Triggering of respiratory burst by tumor necrosis factor in neutrophils adherent to fibronectin. Evidence for a crucial role of CD18 glycoproteins

Ottonello, Luciano; Dapino, Patrizia; Scirocco, M.; Barberá, Pablo; Dallegri, Franco

doi:10.1007/bf01986395

Cited by 6 publications

(4 citation statements)

References 25 publications

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“…These observations suggest that the modulation of ␤ 2 -integrin via GM-CSF was the mechanism of adhesiondependent EOS functional upregulation. Like VCAM-1, EOS adhesion to fibronectin is not dependent on ␤ 2 -integrin expression, but such adhesion can enhance ␤ 2 -dependent GM-CSF-or TNF-␣-stimulated EOS respiratory burst (57,58). Moreover, Sung and coworkers (59) recently reported that GM-CSF enhances the adhesion strength of EOS and VCAM-1.…”

Section: Discussionmentioning

confidence: 99%

Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Nagata

Sedgwick

Kita

et al. 1998

Am J Respir Cell Mol Biol

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Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are members of the immunoglobulin superfamily adhesion molecules on vascular endothelium and important in the development of eosinophil (EOS) accumulation in allergic inflammation. To define the role of these adhesion proteins in EOS inflammation, peripheral blood EOS from allergic donors were incubated in either buffer (control)-, recombinant human (rh)-VCAM-1-, or rh-ICAM-1-coated plates, and the effects of these adhesion proteins on EOS effector functions were determined. VCAM-1 induced spontaneous EOS adhesion whereas EOS adhesion to ICAM-1 required a second signal, such as granulocyte macrophage colony-stimulating factor (GM-CSF). Although only VCAM-1 stimulated EOS superoxide anion (O2-) generation, the addition of GM-CSF (100 pM) to the reactions resulted in a greater and equivalent production of O2- with VCAM-1 and ICAM-1. In the presence of GM-CSF, ICAM-1 and VCAM-1 caused significant release of EOS-derived neurotoxin (EDN). Moreover, only ICAM-1 (no GM-CSF) promoted calcium ionophore A23187 (0.2 microM)-induced EOS leukotriene C4 (LTC4). Enhanced O2- generation, EDN release, and LTC4 generation observed with ICAM-1 and VCAM-1 were significantly inhibited by anti-beta2-integrin antibody. These results suggest that ICAM-1 and VCAM-1 are important in determining the eventual function of airway EOS.

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Section: Discussionmentioning

confidence: 99%

Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Nagata

Sedgwick

Kita

et al. 1998

Am J Respir Cell Mol Biol

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“…Cytochrome b 558 is localized with CD11b/CD18 in secretory vesicles [142]. In this light, adhesion-dependent enhancement of oxidative burst induced by LPS, TNF, fMLP, or phorbol esters may be due to the mobilization to the membrane of both CD11b/CD18 (Mac-1) and cytochrome b 558 [155][156][157][158]. Indeed, this form of activation may explain both vascular sequestration and the increased oxidant capacity of PMNs during endotoxemia.…”

Section: Pmn Primingmentioning

confidence: 99%

Neutrophil migration during endotoxemia

Wagner

Roth

1999

Journal of Leukocyte Biology

177

125

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Endotoxemia is marked by a global activation of inflammatory responses, which can lead to shock, multiple organ failure, and the suppression of immune and wound healing processes. Neutrophils (PMNs) play a central role in some of these responses by accumulating in tissues and releasing reactive oxygen species and proteases that injure host structures. This review focuses on altered PMN migratory responses that occur during endotoxemia and their consequences in the development of pulmonary infection. The inflammatory mediators that might be responsible for these altered responses are discussed. The oxidant potential of PMNs is increased after exposure to endotoxin both in vitro and during clinical and experimental endotoxemia. However, other functions such as chemotaxis and phagocytosis are often depressed in these same cells. Endotoxin exposure renders PMNs hyperadhesive to endothelium. The sum of these effects produces activated inflammatory cells that are incapable of leaving the vasculature. As such, the endotoxic PMN is more likely to promote tissue injury from within microvascular beds than to clear pathogens from extravascular sites. Moreover, the functional characteristics of endotoxic PMNs are similar to those observed during trauma, burn injury, sepsis, surgery, and other inflammatory conditions. Accordingly, several clinical conditions might have a common effector in the activated, yet migratorially dysfunctional, PMN. Direct effects of endotoxin on PMNs as well as effects of endogenous mediators released during endotoxemia are discussed. Understanding PMN behavior during endotoxemia may provide basic and critical insights that can be applied to a number of inflammatory scenarios. J. Leukoc. Biol. 66: 10-24; 1999.

