Effects of inflammatory cytokines on the permeability of human lung microvascular endothelial cell monolayers and differential eosinophil transmigration

Sedgwick, Julie B.; Menon, I. A.; Gern, James E.; Busse, William W.

doi:10.1067/mai.2002.128581

Cited by 98 publications

(68 citation statements)

References 21 publications

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“…/insert) were grown to confluence on 5 mm filters in 6.5 mm Transwell inserts (Corning, NY, USA). Confluence of the monolayers (usually 3 days after seeding) was confirmed by measuring transendothelial electrical resistance with an Endohm device (WPI, Sarasota, Fla) [54,55]. The monolayers grown in the inserts were activated by 0.5 U/mL thrombin for 15 min or by 10 pM TNF-a for 4 h at 371C and placed into 24-well plates containing eotaxin (3 nM) or vehicle in the bottom wells.…”

Section: Eosinophil Adhesion To Endothelial Cells Under Flow Conditionsmentioning

confidence: 99%

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Interaction of eosinophils with endothelial cells is modulated by prostaglandin EP4 receptors

et al. 2011

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Eosinophil extravasation across the endothelium is a key feature of allergic inflammation. Here, we investigated the role of PGE 2 and its receptor, E-type prostanoid receptor (EP)-4, in the regulation of eosinophil interaction with human pulmonary microvascular endothelial cells. PGE 2 and the EP4 receptor agonist ONO AE1-329 significantly reduced eotaxininduced eosinophil adhesion to fibronectin, and formation of filamentous actin and gelsolin-rich adhesive structures. These inhibitory effects were reversed by a selective EP4 receptor antagonist, ONO AE3-208. PGE 2 and the EP4 agonist prevented the activation and cell-surface clustering of b2 integrins, and L-selectin shedding of eosinophils. Under physiological flow conditions, eosinophils that were treated with the EP4 agonist showed reduced adhesion to endothelial monolayers upon stimulation with eotaxin, as well as after TNF-a-induced activation of the endothelial cells. Selective activation of EP1, EP2, and EP3 receptors did not alter eosinophil adhesion to endothelial cells, whereas the EP4 antagonist prevented PGE 2 from decreasing eosinophil adhesion. Finally, eosinophil transmigration across thrombin-and TNF-a-activated endothelial cells was effectively reduced by the EP4 agonist. These data suggest that PGE 2 -EP4 signaling might be protective against allergic responses by inhibiting the interaction of eosinophils with the endothelium and might hence be a useful therapeutic option for controlling inappropriate eosinophil infiltration.Keywords: Adhesion . Endothelium . Eosinophils . Migration . Prostaglandins Supporting Information available online IntroductionEosinophil granulocytes are important effector cells in allergic inflammation and are recruited to the tissue by chemotactic signals [1][2][3][4][5]. The infiltrating eosinophils release several toxic and proinflammatory mediators which induce epithelial injury, airway hyper-responsiveness, and airway remodeling [6][7][8]. Therefore, eosinophils are regarded as potential therapeutic targets in allergic diseases and asthma [9].Prostaglandins (PGs) play diverse roles in inflammation, depending on the cellular context, the type of PG being released, and the differential expression of PG receptors [10,11]. While PGD 2, which is the predominant PG formed in mast cells, exerts proinflammatory effects by regulating the recruitment of eosino- Eur. J. Immunol. 2011. 41: 2379-2389 DOI 10.1002 Leukocyte signaling 2379 phils, basophils, and Th2 lymphocytes to the sites of allergic inflammation [12], PGE 2 seems to attenuate inflammatory responses and reduce tissue injury in airways [13]. PGE 2 was found to exert bronchoprotective effects in patients with asthma [14]. In rats, the ovalbumin-induced early and late phase airway responses were inhibited by intratracheally administered PGE 2 [15]. The activity of PGE 2 is mediated by four subtypes of E-type prostanoid receptors (EP), EP1, EP2, EP3, and EP4 [16]. These G protein-coupled receptors have distinct biological imprints depending on their affinity with...

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Section: Eosinophil Adhesion To Endothelial Cells Under Flow Conditionsmentioning

confidence: 99%

“…Endothelial cell attachment and growth was promoted by precoating with 1% gelatin for 1 h at 371C. Fresh medium was added every 2 days and cells were passaged after reaching 90% confluence (5-6 days); the cells were used between 5 and 10 passages [54,55]. …”

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Interaction of eosinophils with endothelial cells is modulated by prostaglandin EP4 receptors

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“…Every nucleated cell can express these cytokines, and all cells other than erythrocytes can respond to them. In in vitro experiments, these cytokines induce gene expression (including chemokines and adhesion molecules) and increase permeability across microvascular endothelium (53,66,68). In vivo, the instillation or transgenic expression of these cytokines causes inflammation, including neutrophil accumulation and plasma extravasation (11,17,22,23,59).…”

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confidence: 99%

Roles for early response cytokines duringEscherichia colipneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1

Mizgerd¹,

Lupa²,

Hjoberg³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Our study as well as those of other authors revealed that human lung epithelial cells produced CRP (7)(8)(9). Epithelial and endothelial cell permeability may be increased during lung inflammation, allowing the movement of proteins across the lung-blood barrier (39). Therefore, CRP secreted by human lung epithelial cells may enter the systemic circulation and increase serum CRP levels in the presence or absence of a hepatic response.…”

Section: Discussionmentioning

confidence: 53%

Atorvastatin reduces lipopolysaccharide-induced expression of C-reactive protein in human lung epithelial cells

Xing

Duan

et al. 2011

Mol Med Report

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Abstract. Accumulating evidence suggests that statins possess anti-inflammatory properties and may decrease C-reactive protein (CRP) levels in plasma. However, no studies have as yet addressed whether or not statins regulate the expression of CRP in human lung epithelial cells (A549). In this study, we determined whether atorvastatin modulates the lipopolysaccharide (LPS)-induced expression of CRP in A549 cells. A549 cells were incubated in Dulbecco's modified Eagle's medium containing LPS in the absence or presence of various concentrations of atorvastatin. After incubation, the medium was collected and the amount of CRP was measured by an enzyme-linked immunosorbent assay. The cells were harvested and CRP messenger ribonucleic acid (mRNA) was analyzed by reverse transcription polymerase chain reaction. Incubation with LPS induced a significant time-and dose-dependent increase in CRP mRNA expression and CRP production in A549 cells, whereas atorvastatin significantly decreased LPS-induced CRP mRNA expression and CRP production in a dose-dependent manner. The present study revealed that A549 cells are capable of LPS-induced CRP expression, and that atorvastatin down-regulates the LPS-induced expression of CRP in cultured A549 cells. Our results suggest that statins ameliorate lung inflammation by regulating CRP production in human lung epithelial cells.

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Effects of inflammatory cytokines on the permeability of human lung microvascular endothelial cell monolayers and differential eosinophil transmigration

Cited by 98 publications

References 21 publications

Interaction of eosinophils with endothelial cells is modulated by prostaglandin EP4 receptors

Interaction of eosinophils with endothelial cells is modulated by prostaglandin EP4 receptors

Roles for early response cytokines duringEscherichia colipneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1

Atorvastatin reduces lipopolysaccharide-induced expression of C-reactive protein in human lung epithelial cells

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