Differential effect of surfactant and its saturated phosphatidylcholines on human blood macrophages

Gille, Christian; Spring, Bärbel; Bernhard, Wolfgang; Gebhard, Cathérine; Basile, Denise; Lauber, Kirsten; Poets, Christian F.; Orlikowsky, Thorsten

doi:10.1194/jlr.m600451-jlr200

Cited by 37 publications

(33 citation statements)

References 32 publications

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“…As shown earlier (20,22), αCD3 mAb-mediated T-cell proliferation in uninfected CBMCs was diminished as compared with that of PBMCs (28% (15-80%) vs. 64% (40-85%), Figure 5b). Infection of monocytes resulted in a greatly diminished αCD3-mediated T-cell proliferation in PBMCs as compared with their uninfected counterparts (21% (12-82%), Figure 5b), whereas T-cell proliferation in CBMCs was increased (82% (46-89%), Figure 5b).…”

Section: Remaining Cbmos Are Capable Of Inducing T-cell Proliferationmentioning

confidence: 81%

“…Therefore, we analyzed an obligatory monocyte-dependent function and chose αCD3 mAb-stimulated T-cell proliferation, which depends on monocyte capacity to provide costimulatory signals (20,21). PBMOs and CBMOs were infected with E. coli-GFP and, after removal of free bacteria, T cells were stimulated with αCD3 for 48 h and analyzed by flow cytometry.…”

Section: Remaining Cbmos Are Capable Of Inducing T-cell Proliferationmentioning

confidence: 99%

“…T-cell proliferation was assessed by Vybrant CFDA SE Cell Tracer Kit (Molecular Probes, Eugene, OR), as described before (20).…”

Section: T-cell Proliferation Assaymentioning

confidence: 99%

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The CD95/CD95L pathway is involved in phagocytosis-induced cell death of monocytes and may account for sustained inflammation in neonates

et al. 2012

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Background:The propensity for sustained inflammation after bacterial infection in neonates, resulting in inflammatory sequelae such as bronchopulmonary dysplasia and periventricular leucomalacia, is well known, but its molecular mechanisms remain elusive. Termination of inflammatory reactions physiologically occurs early after removal of bacteria by phagocytosis-induced cell death (PIcD) of immune effector cells such as monocytes. PIcD from cord blood monocytes (cBMOs) was shown to be reduced as compared with that of peripheral blood monocytes (PBMOs) from adult donors in vitro. Methods: PBMOs, cBMOs, and Fas (cD95)-deficient (lpr) mouse monocytes were analyzed in an in vitro infection model using green fluorescence protein-labeled Escherichia coli (E. coli-GFP). Phagocytosis and apoptosis were quantified by flow cytometry and cD95L secretion was quantified by enzyme-linked immunosorbent assay. results: We demonstrate the involvement of the cD95/ cD95 ligand pathway (cD95/cD95L) in PIcD and provide evidence that diminished cD95L secretion by cBMOs may result in prolonged activation of neonatal immune effector cells. conclusion: These in vitro results offer for the first time a molecular mechanism accounting for sustained inflammation seen in neonates.

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Section: Remaining Cbmos Are Capable Of Inducing T-cell Proliferationmentioning

confidence: 81%

Section: Remaining Cbmos Are Capable Of Inducing T-cell Proliferationmentioning

confidence: 99%

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The CD95/CD95L pathway is involved in phagocytosis-induced cell death of monocytes and may account for sustained inflammation in neonates

et al. 2012

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“…MOI 1:5 was achieved by dilution with PBS. Actin-dependent phagocytosis was blocked by cytochalasin D (Cyto D, Sigma Chemical Co.; 10 g/mL, 30 min before infection), resulting in a decrease of phagocytosis to less than 5% (17). For analysis of postphagocytic reactions, washed cells were cultured in RPMI supplemented with 10% FCS and gentamicin (Sigma Chemical Co.; 200 g/mL).…”

