Tumour necrosis factor‐α potentiates CR3‐induced respiratory burst by activating p38 MAP kinase in human neutrophils

Forsberg, Maria; Löfgren, Ragnhild; Zheng, Limin; Stendahl, Olle

doi:10.1046/j.1365-2567.2001.01270.x

Cited by 43 publications

(40 citation statements)

References 40 publications

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“…A similar mechanism could operate with regard to ANCA and would be consistent with a previous report that ANCA preferentially engage Fc␥RIIIb (14). However, we found that homotypic Fc␥RIIIb cross-linking led directly to Syk phosphorylation in TNF-␣-primed neutrophils, which concurs with the results of other investigators who previously primed neutrophils with a higher dose of TNF-␣ (16,35). The explanation for this phenomenon remains unknown, but it suggests that Fc␥RIIIb can mediate Syk phosphorylation independent of Fc␥RIIa and that ligation of Fc␥RIIIb by ANCA-Fc may directly induce Syk phosphorylation.…”

Section: Discussionsupporting

confidence: 92%

“…Previously, it was reported that blockade of the common ␤ 2 integrin antigen CD18 completely inhibits the ANCA-induced respiratory burst (8). Mac-1 (CD11b/CD18) may cooperate with Fc␥RIIa and Fc␥RIIIb in neutrophil activation, and specific Mac-1 cross-linking directly induces a respiratory burst in a manner augmented by TNF-␣ (15,16). Another area of interest, which has thus far received little attention, is the involvement of the high-affinity Fc␥ receptor Fc␥RI (CD64) in neutrophil activation by ANCA.…”

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confidence: 99%

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Activation of Syk in Neutrophils by Antineutrophil Cytoplasm Antibodies Occurs via Fcγ Receptors and CD18

Hewins¹,

Williams²,

Wakelam³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Antineutrophil cytoplasm antibodies (ANCA) activate TNF-␣-primed neutrophils to undergo a respiratory burst. The intracellular signals that mediate activation have not been studied extensively but could increase the understanding of the pathogenesis small vessel vasculitis. It was demonstrated that ANCA-IgG induced phosphorylation of the tyrosine kinase Syk in TNF-␣-primed neutrophils from healthy donors. Syk was not phosphorylated in response to ANCA F(ab') 2 . Furthermore, Syk phosphorylation was attenuated by blockade of both low-affinity Fc␥ receptors and CD18. Similarly, low-affinity Fc␥ receptor blockade reduced ANCA-induced superoxide production. In patient-derived neutrophils, the high-affinity Fc␥ receptor Fc␥RI was also demonstrated to be involved in ANCA-induced superoxide production. However, Syk phosphorylation was not attenuated by blockade of the Fc␥RI, present on neutrophils from vasculitis patients. The tyrosine kinase inhibitor 4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine inhibited the ANCA-induced respiratory burst and Syk phosphorylation, suggesting that Src kinases lie upstream of Syk activation but downstream of ANCA engagement of Fc␥ receptors. Piceatannol, another tyrosine kinase inhibitor, also inhibited ANCA-induced Syk phosphorylation and the ANCA-stimulated respiratory burst, supporting the proposed functional role for Syk in ANCA signaling. ANCAinduced phosphorylation of Cbl and intracellular calcium transients, potential downstream mediators of Syk activation, were also blocked by tyrosine kinase inhibitors. While it has previously been shown that pertussis toxin diminishes the ANCAinduced respiratory burst, indicating heterotrimeric G protein involvement, Syk phosphorylation and calcium transients were unaffected by pertussis toxin. Collectively, these data show that Syk phosphorylation is induced during ANCA-triggered neutrophil activation.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Activation of Syk in Neutrophils by Antineutrophil Cytoplasm Antibodies Occurs via Fcγ Receptors and CD18

Hewins¹,

Williams²,

Wakelam³

et al. 2004

Journal of the American Society of Nephrology

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“…Degranulation in neutrophils and macrophages is regulated by p38 MAPK (53,54), and it was recently suggested that p38 MAPK enhances phagosomal maturation by increasing granule mobility via Rab (34). We therefore speculated that p38 MAPK could be part of the signal transduction involved in the Cdc42-regulated translocation of granules.…”

Section: Discussionmentioning

confidence: 96%

Inactivation of Cdc42 Is Necessary for Depolymerization of Phagosomal F-Actin and Subsequent Phagosomal Maturation

