A co-stimulatory signal through ICAM-β2 integrin-binding potentiates neutrophil phagocytosis

Schnitzler, Norbert; Haase, G.; Podbielski, Andreas; Lütticken, Rudolf; Schweizer, Klaus

doi:10.1038/5597

Cited by 62 publications

(58 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This response, stimulated by chemotactic factors, was markedly augmented by CD11b-dependent adhesion via the interaction of CD11b with ICAM-1 expressed on the endothelial cell surface (22,29). CD11b was also shown to be associated with components of the NADPH complex, p47 phox and gp91 phox , after TNF-␣ challenge (unpublished data).…”

Section: Discussionmentioning

confidence: 97%

Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury

Gao

Liu

Broman

et al. 2005

Physiological Genomics

View full text Add to dashboard Cite

ϩ/ϩ mice interfered with lung PMN infiltration induced by E. coli and prevented the increase in lung microvessel permeability and edema formation, with most of the protection seen in the 1-h period after the E. coli. Thus our results demonstrate that CD11b plays a crucial role in mediating lung PMN sequestration and vascular injury in the early phase of gram-negative septicemia. The NIF ϩ/ϩ mouse model, in which CD11b is inactivated by binding to NIF, is a potentially useful model for in vivo assessment of the role of PMN CD11b in the mechanism of vascular inflammation. neutrophil inhibitory factor; NIF ϩ/ϩ mice; CD11b/CD18 integrin; neutrophil function; sepsis-induced lung injury; polymorphonuclear leukocyte RECRUITMENT OF polymorphonuclear neutrophils (PMNs) in lungs has been implicated in the development of acute lung injury (ALI) (17, 28). The process of recruitment involves PMN adhesion to endothelial cells via ␤ 2 -integrins and transendothelial migration of PMNs into tissues (33). The PMN adhesion cascade comprises elements of tethering, rolling, activation, and firm adhesion (4, 33). Rolling and capture of PMNs are in large part mediated by endothelial P-selectin binding to P-selectin glycoprotein ligand-1 (PSGL-1). Stable adhesion of PMNs is mediated by the binding of PMN ␤ 2 -integrins CD11a/CD18 and CD11b/CD18 to intercellular adhesion molecule-1 (ICAM-1) on the endothelial cell surface (33). The ␤ 2 -integrins, lymphocyte function associated antigen-1 (LFA-1; CD11a/CD18) and Mac-1 (CD11b/CD18), are the major negative regulators of PMN rolling velocity; hence, deletion of ␤ 2 -integrin in mice (CD18 Ϫ/Ϫ mice) was shown to increase the PMN rolling velocity (8, 16). ␤ 2 -Integrins are also capable of binding to multiple ligands; Mac-1 recognizes extracellular matrix proteins (fibronectin, laminin, collagen, and elastin), ICAM-1 and ICAM-2 (11), blood coagulation proteins [fibrinogen (1), factor X (2), and kininogen (15)], neutrophil inhibitory factor (NIF) (25), complement pathway product (iC3b) (3), and nonprotein ligands [e.g., lipopolysaccharide (LPS), ␤-glucan (35), and heparin (6)]. The broad binding specificity of Mac-1 is not shared by LFA-1 even though the two have overlapping functional properties (44). Functional defects have been reported for Mac-1 gene deletion in mice; these include impaired PMN respiratory burst response (5), absence of PMN spreading and adhesion (5,7,21,34), and reduced susceptibility to ischemia/reperfusioninduced tissue injury (32).NIF is a 47-kDa protein isolated from the parasite Ancylostoma caninum that interferes with the host-defense response by apparently inactivating CD11b (25). Recombinant NIF inhibited the adhesion of activated human PMNs to the endothelium and release of PMN H 2 O 2 over a concentration range (IC 50 10-20 nM) (25). NIF binding sites on PMNs showed selective, high-affinity binding to the I-domain of CD11b (25) and low-affinity binding to CD11a in phorbol ester-stimulated PMNs (20). NIF protein has 257 amino acids preceded by a 17-amino acid lea...

