Migration of CD18-deficient neutrophils in vitro: evidence for a CD18-independent pathway induced by IL-8

Morland, Clare M.; Morland, Bruce; Darbyshire, P; Stockley, Robert A.

doi:10.1016/s0925-4439(99)00089-7

Cited by 25 publications

(17 citation statements)

References 27 publications

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“…The basis of the engagement of CD18-independent mechanisms is not clear. In an in vitro system in which CD18-indepenent pathways of transendothelial PMN migration were identified, IL-8 was shown to promote the CD18-independent emigration of PMN (8,24,26,39). In another study we showed that the E. coli induced the release of macrophage inflammatory protein-2 (our unpublished observation), the murine homologue of IL-8, in lung tissue, which could account for the observed CD18-independent tissue PMN sequestration and migration responses.…”

Section: Discussionmentioning

confidence: 70%

“…Activation of PMN adherent to the microvessels plays a key role in the inflammatory response and contributes to the mechanism of microvascular injury by the release of oxidants, proteases, chemokines, and other mediators (3,(5)(6)(7)(8). Assessment of PMN adhesion has shown that CD11/CD18 integrin complexes expressed on PMN are essential for PMN adhesion to the vascular endothelium and migration of PMN across the endothelial barrier (9 -14).…”

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confidence: 99%

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Differential Role of CD18 Integrins in Mediating Lung Neutrophil Sequestration and Increased Microvascular Permeability Induced byEscherichia coliin Mice

Gao

Sekosan

et al. 2001

The Journal of Immunology

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The in vivo contributions of CD18 integrin-dependent and -independent mechanisms in mediating the increases in lung neutrophil (polymorphonuclear leukocyte; PMN) sequestration and microvascular permeability are not well understood. We determined the time course of these responses to Gram-negative sepsis in the mouse lung and addressed the specific contributions of CD18 integrins and ICAM-1. PMN sequestration in the lung was assessed by morphometric analysis, and transalveolar PMN migration was assessed by bronchoalveolar lavage. Lung tissue PMN number increased by 6-fold within 1 h after i.p. Escherichia coli challenge; this value peaked at 3 h (7-fold above control) and decreased at 12 h (3.5-fold above control). PMN migration into the airspace was delayed; the value peaked at 6 h and remained elevated up to 12 h. Saturating concentrations of anti-CD18 and anti-ICAM-1 mAbs reduced lung tissue PMN sequestration and migration; however, peak responses at 3 and 6 h were inhibited by 40%, indicating that only a small component of PMN sequestration and migration was CD18 dependent at these times. In contrast to the time-dependent decreased role of CD18 integrins in mediating PMN sequestration and migration, CD18 and ICAM-1 blockade prevented the increase in lung microvascular permeability and edema formation at all times after E. coli challenge. Thus, Gram-negative sepsis engages CD18/ICAM-1-independent mechanisms capable of the time-dependent amplification of lung PMN sequestration and migration. The increased pulmonary microvascular permeability induced by E. coli is solely the result of engagement of CD18 integrins even when PMN accumulation and migration responses are significantly CD18 independent.

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Section: Discussionmentioning

confidence: 70%

mentioning

confidence: 99%

Differential Role of CD18 Integrins in Mediating Lung Neutrophil Sequestration and Increased Microvascular Permeability Induced byEscherichia coliin Mice

Gao

Sekosan

et al. 2001

The Journal of Immunology

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“…However, in light of new published data this distinction obviously oversimplifies this multiform process. Which of these both transmigration mechanisms are actually operative is also in part dependent on the chronicity of reactions as well as on the various chemotaxins (43,44). Thus, a CD18-independent transendothelial migration of PMN can be stimulated in vitro by the host-derived chemoattractants IL-8 and leukotriene B 4 (45).…”

Section: Discussionmentioning

confidence: 99%

Respiratory Syncytial Virus Infection of Human Lung Endothelial Cells Enhances Selectively Intercellular Adhesion Molecule-1 Expression

