Lipopolysaccharide primes neutrophils for a rapid response to IL-10

Cassatella, Marco A.; Tamassia, Nicola; Crepaldi, Luca; McDonald, Patrick P.; Ear, Thornin; Calzetti, Federica; Gasperini, Sara; Zanderigo, Floriana; Bazzoni, Flavia

doi:10.1002/eji.200526088

Cited by 24 publications

(21 citation statements)

References 39 publications

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“…Neutrophils represent key cellular targets for the immunosuppressive effects of IL-10 ( Bazzoni et al 2010). Exposure of neutrophils to inflammatory stimuli like LPS induces expression of IL-10R1 rendering the cells responsive to the immunosuppressive effects of IL-10 (Cassatella et al 2005;Crepaldi et al 2001;Tamassia et al 2008). Accordingly, neutrophils isolated from human patients with sepsis constitutively express high levels of IL-10R1 and are fully responsive to IL-10 (Tamassia et al 2008).…”

Section: Discussionmentioning

confidence: 98%

Deficiency of the CGRP receptor component RAMP1 attenuates immunosuppression during the early phase of septic peritonitis

et al. 2012

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Section: Discussionmentioning

confidence: 98%

Deficiency of the CGRP receptor component RAMP1 attenuates immunosuppression during the early phase of septic peritonitis

et al. 2012

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“…We further report here that GM-CSF or IL-4 also up-regulated SOCS3 mRNA expression. An increased expression of SOCS3 mRNA [21] and protein [27] was observed in neutrophils in response to IL-10, particularly when cells were pretreated with LPS. Presently, as there are few studies dealing with the regulation of SOCS in human neutrophils, it is difficult to explain why one team reported a high basal level of SOCS3 mRNA level expression, and three others reported different degrees of such expression.…”

Section: Discussionmentioning

confidence: 99%

“…Among these, it was observed that G-CSF and GM-CSF induced SOCS3 in human neutrophils [20,22,23,27]. Although IL-4 was reported to induce SOCS3 in murine B cells [25], there are presently no studies investigating the role of SOCS in IL-4-induced neutrophils.…”

Section: Introductionmentioning

confidence: 97%

Molecular mechanisms involved in interleukin-4-induced human neutrophils: expression and regulation of suppressor of cytokine signaling

Ratthé

Pelletier

Chiasson

et al. 2007

Journal of Leukocyte Biology

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Interleukin-4 (IL-4) is a CD132-dependent cytokine known to activate the Jak-STAT pathway in different cells and cell lines. Although IL-4 has been demonstrated previously to be an agonist in human neutrophils, its capacity to activate different cell signaling pathways in these cells has never been investigated. Two types of IL-4 receptor (IL-4R) exist: the Type I (CD132/IL-4Ralpha heterodimer) and the Type II (IL-4Ralpha/IL-13Ralpha1 heterodimer). In a previous study, we demonstrated that neutrophils express the Type I receptor. Herein, using flow cytometry, we demonstrated that neutrophils, unlike U-937 cells, do not express IL-13Ralpha1 and IL-13Ralpha2 and confirmed the expression of CD132 and IL-4Ralpha on their surface. We also demonstrated that IL-4 induced phosphorylation of Syk, p38, Erk-1/2, JNK, Jak-1, Jak-2, STAT6, and STAT1 and that treatment of cells with the inhibitors piceatannol, SB203580, PD98059, or AG490 reversed the ability of IL-4 to delay neutrophil apoptosis. Using RT-PCR, we demonstrated for the first time that neutrophils express mRNA for all suppressor of cytokine signaling (SOCS) members, namely SOCS1-7 and cytokine-inducible Src homology 2 protein. It is interesting that IL-4 increased expression of SOCS3 at the mRNA and protein levels. The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4. We conclude that neutrophils express only the Type I IL-4R on their surface and that IL-4 signals via different cell signaling pathways, including the Jak/STAT/SOCS pathway.

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“…[16][17][18] The induction of IL-8, a chemoattractant for neutrophils, suggests a role in early recruitment of inflammatory cells to the site of infection and whilst both IL-6 and -10 are known mainly for their roles in the adaptive immune system, both also have roles in innate responses. [34][35][36][37] The presence of IL-6 and -10 was particularly interesting from the perspective of IFN-l1 playing a role in linking innate and adaptive immunity. IL-6 plays a key role in the transition from a response dominated by cells of the innate immune system into one capable of mounting subsequent adaptive immunity, promoting the transition from a neutrophil-mediated infiltrate into one of monocytes, macrophages and lymphocytes.…”

Section: 24-31mentioning

confidence: 99%

Modulation of the human cytokine response by interferon lambda-1 (IFN-λ1/IL-29)

et al. 2006

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The interferon lambda family (IFN-l1/2/3) is a newly described group of cytokines that are related to both the type-1 interferons and IL-10 family members. These novel cytokines are induced during viral infection and, like type-1 interferons, display significant anti-viral activity. In order to understand their function in more depth, we have examined the ability of IFN-l1/IL-29 to regulate cytokine production by human immune cells. Whole peripheral blood mononuclear cells (PBMC) exposed to IFN-l1 specifically upregulated IL-6, -8 and -10 but there were no visible effects on TNF or IL-1. This response was produced in a dose-dependant fashion and was inhibited by IL-10. Examination of purified cell populations isolated from PBMC demonstrated that monocytes, rather than lymphocytes, were the major IFN-l1-responsive cellular subset, producing IL-6, -8 and -10 in response to IFN-l1. Monocyte responses induced by low-level LPS stimulation were also synergistically enhanced by the presence of IFN-l1. Human macrophages were also shown to react to IFN-l1 similarly to monocytes, by producing the cytokines IL-6, -8 and -10. In conclusion, we have shown that IFN-l1, a cytokine produced in response to viral infection, activates both monocytes and macrophages producing a restricted panel of cytokines and may therefore be important in activating innate immune responses at the site of viral infection.

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Lipopolysaccharide primes neutrophils for a rapid response to IL-10

Cited by 24 publications

References 39 publications

Deficiency of the CGRP receptor component RAMP1 attenuates immunosuppression during the early phase of septic peritonitis

Deficiency of the CGRP receptor component RAMP1 attenuates immunosuppression during the early phase of septic peritonitis

Molecular mechanisms involved in interleukin-4-induced human neutrophils: expression and regulation of suppressor of cytokine signaling

Modulation of the human cytokine response by interferon lambda-1 (IFN-λ1/IL-29)

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