show abstract

Section: Discussionmentioning

confidence: 97%

Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury

Gao

Liu

Broman

et al. 2005

Physiological Genomics

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown that staphylococci and streptococci differ in their sensitivity to phagocytosis, depending on the expression of neutrophil surface receptors. 26 Hence, the impact of zinc deficiency on phagocytosis by monocytes may also vary with the bacterial species.…”

Section: Discussionmentioning

confidence: 99%

Differential impact of zinc deficiency on phagocytosis, oxidative burst, and production of pro-inflammatory cytokines by human monocytes

et al. 2014

View full text Add to dashboard Cite

Zinc deficiency has a fundamental influence on the immune defense, with multiple effects on different immune cells, resulting in a major impairment of human health. Monocytes and macrophages are among the immune cells that are most fundamentally affected by zinc, but the impact of zinc on these cells is still far from being completely understood. Therefore, this study investigates the influence of zinc deficiency on monocytes of healthy human donors. Peripheral blood mononuclear cells, which include monocytes, were cultured under zinc deficient conditions for 3 days. This was achieved by two different methods:by application of the membrane permeable chelator N,N,N 0 ,N 0 -tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN) or by removal of zinc from the culture medium using a CHELEX 100 resin. Subsequently, monocyte functions were analyzed in response to Escherichia coli, Staphylococcus aureus, and Streptococcus pneumoniae. Zinc depletion had differential effects. On the one hand, elimination of bacterial pathogens by phagocytosis and oxidative burst was elevated. On the other hand, the production of the inflammatory cytokines tumor necrosis factor (TNF)-a and interleukin (IL)-6 was reduced. This suggests that monocytes shift from intercellular communication to basic innate defensive functions in response to zinc deficiency.These results were obtained regardless of the method by which zinc deficiency was achieved. However, CHELEX-treated medium strongly augmented cytokine production, independently from its capability for zinc removal. This side-effect severely limits the use of CHELEX for investigating the effects of zinc deficiency on innate immunity.

show abstract

“…Airway response to bacterial pathogens is modulated by increased expression of ICAM-1 [66,134]. Interaction of ICAM-1 with CD11/CD18 on leukocytes is determinant for leukocyte adhesion to airway epithelial cells [90,135] and decreased ICAM-1 expression or function may result in impaired leukocyte recruitment and/or antimicrobial activity [134,136,137]. Therefore, the current evidence suggests that airway epithelial cells are key orchestrators of inflammatory response through the release of both pro-inflammatory cytokines and the upregulation of ICAM-1 adhesion molecules.…”

Section: Epithelial Cellsmentioning

confidence: 99%

Mucosal inflammation in idiopathic bronchiectasis: cellular and molecular mechanisms

Fuschillo¹,

Felice²,

Balzano³

2008

Eur Respir J

184

124

View full text Add to dashboard Cite

Bronchiectasis is a chronic and debilitating lung disease, characterised by irreversible dilatation of the bronchi as consequence of airway injury and remodelling due to recurrent or chronic airway inflammation and infection. The underlying aetiologies include autoimmune diseases, severe infections, genetic abnormalities and acquired disorders.The pathogenesis of bronchiectasis is poorly understood. Three distinct pathogenetic elements, namely infection, inflammation and enzymatic actions, which interact with each other, have been implicated in the pathophysiology of bronchiectasis.Some recent observations indicate that airway inflammation in bronchiectasis comes from a deregulated cytokine network independent of bacterial airway colonisation.In the present review, current knowledge about cellular and molecular inflammatory events in the dynamic process of host-pathogen interaction that are thought to play a relevant role in the pathogenic mechanisms of airway wall destruction leading to bronchiectasis are discussed.

show abstract

A co-stimulatory signal through ICAM-β2 integrin-binding potentiates neutrophil phagocytosis

Cited by 62 publications

References 23 publications

Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury

Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury

Differential impact of zinc deficiency on phagocytosis, oxidative burst, and production of pro-inflammatory cytokines by human monocytes

Mucosal inflammation in idiopathic bronchiectasis: cellular and molecular mechanisms

Contact Info

Product

Resources

About