Adhesion and transcellular migration of neutrophils and B lymphocytes on fibroblasts

Couture, Patrick; Paradis-Massie, Jérémie; Oualha, Nadia; Thibault, Gaétan

doi:10.1016/j.yexcr.2009.04.013

Cited by 23 publications

(18 citation statements)

References 56 publications

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“…This step depends initially on chemokine secretion and ICAM-1 and VCAM-1 expression at the inflammation site (Kukielka et al, 1993; Cook-Mills et al, 2011). Couture et al (2009), have shown that TNF-α and PMA increase neutrophil recruitment by CF. Previous results from our laboratory have shown that in CF, TLR4 activation by LPS, induces monocyte recruitment by CF themselves, due initially to the monocyte migration favored by MCP-1 secretion; whereas ICAM-1 and VCAM-1 expression in turn favors monocyte adhesion (Humeres et al, 2016).…”

Section: Discussionmentioning

confidence: 96%

IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation

et al. 2018

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Cardiac fibroblasts (CFs) contribute to theinflammatory response to tissue damage, secreting both pro- and anti-inflammatory cytokines and chemokines. Interferon beta (IFN-β) induces the phosphorylation of signal transducer and activator of transcription (STAT) proteins through the activation of its own receptor, modulating the secretion of cytokines and chemokines which regulate inflammation. However, the role of IFN-β and STAT proteins in modulating the inflammatory response of CF remains unknown. CF were isolated from adult male rats and subsequently stimulated with IFN-β to evaluate the participation of STAT proteins in secreting chemokines, cytokines, cell adhesion proteins expression and in their capacity to recruit neutrophils. In addition, in CF in which the TRL4 receptor was pre-activated, the effect of INF-β on the aforementioned responses was also evaluated. Cardiac fibroblasts stimulation with IFN-β showed an increase in STAT1, STAT2, and STAT3 phosphorylation. IFN-β stimulation through STAT1 activation increased proinflammatory chemokines MCP-1 and IP-10 secretion, whereas IFN-β induced activation of STAT3 increased cytokine secretion of anti-inflammatory IL-10. Moreover, in TLR4-activated CF, IFN-β through STAT2 and/or STAT3, produced an anti-inflammatory effect, reducing pro-IL-1β, TNF-α, IL-6, MCP-1, and IP-10 secretion; and decreasing neutrophil recruitment by decreasing ICAM-1 and VCAM-1 expression. Altogether, our results indicate that IFN-β exerts both pro-inflammatory and anti-inflammatory effects in non-stimulated CF, through differential activation of STAT proteins. When CF were previously treated with an inflammatory agent such as TLR-4 activation, IFN-β effects were predominantly anti-inflammatory.

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Section: Discussionmentioning

confidence: 96%

IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation

et al. 2018

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“…An alternative explanation is that fibroblast-derived mediators are more attractive to B-cells than T-cells. For example, it has been reported that B-cells adhere more efficiently to human dermal fibroblasts than T-cells (Couture et al, 2009). Moreover, B-cells, but not T-cells, were able to migrate through a fibroblast barrier (monolayer) (Couture et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…For example, it has been reported that B-cells adhere more efficiently to human dermal fibroblasts than T-cells (Couture et al, 2009). Moreover, B-cells, but not T-cells, were able to migrate through a fibroblast barrier (monolayer) (Couture et al, 2009). In fact in that study the fibroblasts appeared to selectively promote B-cell migration.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the effects of stromal cells on the migration of lymphocytes into and through inflamed tissue using 3-D culture models

Jeffery

Buckley

Moss

et al. 2013

Journal of Immunological Methods

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Stromal cells may regulate the recruitment and behaviour of leukocytes during an inflammatory response, potentially through interaction with the endothelial cells (EC) and the leukocytes themselves. Here we describe new in vitro methodologies to characterise the effects of stromal cells on the migration of lymphocytes through endothelium and its underlying matrix. Three-dimensional tissue-like constructs were created in which EC were cultured above a stromal layer incorporating fibroblasts either as a monolayer on a porous filter or dispersed within a matrix of collagen type 1. A major advantage of these constructs is that they enable each step in leukocyte migration to be analysed in sequence (migration through EC and then stroma), as would occur in vivo. Migrated cells can also be retrieved from the constructs to identify which subsets traffic more effectively and how their functional responses evolve during migration. We found that culture of EC with dermal fibroblasts promoted lymphocyte transendothelial migration but not onward transit through matrix. A critical factor influencing the effect of fibroblasts on recruitment proved to be their proximity to the EC, with direct contact tending to disrupt migration. Comparison of the different approaches indicates that choice of an appropriate 3-D model enables the steps in lymphocyte entry into tissue to be studied in sequence, the regulatory mechanism to be dissected, and the effects of changes in stroma to be investigated.

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“…Hypoxia, TNF-α, IL-1β, and LPS have been shown to induce expression of ICAM-1 on the vascular endothelial surface [81,109,123]. VCAM-1 and ICAM-1 interact with alpha-4 integrin (VLA-4) expressed on B-lymphocytes, and beta-2 integrins expressed on neutrophils and monocytes/macrophages resulting in extravasation [124,125].…”

Section: Vascular Dysfunctionmentioning

confidence: 99%

Cellular Pathways of Death and Survival in Acute Myocardial Infarction

Kent¹

2013

J Clin Exp Cardiolog

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During acute myocardial infarction (MI), the cumulative loss of functioning cardiomyocytes (CM) progresses as an imbrication of necrosis, apoptosis, and autophagy. Coronary artery occlusion and subsequent hypoxia causes some CMs to undergo necrosis with most cellular damage occurring near the area of occlusion. The inflammation that ensues plays a critical role in the reparative process and occurs in parallel as CMs struggle to survive. The release of inflammatory pro-apoptotic cytokines compounded with activation of apoptosis results in the programmed death of ischemic CMs. Concurrently, the level of autophagic flux in border zone CMs will determine whether or not these CMs are able to survive hypoxic cellular conditions. The interplay of these processes and the balance that occurs in the peri-infarct area plays a pivotal role in preserving the functional capacity of CMs, specifically through the upregulation of autophagy and downregulation of apoptosis and inflammation. A detailed understanding of these signaling pathways in acute MI is necessary to develop novel therapeutics to promote CM survival and diminish CM death following MI. This review discusses the cellular processes of necrosis, apoptosis, autophagy, and inflammation that occur during acute MI. Also, the common signaling mediators that each process employs and their relationship to each other are discussed to provide a better understanding of these synergistic effects during MI.

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Adhesion and transcellular migration of neutrophils and B lymphocytes on fibroblasts

Cited by 23 publications

References 56 publications

IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation

IFN-β Plays Both Pro- and Anti-inflammatory Roles in the Rat Cardiac Fibroblast Through Differential STAT Protein Activation

Analysis of the effects of stromal cells on the migration of lymphocytes into and through inflamed tissue using 3-D culture models

Cellular Pathways of Death and Survival in Acute Myocardial Infarction

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