Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.

Till, Gerd O.; Johnson, Kent J.; Kunkel, Robin G.; Ward, Peter A.

doi:10.1172/jci110548

Cited by 501 publications

(202 citation statements)

References 18 publications

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“…Thus, we cannot rule out completely the possibility that C3a and C5a could participate in this model. It has been reported that complement mediated increases in microvascular permeability is entirely dependent on PMNs (Till et al 1982). However, our results in this study suggest that latex microbeads infusion increases permeability independently of PMNs.…”

Section: Discussioncontrasting

confidence: 81%

Stimulation of Pulmonary Intravascular Macrophages Increases Microvascular Permeability in Awake Sheep.

Suzuki

Tanita²,

Kubo³

et al. 1993

Tohoku J. Exp. Med.

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The purpose of this study is to determine if stimulation of pulmonary intravascular macrophages (PIMs) increase microvascular permeability in sheep. We infused latex microbeads, l ,um in diameter, for 1 hr continuously and analysed lung hemodynamic and lymph-dynamic changes. More than 70% of latex microbeads in the lung were assigned to PIMs, and caught in their phagosomes as determined by morphological examination. This implies that infused latex microbeads predominantly stimulate PIMs. Pulmonary arterial pressure increased during the infusion period, and returned to baseline after the infusion period. Lung lymph flow increased and remained high while the lymph to plasma protein ratio ultimately increased above baseline. This implies that infusion of latex microbeads increases pulmonary microvascular permeability. The increase in lung lymph protein clearance was blocked completely by pretreatment with indomethacin, but not with a thromboxane synthetase inhibitor (OKY-046). These data indicate that the increase in microvascular permeability is mediated by an arachidonic acid cyclooxygenase metabolites but not by thromboxane. We conclude that PIMs can act as an initiator to increase pulmonary microvascular permeability by releasing arachidonic acid cyclooxygenase metabolites through their stimulation with latex beads. index terms ; sheep with chronic lung lymph fistulas; latex microbeads; arachidonic acid cyclooxygenase metabolites Previous reports using sheep with chronic lung lymph fistulas have indicated that infusion of bacteria and endotoxin leads to increase in pulmonary microvascular permeability (Brigham et al. 1974(Brigham et al. , 1979. This response is interpreted as acute inflammation in the alveolar capillaries based on microscopic examinations

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Section: Discussioncontrasting

confidence: 81%

Stimulation of Pulmonary Intravascular Macrophages Increases Microvascular Permeability in Awake Sheep.

Suzuki

Tanita²,

Kubo³

et al. 1993

Tohoku J. Exp. Med.

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“…Attenuation of neutrophil accumulation in the lungs, by using molecules inhibiting neutrophil adhesion, decreased the severity of lung injury (37). In addition, data from animal studies indicate that neutrophil depletion markedly attenuates the severity of endotoxemia-induced ALI (38,39).…”

Section: Discussionmentioning

confidence: 99%

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

Kambas

Markiewski

Pneumatikos

et al. 2008

The Journal of Immunology

116

111

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Acute respiratory distress syndrome (ARDS) is characterized by the presence of fibrin-rich inflammatory exudates in the intra-alveolar spaces and the extensive migration of neutrophils into alveoli of the lungs. Tissue factor (TF)-dependent procoagulant properties of bronchoalveaolar lavage fluid (BALF) obtained from ARDS patients favor fibrin deposition, and are likely the result of cross-talk between inflammatory mediators and hemostatic mechanisms. However, the regulation of these interactions remains elusive. Prompted by previous findings suggesting that neutrophils, under certain inflammatory conditions, can express functional TF, we investigated the contribution of intra-alveolar neutrophils to the procoagulant properties of BALF from patients with ARDS. Our results confirm that the procoagulant properties of BALF from ARDS patients are the result of TF induction, and further indicate that BALF neutrophils are a main source of TF in intra-alveolar fluid. We also found that BALF neutrophils in these patients express significantly higher levels of TF than peripheral blood neutrophils. These results suggest that the alveolar microenvironment contributes to TF induction in ARDS. Additional experiments indicated that the ability of BALF to induce TF expression in neutrophils from healthy donors can be abolished by inhibiting C5a or TNF-α signaling, suggesting a primary role for these inflammatory mediators in the up-regulation of TF in alveolar neutrophils in ARDS. This cross-talk between inflammatory mediators and the induction of TF expression in intra-alveolar neutrophils may be a potential target for novel therapeutic strategies to limit ARDS-associated disturbances of coagulation.

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“…These oxygen radicals have been shown to be injurious to cells and tissues [10,11]. In addition O 2~ is able to react with plasma and generate a chemotactic factor for neutrophils, thus amplifying the inflammatory response [12].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Oxygen Radical Production by Dialysis Membranes

Kuwahara¹,

Markert²,

Wauters³

1988

Nephrology Dialysis Transplantation

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Abstract. The ability of different dialysis membranes to activate polymorphonuclear neutrophil oxygen radical production was investigated with chemiluminescence. All the six membranes, namely cuprophan, cellulose acetate, polycarbonate, polysulphone, polyacrilonitrile and polymethylmethacrylate were able to interact with neutrophils and stimulate their oxygen radical production, the highest responses being seen with polyacrilonitrile, polymethylmethacrylate and polycarbonate. To analyse the role of complement in this interaction, fresh plasma, heatinactivated and zymosan-activated plasma were added: with fresh plasma oxygen radical production was stimulated on cuprophan, cellulose acetate and polysulphone, not modified on polycarbonate, and decreased on polyacrilonitrile and polymethylmethacrylate. With heatinactivated plasma, the responses were decreased or abrogated on all the membranes except polycarbonate and polymethylmethacrylate, whereas with zymosanactivated plasma similar responses to fresh plasma were observed. In addition, when plasma was used to precoat the membrane, cuprophan, cellulose acetate and polysulphone disclosed an enhanced neutrophil oxidative burst, while precoated polyacrilonitrile and polymethylmethacrylate were less stimulatory than uncoated membranes. In contrast the precoating of polycarbonate did not modify oxygen radical production. These data suggest that neutrophil activation occurs by direct membraneneutrophil interaction. Plasmatic factors modulate this interaction but complement seems involved on cellulosic and polysulphone membranes only. Therefore, it appears that oxygen radicals produced from contact of neutrophils with the dialysis membrane might play an initial and/or additional role in the events occurring at the initiation of haemodialysis.

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Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.

Cited by 501 publications

References 18 publications

Stimulation of Pulmonary Intravascular Macrophages Increases Microvascular Permeability in Awake Sheep.

Stimulation of Pulmonary Intravascular Macrophages Increases Microvascular Permeability in Awake Sheep.

C5a and TNF-α Up-Regulate the Expression of Tissue Factor in Intra-Alveolar Neutrophils of Patients with the Acute Respiratory Distress Syndrome

Neutrophil Oxygen Radical Production by Dialysis Membranes

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