Arnold

König

2005

The Journal of Immunology

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Respiratory syncytial virus (RSV) is worldwide the most frequent cause of bronchiolitis and pneumonia in infants requiring hospitalization. In the present study, we supply evidence that human lung microvascular endothelial cells, human pulmonary lung aorta endothelial cells, and HUVEC are target cells for productive RSV infection. All three RSV-infected endothelial cell types showed an enhanced cell surface expression of ICAM-1 (CD54), which increased in a time- and RSV-dose-dependent manner. By using noninfectious RSV particles we verified that replication of RSV is a prerequisite for the increase of ICAM-1 cell surface expression. The up-regulated ICAM-1 expression pattern correlated with an increased cellular ICAM-1 mRNA amount. In contrast to ICAM-1, a de novo expression of VCAM-1 (CD106) was only observed on RSV-infected HUVEC. Neither P-selectin (CD62P) nor E-selectin (CD62E) was up-regulated by RSV on human endothelial cells. Additional experiments performed with neutralizing Abs specific for IL-1α, IL-1β, IL-6, and TNF-α, respectively, excluded an autocrine mechanism responsible for the observed ICAM-1 up-regulation. The virus-induced ICAM-1 up-regulation was dependent on protein kinase C and A, PI3K, and p38 MAPK activity. Adhesion experiments using polymorphonuclear neutrophil granulocytes (PMN) verified an increased ICAM-1-dependent adhesion rate of PMN cocultured with RSV-infected endothelial cells. Furthermore, the increased adhesiveness resulted in an enhanced transmigration rate of PMN. Our in vitro data suggest that human lung endothelial cells are target cells for RSV infection and that ICAM-1 up-regulated on RSV-infected endothelial cells might contribute to the enhanced accumulation of PMN into the bronchoalveolar space.

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“…In vitro studies of neutrophil locomotion indicate that different chemotactic factors may select different pathways. For example, neutrophil emigration through human umbilical vein endothelial cell monolayers is not blocked by antibodies to ␤ 2 -integrins if the stimulus is IL-8 or leukotriene (LT) B 4 , but transendothelial migration in response to the chemotactic tripeptide [N-formyl-methionyl-leucyl-phenylalanine (fMLF)] is ␤ 2 -integrin dependent (179). Clear evidence for such chemotactic factor selection in vivo has not been published.…”

Section: Introductionmentioning

confidence: 99%

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Burns

Smith²,

Walker³

2003

Physiological Reviews

266

273

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Neutrophil emigration in the lung differs substantially from that in systemic vascular beds where extravasation occurs primarily through postcapillary venules. Migration into the alveolus occurs directly from alveolar capillaries and appears to progress through a sequence of steps uniquely influenced by the cellular anatomy and organization of the alveolar wall. The cascade of adhesive and stimulatory events so critical to the extravasation of neutrophils from postcapillary venules in many tissues is not evident in this setting. Compelling evidence exists for unique cascades of biophysical, adhesive, stimulatory, and guidance factors that arrest neutrophils in the alveolar capillary bed and direct their movement through the endothelium, interstitial space, and alveolar epithelium. A prominent path accessible to the neutrophil appears to be determined by the structural interactions of endothelial cells, interstitial fibroblasts, as well as type I and type II alveolar epithelial cells.

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Migration of CD18-deficient neutrophils in vitro: evidence for a CD18-independent pathway induced by IL-8

Cited by 25 publications

References 27 publications

Differential Role of CD18 Integrins in Mediating Lung Neutrophil Sequestration and Increased Microvascular Permeability Induced byEscherichia coliin Mice

Differential Role of CD18 Integrins in Mediating Lung Neutrophil Sequestration and Increased Microvascular Permeability Induced byEscherichia coliin Mice

Respiratory Syncytial Virus Infection of Human Lung Endothelial Cells Enhances Selectively Intercellular Adhesion Molecule-1 Expression

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

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