ArticleMediators of inflammation2018
Complement C5a Alters the Membrane Potential of Neutrophils during Hemorrhagic Shock.
Article in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Inwardly rectifying potassium channels promote directional sensing during neutrophil chemotaxis.The Journal of cell biology · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Inwardly rectifying potassium channels regulate membrane potential polarization and direction sensing during neutrophil chemotaxis.bioRxiv : the preprint server for biology · 2025Article
- Multimodal monitoring of neutrophil activity during cardiac surgery.Frontiers in immunology · 2025Article
- Multimodal analysis of granulocytes, monocytes, and platelets in patients with cystic fibrosis before and after Elexacaftor-Tezacaftor-Ivacaftor treatment.Frontiers in immunology · 2023Article
- An exploratory study investigating the effect of targeted hyperoxemia in a randomized controlled trial in a long-term resuscitated model of combined acute subdural hematoma and hemorrhagic shock in cardiovascular healthy pigs.Frontiers in immunology · 2023Article
- Modulation of Neutrophil Activity by Soluble Complement Cleavage Products-An In-Depth Analysis.Cells · 2022Article
- Simultaneous Measurement of Changes in Neutrophil Granulocyte Membrane Potential, Intracellular pH, and Cell Size by Multiparametric Flow Cytometry.Biomedicines · 2021Article
- Ion and Water Transport in Neutrophil Granulocytes and Its Impairment during Sepsis.International journal of molecular sciences · 2021Review
- C5a-C5aR1 Axis Activation Drives Envenomation Immunopathology by the SnakeFrontiers in immunology · 2021Article
- Interleukin 8 Elicits Rapid Physiological Changes in Neutrophils That Are Altered by Inflammatory Conditions.Journal of innate immunity · 2021Article
- Activation of Neutrophil Granulocytes by Platelet-Activating Factor Is Impaired During Experimental Sepsis.Frontiers in immunology · 2021Article
- Complement C5a Induces Pro-inflammatory Microvesicle Shedding in Severely Injured Patients.Frontiers in immunology · 2020Article
- Targeting Complement Pathways in Polytrauma- and Sepsis-Induced Multiple-Organ Dysfunction.Frontiers in immunology · 2019Review
- Neutrophil heterogeneity and its role in infectious complications after severe trauma.World journal of emergency surgery : WJES · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPolymorphonuclear granulocytes (PMN) play a crucial role in host defense. Physiologically, exposure of PMN to the complement activation product C5a results in a protective response against pathogens, whereas in the case of systemic inflammation, excessive C5a substantially impairs neutrophil functions. To further elucidate the inability of PMN to properly respond to C5a, this study investigates the role of the cellular membrane potential of PMN in response to C5a.
methodsElectrophysiological changes in cellular and mitochondrial membrane potential and intracellular pH of PMN from human healthy volunteers were determined by flow cytometry after exposure to C5a. Furthermore, PMN from male Bretoncelles-Meishan-Willebrand cross-bred pigs before and three hours after severe hemorrhagic shock were analyzed for their electrophysiological response.
resultsPMN showed a significant dose- and time-dependent depolarization in response to C5a with a strong response after one minute. The chemotactic peptide fMLP also evoked a significant shift in the membrane potential of PMN. Acidification of the cellular microenvironment significantly enhanced depolarization of PMN. In a clinically relevant model of porcine hemorrhagic shock, the C5a-induced changes in membrane potential of PMN were markedly diminished compared to healthy littermates. Overall, these membrane potential changes may contribute to PMN dysfunction in an inflammatory environment.
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