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“…Whereas TNF␣ can prime neutrophils in suspension (9, 10), many TNF␣-induced cellular responses, including oxidant release, have been reported in association with ␤ 2 -mediated, integrin-mediated adherence (11)(12)(13). Neutrophils utilize a variety of adhesion molecules (14), but studies employing either genetically manipulated mice (15), antibody blocking studies (16), and studies with adhesion molecule-deficient patients (17) have shown that integrins, in particular ␤ 2 and ␤ 3 , are fundamentally important in adhesive events (16,18).…”

mentioning

confidence: 99%

Tumor Necrosis Factor-α Activation of the c-Jun N-terminal Kinase Pathway in Human Neutrophils

Avdi¹,

Nick²,

Whitlock³

et al. 2001

Journal of Biological Chemistry

104

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The intensity and duration of an inflammatory response depends on the balance of factors that favor perpetuation versus resolution. At sites of inflammation, neutrophils adherent to other cells or matrix components are exposed to tumor necrosis factor-␣ (TNF␣). Although TNF␣ has been implicated in induction of pro-inflammatory responses, it may also inhibit the intensity of neutrophilic inflammation by promoting apoptosis. Since TNF␣ is not only an important activator of the stress-induced pathways leading to p38 MAPk and c-Jun N-terminal kinase (JNK) but also a potent effector of apoptosis, we investigated the effects of TNF␣ on the JNK pathway in adherent human neutrophils and the potential involvement of this pathway in neutrophil apoptosis. Stimulation with TNF␣ was found to result in ␤ 2 integrin-mediated activation of the cytoplasmic tyrosine kinases Pyk2 and Syk, and activation of a three-part MAPk module composed of MEKK1, MKK7, and/or MKK4 and JNK1. JNK activation was attenuated by blocking antibodies to ␤ 2 integrins, the tyrosine kinase inhibitors, genistein, and tyrphostin A9, a Pyk2-specific inhibitor, and piceatannol, a Syk-specific inhibitor. Exposure of adherent neutrophils to TNF␣ led to the rapid onset of apoptosis that was demonstrated by augmented annexin V binding and caspase-3 cleavage. TNF␣؊induced increases in annexin V binding to neutrophils were attenuated by blocking antibodies to ␤ 2 integrins, and the caspase-3 cleavage was attenuated by tyrphostin A9. Hence, exposure of adherent neutrophils to TNF␣ leads to utilization of the JNK-signaling pathways that may contribute to diverse functional responses including induction of apoptosis and subsequent resolution of the inflammatory response.The rapid influx of polymorphonuclear leukocytes (neutrophils) into sites of injury is an important component of the acute inflammatory response in humans (1). The resulting adherence and chemotaxis of leukocytes in the appropriate cytokine milieu are not only necessary for efficient clearance of microorganisms (2) but may also participate in appropriate resolution of the inflammatory response through the subsequent induction of cell death by apoptosis.Tumor necrosis factor-␣ (TNF␣), 1 a pluripotent cytokine, is produced by a variety of leukocytes in response to stimulation by lipopolysaccharide (3). In turn, exposure to TNF␣ induces wide ranging biological effects including cell differentiation, proliferation, apoptosis, and multiple pro-inflammatory effects. TNF␣ exerts potent effects on neutrophils that have been suggested to contribute to the inflammatory response in sepsis (4, 5) and the adult respiratory distress syndrome (6). However, TNF␣ also exerts anti-inflammatory effects as demonstrated by an enhanced inflammatory response in TNF␣ Ϫ/Ϫ mice after infection (7), an effect that has been ascribed to the ability of TNF␣ to induce apoptosis in neutrophils (8).Whereas TNF␣ can prime neutrophils in suspension (9, 10), many TNF␣-induced cellular responses, including oxidant release, have been repo...

show abstract

Triggering of respiratory burst by tumor necrosis factor in neutrophils adherent to fibronectin. Evidence for a crucial role of CD18 glycoproteins

Cited by 6 publications

References 25 publications

Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Neutrophil migration during endotoxemia

Tumor Necrosis Factor-α Activation of the c-Jun N-terminal Kinase Pathway in Human Neutrophils

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