Detrimental hemodynamic and inflammatory effects of microparticles originating from septic rats*

Mortaza, Satar; Martinez, Maria Carmen; Baron-Menguy, Céline; Burban, Mélanie; Bourdonnaye, Mathilde de la; Fizanne, Lionel; Pierrot, Marc; Calès, Paul; Henrion, Didier; Andriantsitohaina, Ramaroson; Mercat, Alain; Asfar, Pierre; Meziani, Ferhat

doi:10.1097/ccm.0b013e3181a00629

Cited by 72 publications

(61 citation statements)

References 29 publications

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“…Very recently, we found that rats with sepsis induced by peritonitis exhibit a specific phenotype of MPs, with MPs from leukocytes increased. Inoculation of these MPs in healthy rats reproduced hemodynamic, septic inflammatory patterns associated with oxidative and nitrative stresses in heart and aorta (12). Although septic MPs from humans (10) or rats (11) exert different effects in terms of oxidative and nitrative stresses in the aorta, they exhibit similar effects in the heart.…”

Section: Discussionmentioning

confidence: 97%

Circulating microparticles from septic shock patients exert differential tissue expression of enzymes related to inflammation and oxidative stress*

Mastronardi¹,

Mostefai²,

Meziani³

et al. 2011

Critical Care Medicine

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Section: Discussionmentioning

confidence: 97%

Circulating microparticles from septic shock patients exert differential tissue expression of enzymes related to inflammation and oxidative stress*

Mastronardi¹,

Mostefai²,

Meziani³

et al. 2011

Critical Care Medicine

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“…Consistent with these diverse effects, the overall clinical impact of neutrophil-derived microparticles is uncertain. Circulating leukocyte and erythrocyte microparticles isolated from septic rats induced hemodynamic instability in normal rats (43). In contrast, nonplatelet microparticles isolated from humans with sepsis improved the vasoconstrictor response of murine aortic rings (31).…”

Section: Circulating Neutrophils During Systemic Inflammationmentioning

confidence: 99%

Neutrophil Intercellular Communication in Acute Lung Injury. Emerging Roles of Microparticles and Gap Junctions

Dengler¹,

Downey

Tuder

et al. 2013

Am J Respir Cell Mol Biol

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A hallmark of acute inflammation involves the recruitment of polymorphonuclear leukocytes (neutrophils) to infected or injured tissues. The processes underlying this recruitment are complex, and include multiple mechanisms of intercellular communication between neutrophils and the inflamed tissue. In recent studies of the systemic and pulmonary vasculature, interest has increased in novel forms of intercellular communication, such as microparticle exchange and gap junctional intercellular communication. To understand the roles of these novel forms of communication in the onset, progression, and resolution of inflammatory lung injury (such as acute respiratory distress syndrome), we review the literature concerning the contributions of microparticle exchange and gap junctional intercellular communication to neutrophilalveolar crosstalk during pulmonary inflammation. By focusing on these cell-cell communications, we aim to demonstrate significant gaps of knowledge and identify areas of considerable need for further investigations of the processes of acute lung inflammation.Keywords: neutrophil; connexin; gap junction; microparticles; acute lung injury Although investigations of acute respiratory distress syndrome (ARDS) have yet to yield an efficacious pathophysiologytargeted therapy, they have provided important insights into the intercellular communications regulating neutrophil activation and alveolar transmigration. These communications include juxtacrine and paracrine (e.g., chemokines, cytokines, and proteinases), crosstalk between neutrophils and lung parenchymal cells, and the signaling conducted through cell-surface receptors such as leukocyte integrins and cognate adhesion molecules (e.g., intercellular adhesion molecules) expressed by lung parenchymal cells (1). The past decade has seen an increasing recognition of alternative forms of intercellular communications during the onset and resolution of inflammatory lung disease. These communications include microparticle exchange as well as gap junctional intercellular communication (GJIC). This Perspective will focus on these alternative forms of communication between neutrophils and lung parenchymal cells during the genesis of ARDS, highlighting opportunities for further investigations. MICROPARTICLE EXCHANGEMicroparticles are spherical, lipid bilayer-encapsulated extracellular bodies ranging from 50-1,000 nm in diameter. Microparticles can be secreted by almost every cell type, including lung parenchymal cells and inflammatory cells. Multiple forms of microparticles exist, reflecting different modes of production. "Exosomes" and "shedding vesicles" are derived from living cells, whereas "apoptotic bodies" are secreted by apoptotic and/or necrotic cells (2). Exosomes have an endosomal origin, and are stored as intraluminal vesicles within multivesicular bodies (3). Upon stimulation, exosomes are secreted by fusion with the cell membrane, forming a relatively homogenous group of microparticle sizes (50-150 nm). In contrast, shedding vesicles and apoptotic ...

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“…Similarly, injection of circulating MPs from septic rats into healthy ones induced the detrimental hemodynamic and inflammatory patterns of sepsis, associated with oxidative stresses, whereas MPs from healthy rats had no effect. 127 Overall, MPs are diverse and biologically active, providing another bridge between inflammation and coagulation. They are increasingly recognized as a diagnostic, prognostic, and therapeutic target for thrombotic and inflammatory/infectious disorders.…”

Section: Microparticlesmentioning

confidence: 99%

Cross Talk Pathways Between Coagulation and Inflammation

Foley

Conway

2016

Circulation Research

454

414

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Anatomic pathology studies performed over 150 years ago revealed that excessive activation of coagulation occurs in the setting of inflammation. However, it has taken over a century since these seminal observations were made to delineate the molecular mechanisms by which these systems interact and the extent to which they participate in the pathogenesis of multiple diseases. There is, in fact, extensive cross talk between coagulation and inflammation, whereby activation of one system may amplify activation of the other, a situation that, if unopposed, may result in tissue damage or even multiorgan failure. Characterizing the common triggers and pathways are key for the strategic design of effective therapeutic interventions. In this review, we highlight some of the key molecular interactions, some of which are already showing promise as therapeutic targets for inflammatory and thrombotic disorders. (Circ Res.

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Detrimental hemodynamic and inflammatory effects of microparticles originating from septic rats*

Abstract: Rats with sepsis induced by peritonitis exhibited a specific phenotype of MPs. Inoculation of sMPs in healthy rats reproduced hemodynamic, septic inflammatory patterns, associated with oxidative and nitrosative stresses.

Cited by 72 publications

References 29 publications

Circulating microparticles from septic shock patients exert differential tissue expression of enzymes related to inflammation and oxidative stress*

Circulating microparticles from septic shock patients exert differential tissue expression of enzymes related to inflammation and oxidative stress*

Neutrophil Intercellular Communication in Acute Lung Injury. Emerging Roles of Microparticles and Gap Junctions

Cross Talk Pathways Between Coagulation and Inflammation

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