Lerm

Brodin

Ruishalme

et al. 2007

The Journal of Immunology

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Phagocytosis is a complex process involving the activation of various signaling pathways, such as the Rho GTPases, and the subsequent reorganization of the actin cytoskeleton. In neutrophils, Rac and Cdc42 are activated during phagocytosis but less is known about the involvement of these GTPases during the different stages of the phagocytic process. The aim of this study was to elucidate the role of Cdc42 in phagocytosis and the subsequent phagosomal maturation. Using a TAT-based protein transduction technique, we introduced dominant negative and constitutively active forms of Cdc42 into neutrophil-like HL60 (human leukemia) cells that were allowed to phagocytose IgG-opsonized yeast particles. Staining of cellular F-actin in cells transduced with constitutively active Cdc42 revealed that the activation of Cdc42 induced sustained accumulation of periphagosomal actin. Moreover, the fusion of azurophilic granules with the phagosomal membrane was prevented by the accumulated F-actin. In contrast, introducing dominant negative Cdc42 impaired the translocation per se of azurophilic granules to the periphagosomal area. These results show that efficient phagosomal maturation and the subsequent eradication of ingested microbes in human neutrophils is dependent on a strictly regulated Cdc42. To induce granule translocation, Cdc42 must be in its active state but has to be inactivated to allow depolymerization of the F-actin cage around the phagosome, a process essential for phagolysosome formation.

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“…Besides its key contribution to the anti-Aspergillus innate response (9,14,23,39), TNF-␣ represents an essential cytokine involved in DC maturation (42). Indeed, the TNF-␣ present in the supernatants from A. fumigatus-infected DC could determine the induction of a partial maturation of DC, characterized by the acquisition of CD83 and the absence of CCR7.…”

Section: Fumigatus-matured DC and Il-12 Family Members 1485mentioning

confidence: 99%

Human Dendritic Cells followingAspergillus fumigatusInfection Express the CCR7 Receptor and a Differential Pattern of Interleukin-12 (IL-12), IL-23, and IL-27 Cytokines, Which Lead to a Th1 Response

Gafa

Lande²,

Gagliardi³

et al. 2006

Infect Immun

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Aspergillus fumigatus is the most prevalent airborne fungal pathogen and causes fatal invasive aspergillosis in immunocompromised patients. Given the essential role of dendritic cells (DC) in initiating and regulating immune responses, we investigated the impact of A. fumigatus conidial infection on human DC. A. fumigatus conidia were rapidly internalized and induced the release of tumor necrosis factor alpha within the first 8 h. After A. fumigatus infection, the majority of DC underwent full maturation, although CCR7 expression was observed only in DC that had internalized the conidia. Additionally, the analysis of regulatory cytokines showed that infected DC simultaneously produced interleukin-12p70 (IL-12p70) and significant amounts of IL-10. IL-10 neutralization was not able to further increase IL-12p70 production from infected DC. Whereas the central role of IL-12 in the generation of Th1 cells has long been appreciated, recently two other members of the IL-12 family, IL-23 and IL-27, were reported to play important roles in the regulation of gamma interferon (IFN-␥) production from naïve and memory T cells. A. fumigatus-infected DC were also able to express high levels of IL-23p19 and low levels of IL-27p28 at later stages of infection. According to this expression pattern, A. fumigatus-infected DC were able to prime IFN-␥ production of naïve T cells. Thus, this study on the expression of the new IL-12 family members controlling the Th1 response sheds light on a novel aspect of the contribution of DC to anti-Aspergillus immunity.

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Tumour necrosis factor‐α potentiates CR3‐induced respiratory burst by activating p38 MAP kinase in human neutrophils

Cited by 43 publications

References 40 publications

Activation of Syk in Neutrophils by Antineutrophil Cytoplasm Antibodies Occurs via Fcγ Receptors and CD18

Activation of Syk in Neutrophils by Antineutrophil Cytoplasm Antibodies Occurs via Fcγ Receptors and CD18

Inactivation of Cdc42 Is Necessary for Depolymerization of Phagosomal F-Actin and Subsequent Phagosomal Maturation

Human Dendritic Cells followingAspergillus fumigatusInfection Express the CCR7 Receptor and a Differential Pattern of Interleukin-12 (IL-12), IL-23, and IL-27 Cytokines, Which Lead to a Th1 Response

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