Phospholipase A2 is Involved in Chemotaxis Of Human Leukocytes

Tibes, Ulrich; Hinder, Markus; Scheuer, Werner; Friebe, W.-G.; Schramm, Stephan; Kaiser, Beate

doi:10.1007/978-1-4615-4793-8_29

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…89,90 LPC has been shown to both increase production of proinflammatory cytokines, 69 and have anti-inflammatory effects such as inhibiting high-mobility group protein B1 (HMGB1) secretion(16 h post-treatment with LPC). 91 These effects are dependent on different receptors as well as cell types, but not yet fully understood.…”

Section: Steps Involved In Clearancementioning

confidence: 99%

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

2016

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The turnover and clearance of cells is an essential process that is part of many physiological and pathological processes. Improper or deficient clearance of apoptotic cells can lead to excessive inflammation and autoimmune disease. The steps involved in cell clearance include: migration of the phagocyte toward the proximity of the dying cells, specific recognition and internalization of the dying cell, and degradation of the corpse. The ability of phagocytes to recognize and react to dying cells to perform efficient and immunologically silent engulfment has been well-characterized in vitro and in vivo. However, how apoptotic cells themselves initiate the corpse removal and also influence the cells within the neighboring environment during clearance was less understood. Recent exciting observations suggest that apoptotic cells can attract phagocytes through the regulated release of 'find-me' signals. More recent studies also suggest that these find-me signals can have additional roles outside of phagocyte attraction to help orchestrate engulfment. This review will discuss our current understanding of the different find-me signals released by apoptotic cells, how they may be relevant in vivo, and their additional roles in facilitating engulfment.

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Section: Steps Involved In Clearancementioning

confidence: 99%

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

2016

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“…cPLA 2 activity is regulated by calcium binding and phosphorylation (11,12). Compounds that inhibit cPLA 2 and secretory PLA 2 (sPLA 2 ) activities block chemotaxis of human leukocytes in culture (40). Chemokines are a low-molecularweight subclass of cytokines that promote leukocyte chemotaxis.…”

Section: Eicosanoids; Clara Cells; Macrophagesmentioning

confidence: 99%

Attenuation of the pulmonary inflammatory response following butylated hydroxytoluene treatment of cytosolic phospholipase A₂null mice

Meyer¹,

Dwyer‐Nield²,

Hurteau³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Administration of butylated hydroxytoluene (BHT) to mice causes lung damage characterized by the death of alveolar type I pneumocytes and the proliferation and subsequent differentiation of type II cells to replace them. Herein, we demonstrate this injury elicits an inflammatory response marked by chemokine secretion, alveolar macrophage recruitment, and elevated expression of enzymes in the eicosanoid pathway. Cytosolic phospholipase A(2) (cPLA(2)) catalyzes release of arachidonic acid from membrane phospholipids to initiate the synthesis of prostaglandins and other inflammatory mediators. A role for cPLA(2) in this response was examined by determining cPLA(2) expression and enzymatic activity in distal respiratory epithelia and macrophages and by assessing the consequences of cPLA(2) genetic ablation. BHT-induced lung inflammation, particularly monocyte infiltration, was depressed in cPLA(2) null mice. Monocyte chemotactic protein-1 (MCP-1) content in bronchoalveolar lavage fluid increases after BHT treatment but before monocyte influx, suggesting a causative role. Bronchiolar Clara cells isolated from cPLA(2) null mice secrete less MCP-1 than Clara cells from wild-type mice, consistent with the hypothesis that cPLA(2) is required to secrete sufficient MCP-1 to induce an inflammatory monocytic response.

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“…Studies indicated that soluble LPC can recruit phagocytic cells, such as macrophages, and induce phagocyte chemotaxis (Ousman & David, 2000; Peter et al, 2008). LPC might play an indirect role in the migration and recruitment of phagocytic cells, such as monocytes/macrophages, by increasing the regulation of VEC expression of different chemokines (Quinn et al, 1988; Tibes et al, 1999). LPC release is dependent on caspase‐3‐mediated activation in HT29 and MCF7 cells and in vivo and the ATP‐binding cassette transporter A1 (ABCA1) in apoptotic MCF7 casp3 cells and in vivo, both of which are involved in the release of LPC during apoptosis (Lauber et al, 2003; Peter et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

The cross‐talk between soluble “Find me” and “Keep out” signals as an initial step in regulating efferocytosis

Tajbakhsh

Yousefi

Abedi

et al. 2022

Journal Cellular Physiology

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The rapid clearance of apoptotic cells (ACs), known as efferocytosis, prompts the inhibition of inflammatory responses and autoimmunity and maintains homeostatic cell turnover by controlling the release of intracellular contents. The fast clearance of ACs requires professional and nonprofessional phagocytic cells that can accurately and promptly recognize ACs and migrate towards them. Cells undergoing apoptosis alarm their presence by releasing special soluble chemotactic factors, such as lactoferrin, that act as “Find me,” “Keep out,” or “Stay away” signals to recruit phagocytic cells, such as macrophages or prevent granulocyte migration. Efferocytosis effectively serves to prevent damage‐associated molecular pattern release and secondary necrosis and inhibit inflammation/autoimmunity at the very first step. Since less attention has been given to the cross‐talk and balance of “Find me” and “Keep out” signals released from ACs in efferocytosis, we set out to investigate the current knowledge of the roles of “Find me” and “Keep out” signals in the efferocytosis process.

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Phospholipase A2 is Involved in Chemotaxis Of Human Leukocytes

Cited by 4 publications

References 15 publications

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Attenuation of the pulmonary inflammatory response following butylated hydroxytoluene treatment of cytosolic phospholipase A₂null mice

The cross‐talk between soluble “Find me” and “Keep out” signals as an initial step in regulating efferocytosis

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Phospholipase A2 is Involved in Chemotaxis Of Human Leukocytes

Cited by 4 publications

References 15 publications

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Attenuation of the pulmonary inflammatory response following butylated hydroxytoluene treatment of cytosolic phospholipase A2null mice

The cross‐talk between soluble “Find me” and “Keep out” signals as an initial step in regulating efferocytosis

Contact Info

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Resources

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Attenuation of the pulmonary inflammatory response following butylated hydroxytoluene treatment of cytosolic phospholipase A₂null mice