Section: Methodsmentioning

confidence: 99%

Diminished Phagocytosis-Induced Cell Death (PICD) in Neonatal Monocytes upon Infection with Escherichia coli

et al. 2008

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An imbalance in apoptosis or survival of immune cells plays an essential role in the pathophysiology of sepsis. Phagocytosis-induced cell death (PICD) is a common result of the pathogenhost cell interaction mediated by reactive oxygen species (ROS). Neonatal sepsis is frequently characterized by hyperinflammation. Cord blood monocytes (CBMO) are equivalent to monocytes of adults [peripheral blood monocytes (PBMO)], both in terms of phagocytosis and killing of Escherichia coli. We investigated whether CBMO are less sensitive toward PICD compared with PBMO. Monocytes were infected with green fluorescent protein (GFP)-labeled E. coli. Phagocytic activity, cell-count, Annexin V staining, hypoploid DNA content, CD95 and CD95L expression, and caspase-8 and -9 activities were analyzed by flow cytometry, ROS production by chemiluminescence, and CD95L mRNA expression by reverse-transcriptase polymerase chain reaction. With equal phagocytic activity and ROS production, PBMO cell count was decreased by 82 Ϯ 6% versus 28 Ϯ 8% for CBMO after infection. Annexin V binding was enhanced fivefold on PBMO; 56 Ϯ 15% of PBMO showed a hypodiploid DNA content compared with 9 Ϯ 6% of CBMO. Caspases CD95L and CD95L mRNA were up-regulated in PBMO. Our results indicate that CBMO are less sensitive toward E. coli-mediated PICD than PBMO. Modifying monocyte apoptosis may be a target for future interventions in sepsis. (Pediatr Res 63: [33][34][35][36][37][38] 2008)

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“…On the other hand, treatment of macrophages with surfactant lipids or SP-A was shown to induce SR-A expression (89), indicating that local host factors control basal levels of SR-A on alveolar macrophages. Several signaling pathways were shown to regulate expression and activation of SR-A involving arachidonic acid metabolites of iPLA2 and 12/15 lipoxygenase (87).…”

Section: Cd11cmentioning

confidence: 99%

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

Sever-Chroneos

Krupa

Davis

et al. 2011

Journal of Biological Chemistry

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There is limited knowledge about host factors that facilitate eradication of Staphylococcus aureus infection in the lung. Methicillin-resistant S. aureus has remained a major cause of hospital-and health care-associated pneumonia since its appearance over 40 years ago and has recently become a more prominent etiology in community acquired pneumonia. Colonization of nasal epithelium with S. aureus, a normal occurrence in over 20% of the population, increases the risk for the development of staphylococcal pneumonia (1). Furthermore, S. aureus co-infections are a major complication contributing to high morbidity and mortality during both pandemic and seasonal influenza virus pneumonia (2). S. aureus deploys a combination of virulence factors, including adhesins, toxins, and immunomodulatory molecules, that facilitate infection of different host tissues (3, 4).Surfactant protein A (SP-A) 3 is a crucial component of the pulmonary innate immune system in the alveolar spaces (5, 6). SP-A is the major protein constituent of pulmonary surfactant; it is involved in organization of large aggregate surfactant phospholipids lining the alveolar surface and acts as an opsonin for pathogens (7). SP-A is incorporated in the tubular myelin fraction of pulmonary surfactant that covers the alveolar lining fluid of the distal airway epithelium. The presence of pathogen-derived molecules may trigger reorganization of surfactant lipids (8 -11) and exposure of SP-A to bind pathogens at points of entry on the surfactant interface. Alveolar macrophages in the aqueous hypophase may then patrol areas of disturbance on the surfactant layer binding SP-A-opsonized bacteria. SP-A binds pathogens via a carboxyl-terminal carbohydrate recognition domain in a calcium-dependent manner. Amino-terminal collagen-like and coiled-coil do-

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Differential effect of surfactant and its saturated phosphatidylcholines on human blood macrophages

Cited by 37 publications

References 32 publications

The CD95/CD95L pathway is involved in phagocytosis-induced cell death of monocytes and may account for sustained inflammation in neonates

The CD95/CD95L pathway is involved in phagocytosis-induced cell death of monocytes and may account for sustained inflammation in neonates

Diminished Phagocytosis-Induced Cell Death (PICD) in Neonatal Monocytes upon Infection with Escherichia coli

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

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