Section: Discussionmentioning

confidence: 99%

Deformability of passive and activated neutrophils in children with Gram‐negative septicemia

Pöschl

Ruef

Linderkamp

2005

Scandinavian Journal of Clinical and Laboratory Investigation

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Animal experiments suggest that obstruction of small vessels by polymorphonuclear neutrophils (PMNs) may contribute to the disturbed microcirculation in septic shock. The purpose of this investigation was to study deformability and volume of passive and activated PMNs and immature neutrophils in 15 children with Gram-negative septicemia and in 20 healthy children. Membrane cytoplasm tongues of neutrophils were aspirated by means of a micropipette system into 2.5-microm (diameter) pipettes for 60 s. Tongue growth was used as an indicator of deformability and the cell volume was calculated from the cell circumference before aspiration. Septicemic children showed higher percentages of immature neutrophils (38+/-13%) and activated PMN (12+/-5%) than healthy children (3+/-2% and 3+/-2%). In septicemic children, cellular volume of passive neutrophils decreased progressively with increasing maturity from myeloblasts (493+/-105 fL) to mature PMNs (346+/-29 fL) and the final tongue length in the micropipette increased from 2.7+/-1.1 to 8.5+/-1.8 microm during maturation. The final tongue length of activated PMNs was decreased by 60% compared with that of passive PMNs. The increased number of rigid activated and immature neutrophils may contribute to impaired microcirculation in septicemic patients.

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Neutrophil deformability in patients with sepsis, septic shock, and adult respiratory distress syndrome

Cited by 77 publications

References 19 publications

A Neutrophil Elastase Inhibitor, Sivelestat, Improves Leukocyte Deformability in Patients With Acute Lung Injury

A Neutrophil Elastase Inhibitor, Sivelestat, Improves Leukocyte Deformability in Patients With Acute Lung Injury

P-selectin blockade fails to improve acute lung injury in sheep

Deformability of passive and activated neutrophils in children with Gram‐negative septicemia

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