Human Alveolar Macrophages and Granulocyte-macrophage Colony-stimulating Factor-induced Monocyte-derived Macrophages Are Resistant to H2O2 via Their High Basal and Inducible Levels of Catalase Activity

Komuro, Iwao; Keicho, Naoto; Iwamoto, Aikichi; Akagawa, Kiyoko S.

doi:10.1074/jbc.m102081200

Cited by 44 publications

(49 citation statements)

References 46 publications

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“…Treatment of GM-CSF-induced macrophages with antisense oligonucleotides for C/EBPdecreases the amount of the inhibitory isoform produced and increases HIV-1 production (Komuro et al, 2003). This study also showed the inverse regulation of the Src-like tyrosine kinase Hck and suggested that the heterogeneity in macrophage susceptibility to HIV-1 infection was related to distinct regulation of Hck and the inhibitory isoform of C/EBPGM-CSF-induced macrophages present similar morphological and functional features to alveolar macrophages (Komuro et al, 2001). The low level of susceptibility of alveolar macrophages to HIV-1 infection may be related to the expression of the dominant inhibitory C/EBPisoform .…”

Section: Viral Transcription In Macrophagesmentioning

confidence: 52%

Macrophages and HIV-1: dangerous liaisons

Verani¹,

Gras

Pancino

2005

Molecular Immunology

102

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Section: Viral Transcription In Macrophagesmentioning

confidence: 52%

Macrophages and HIV-1: dangerous liaisons

Verani¹,

Gras

Pancino

2005

Molecular Immunology

102

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“…It was earlier demonstrated that GM-CSF-differentiated macrophages exhibit higher catalase activity than M-CSF-differentiated macrophages and that M-CSF-differentiated macrophages release a larger amount of H 2 O 2 than GM-CSF-differentiated macrophages in response to bacterial stimulation (53). It also has been shown that inhibition of catalase by 3-AT increases H 2 O 2 levels in macrophages (54).…”

Section: Discussionmentioning

confidence: 89%

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Yoshioka

Kitao

Kishino

et al. 2006

The Journal of Immunology

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We investigated the cytoprotective effect of NO on H2O2-induced cell death in mouse macrophage-like cell line RAW264. H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. These apoptotic features were significantly inhibited by pretreatment for 24 h with NO donors, sodium nitroprusside and 1-hydroxy-2-oxo-3,3-bis-(2-aminoethyl)-1-triazene, at a low nontoxic concentration. The cytoprotective effect of NO was abrogated by the catalase inhibitor 3-amino-1,2,4-triazole but was not affected by a glutathione synthesis inhibitor, l-buthionine-(S,R)-sulfoximine. NO donors increased the level of catalase and its activity in a concentration-dependent manner. Cycloheximide, a protein synthesis inhibitor, inhibited both the NO-induced increase in the catalase level and the cytoprotective effect of NO. These results indicate that NO at a low concentration protects macrophages from H2O2-induced apoptosis by inducing the production of catalase.

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“…Differentiation was evaluated by morphology, by cell cycle analysis using PI and by the NBT assay (22). Cell surface expression of CD11b (2 l/tube) and CD14 (2 l/tube) were performed by flow cytometric analysis (10,000 events) using a FACScan (BD Biosciences).…”

Section: Hl-60 Cell Differentiationmentioning

confidence: 99%

In Vivo and In Vitro Roles of IL-21 in Inflammation

Pelletier

Bouchard

Girard

2004

The Journal of Immunology

102

126

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IL-21 is a cytokine known to mediate its biological action via the IL-21R, composed of a specific chain, IL-21Rα, and the common γ-chain (CD132). Recent data suggest that IL-21 possesses proinflammatory properties. However, there is no clear evidence that IL-21 induces inflammation in vivo and, curiously, the interaction between IL-21 and neutrophils has never been investigated, despite the fact that these cells express CD132 and respond to other CD132-dependent cytokines involved in inflammatory disorders. Using the murine air pouch model, we found that IL-21 induced inflammation in vivo, based on recruitment of neutrophil and monocyte populations. In contrast to LPS, administration of IL-21 into the air pouch did not significantly increase the concentration of IL-6, CCL5, CCL3, and CXCL2. We demonstrated that HL-60 cells expressed IL-21Rα, which is down-regulated during their differentiation toward neutrophils, and that IL-21Rα is not detected in neutrophils. Concomitant with this, IL-21 induced Erk-1/2 phosphorylation in HL-60 cells, but not in neutrophils. To eliminate the possibility that IL-21 could activate neutrophils even in the absence of IL-21Rα, we demonstrated that IL-21 did not modulate several neutrophil functions. IL-21-induced Erk-1/2 phosphorylation was not associated with proliferation or differentiation of HL-60 toward neutrophils, monocytes, or macrophages. IL-21Rα was detected in human monocytes and monocyte-derived macrophages, but IL-21 increased CXCL8 production only in monocyte-derived macrophages. We conclude that IL-21 is a proinflammatory cytokine, but not a neutrophil agonist. We propose that IL-21 attracts neutrophils indirectly in vivo via a mechanism independent of IL-6, CCL3, CCL5, and CXCL2 production.

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Human Alveolar Macrophages and Granulocyte-macrophage Colony-stimulating Factor-induced Monocyte-derived Macrophages Are Resistant to H2O2 via Their High Basal and Inducible Levels of Catalase Activity

Cited by 44 publications

References 46 publications

Macrophages and HIV-1: dangerous liaisons

Macrophages and HIV-1: dangerous liaisons

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

In Vivo and In Vitro Roles of IL-21 in Inflammation

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