Different Subcellular Localization of Cytochrome b and the Dormant NADPH-Oxidase in Neutrophils and Macrophages: Effect on the Production of Reactive Oxygen Species during Phagocytosis

Johansson, Agneta; Jesaitis, Algirdas J.; Lundqvist, Helen; Magnusson, Karl‐Eric; Sjölin, Carola; Karlsson, Anna; Dahlgren, Cláes

doi:10.1006/cimm.1995.1009

Cited by 71 publications

(56 citation statements)

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“…However, LDL was internalized by PMN by its specific receptor, and this internalization decreased PKC-induced oxidative burst (monitored by DCF formation). In neutrophils, contrary to macrophages, NADPH oxidase has been located preferentially in the phagolysosome [29] and cytoskeleton rearrangements upon phagolysosome formation diminished PKC induction of peroxide formation [30]. Furthermore, LDL has been shown to scavenge peroxides produced by the cells, which readily modified the molecule [3,11].…”

Section: Discussionmentioning

confidence: 99%

“…The measurement of PKC activity was performed as described by the manufacturer (GIBCO) using the protocol described by Thomas et al [27] and modified by Yasuda et al [28] which includes a pseudosubstrate inhibitor PKC (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36). Membrane and cytosol fractions were separated by ultracentrifugation at 100 000 g for 60 min at 48C; the membrane fraction was then solubilized again with 1% (w/v) of Nonidet P-40 and recentrifuged at 100 000 g for 60 min at 48C.…”

Section: Determination Of Pkc Activitymentioning

confidence: 99%

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Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Leclerc

Rivera

Perez-P

et al. 1997

Clinical and Experimental Immunology

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SUMMARYLow density lipoprotein receptors (LDLR), capable of internalizing LDL, are expressed in polymorphonuclear neutrophils (PMN). The expression was assessed using anti-LDLR antibody by flow cytometry. The internalization of LDL was assessed by: (i) quantification of the uptake of labelled LDL with 1,1 0 dicholoflurescein (DCF) by flow cytometry. This effect was not observed in monocytes or lymphocytes, and it was blocked by anti-LDLR antibody. The stimulation of LDL was optimal at 10 ¹ g of protein/ml. LDL was able to suppress DCF formation induced by phorbol myristate acetate (PMA) and PMA was unable to further stimulate LDL-treated cells, suggesting protein kinase-C (PKC) involvement in LDL effects. Using a PKC assay, LDL was shown to induce a two-fold increase in PKC translocation to the membrane. Thus, LDL increases PMN oxidative burst through a PKCdependent pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Determination Of Pkc Activitymentioning

confidence: 99%

Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Leclerc

Rivera

Perez-P

et al. 1997

Clinical and Experimental Immunology

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“…Importantly, the site of oxidant generation depends on the stimulus. In general, soluble agonists such as fMLP promote oxidase assembly at the plasma membrane, and superoxide is generated primarily in the extracellular milieu, whereas microbes target the NADPH oxidase to form phagosomes, and superoxide is generated in the phagosome lumen (15)(16)(17)(18)(19)(20)(21)(22).…”

Section: Helicobacter Pylori Disrupts Nadph Oxidase Targeting In Humamentioning

confidence: 99%

“…5A). Cell activation by HP-NAP and Hp(2-20) is sensitive to PTx and Hp (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) acts via FPRL1 (34). Notably, the fMLP-triggered respiratory burst was efficiently blocked by PTx (4.5 Ϯ 7.8% of control (n ϭ 6)), but responses to Hp were unaffected (103 Ϯ 6% of control (n ϭ 6)).…”

Section: Mechanism Of Hp-induced Superoxide Releasementioning

confidence: 99%

Helicobacter pyloriDisrupts NADPH Oxidase Targeting in Human Neutrophils to Induce Extracellular Superoxide Release

Allen

Beecher

Lynch

et al. 2005

The Journal of Immunology

123

168

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Helicobacter pylori (Hp) infection triggers a chronic influx of polymorphonuclear leukocyte neutrophils (PMNs) into the gastric mucosa. Although Hp reside in a neutrophil-rich environment, how these organisms evade phagocytic killing is largely unexplored. We now show that live Hp (strains 11637, 60190, DT61A, and 11916) are readily ingested by PMNs and induce a rapid and strong respiratory burst that is comparable to PMA. Relative to other particulate stimuli, Hp are more potent activators of PMNs than opsonized zymosan, Staphylococcus aureus, or Salmonella. Strikingly, biochemical and microscopic analyses demonstrate that Hp disrupt NADPH oxidase targeting such that superoxide anions are released into the extracellular milieu and do not accumulate inside Hp phagosomes. Specifically, nascent Hp phagosomes acquire flavocytochrome b558 but do not efficiently recruit or retain p47phox or p67phox. Superoxide release peaks at 16 min coincident with the appearance of assembled oxidase complexes in patches at the cell surface. Oxidant release is regulated by formalin-resistant and heat-sensitive bacterial surface factors distinct from urease and Hp(2–20). Following opsonization with fresh serum, Hp triggers a modest respiratory burst that is confined to the phagosome, and ingested bacteria are eliminated. We conclude that disruption of NADPH oxidase targeting allows unopsonized Hp to escape phagocytic killing, and our findings support the hypothesis that bacteria and PMNs act in concert to damage the gastric mucosa.

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“…Neutrophils were allowed to phagocytize serum-opsonized yeast particles and indirect immunofluorescence was performed as described earlier [17] using lactoferrin as a marker for specific granules.…”

Section: Determination Of Phagolysosome Fusionmentioning

confidence: 99%

Neutrophils in mucosal secretion are functionally active

Ebenfelt

Lundqvist

Dahlgren

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe leucocytes in the secretion on the tonsillar surface have been regarded as inactivated and dying cells with no essential function in the defence of the underlying mucosa. In recent studies, we showed that in acute tonsillitis there are very few, if any, bacteria in the parenchyma, whereas in the secretion on the tonsillar surface there are huge numbers of bacteria and neutrophils, and furthermore, extensive phagocytosis. The present study was performed to elucidate the functional capacity of the neutrophils in the secretion on the tonsillar surface. Secretion samples were taken from the tonsillar surface of healthy volunteers with an imprint technique which allows transfer of secretion from the mucosa to a glass slide with maintained topographic position of the cells. The capacity of the neutrophils to respond to chemotactic stimuli and to phagocytize and further process labelled yeast particles was studied in this in vitro system. The results show that the neutrophils in the secretion have the same properties as in tissue, and also when having arrived in the secretion they can identify and attack new prey.

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Different Subcellular Localization of Cytochrome b and the Dormant NADPH-Oxidase in Neutrophils and Macrophages: Effect on the Production of Reactive Oxygen Species during Phagocytosis

Cited by 71 publications

References 0 publications

Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes

Helicobacter pyloriDisrupts NADPH Oxidase Targeting in Human Neutrophils to Induce Extracellular Superoxide Release

Neutrophils in mucosal secretion are functionally active

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