Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

Moulin, David; Donzé, Olivier; Talabot-Ayer, Dominique; Mézin, Françoise; Palmer, Gaby; Gabay, Cem

doi:10.1016/j.cyto.2007.09.013

Cited by 287 publications

(271 citation statements)

References 27 publications

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“…IL-33 is present in the peripheral blood [23] and in BALF of asthmatic patients whose bronchial epithelium produces this cytokine at high levels [24]. IL-33 drives production of proinflammatory and Th2 cytokines by mast cells and Th2 lymphocytes [25,26], induces chemotaxis of Th2 cells [27], promotes eosinophil and basophil adhesion, and increases eosinophil survival and basophil migration [28]. In the present study, IL-33 reduction by SCTE may help decrease lung and BALF eosinophil numbers.…”

Section: Discussionmentioning

confidence: 99%

A water extract of Samchulkunbi-tang attenuates airway inflammation by inhibiting inos and MMP-9 activities in an ovalbumin-induced murine asthma model

Lee

Shin

Lim

et al. 2012

BMC Complement Altern Med

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BackgroundIn this study, we investigated the effect of Samchulkunbi-tang water extract (SCTE) in an established mouse model of ovalbumin (OVA)-induced allergic asthma. The effects of SCTE on the production of Th1 and Th2 cytokines, eotaxin, and total and OVA-specific immunoglobulin E, inducible nitric oxide synthase expression, and matrix metalloproteinase-9 activity were measured.MethodsMice were sensitized on days 0 and 14 with an intraperitoneal injection of 20 μg ovalbumin (OVA) emulsified in 2 mg aluminum hydroxide in 200 μL PBS buffer. On days 21, 22, and 23, mice received an airway exposure to OVA (1%, w/v, in PBS) for 1 h. SCTE was administered orally to mice at doses of 200 and 400 mg/kg per day from days 18 to 23.ResultsSCTE reduced the number of inflammatory cells, cytokines, and chemokines in bronchoalveolar lavage fluids and iNOS expression and MMP-9 activity in mouse lung tissue. Histological studies using hematoxylin & eosin and periodic acid-schiff staining showed that SCTE substantially inhibited OVA-induced inflammatory cell infiltration in lung tissue and goblet cell hyperplasia in the airway. SCTE also reduced IL-4 and IL-13 expression in concanavalin-A-stimulated splenocytes. These results were similar to those obtained with montelukast as a positive control.ConclusionsCollectively, these results suggest that SCTE may be an effective oral treatment for allergic airway inflammation by virtue of its anti-inflammatory activity.

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Section: Discussionmentioning

confidence: 99%

A water extract of Samchulkunbi-tang attenuates airway inflammation by inhibiting inos and MMP-9 activities in an ovalbumin-induced murine asthma model

Lee

Shin

Lim

et al. 2012

BMC Complement Altern Med

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“…48,49 Much like IL-25, it is important for driving IL-13 production by ILC2 during infection 31,35 and can also be recognized by other cell types. [50][51][52][53] Furthermore, whereas exogenous administration of IL-33 at early time points after T. muris infection promotes worm clearance, injection at later stages of infection does not induce expulsion, 29 suggesting that there is an early window of opportunity in which it exerts its effects. The relative importance of IL-33 as compared with IL-25 is not clear, as there is some functional redundancy between the two, and it thus remains to be determined whether both are equally important upon parasite infection.…”

Section: Transmissionmentioning

confidence: 99%

Immunity to gastrointestinal nematode infections

2018

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“…IL-33 signals through a heterodimeric membrane receptor composed of ST2 and the IL-1R1 accessory protein and activates basophils [20,21], mast cells [22,23], eosinophils [24,25], NK and NKT cells [26], Th2 lymphocytes [5,27] and macrophages [14]. In accordance with its Th2 functions, administration of IL-33 into naive mice induces severe inflammation in the lung and digestive tract with elevated levels of IL-4, IL-5 and IL-13, splenomegaly and increased serum Ig [10].…”

Section: Introductionmentioning

confidence: 99%

IL‐33‐activated dendritic cells are critical for allergic airway inflammation

et al. 2011

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IL-33, a new member of the IL-1 family cytokine, is involved in Th2-type responses in a wide range of diseases and signals through the ST2 receptor expressed on many immune cells. Since the effects of IL-33 on DCs remain controversial, we investigated the ability of IL-33 to modulate DC functions in vitro and in vivo. Here, we report that IL-33 activates myeloid DCs to produce IL-6, IL-1b, TNF, CCL17 and to express high levels of CD40, CD80 OX40L and CCR7. Importantly, IL-33-activated DCs prime naive lymphocytes to produce the Th2 cytokines IL-5 and IL-13, but not IL-4. In vivo, IL-33 exposure induces DC recruitment and activation in the lung. Using an OVA-induced allergic lung inflammation model, we demonstrate that the reduced airway inflammation in ST2-deficient mice correlates with the failure in DC activation and migration to the draining LN. Finally, we show that adoptive transfer of IL-33-activated DCs exacerbates lung inflammation in a DC-driven model of allergic airway inflammation. These data demonstrate for the first time that IL-33 activates DCs during antigen presentation and thereby drives a Th2-type response in allergic lung inflammation. IntroductionAllergic asthma is a chronic disorder characterized by eosinophilic airway inflammation, mucus hypersecretion, antigenspecific-IgE antibodies, airway remodeling and increased airway hyperreactivity [1,2]. The process of airway inflammation involves various cells types, such as eosinophils, mast cells, epithelial cells, lymphocytes and DCs. Th2 cells have been shown to play a predominant role in allergic asthma and Th2 cytokines, such as IL-4, IL-5 and IL-13, exacerbate disease severity [3,4]. IL-33, the recently discovered Th2 cytokine, is found at high levels in the plasma of asthmatic patients [5,6] and in the lungs of mice during experimental allergic asthma [7,8].IL-33 is a member of IL-1 family [9][10][11]. Like IL-1b or IL-18, IL-33 is synthesized as a precursor and can be cleaved by caspase-1 and 3 but the cleavage products are biologically less active than the precursor [12,13]. In contrast to the other IL-1 family members, IL-33 is mainly expressed in non-hematopoietic cells such as fibroblasts, epithelial cells and endothelial cells [10,14,15]. Because of its nuclear localization sequence, IL-33 is usually present in the nucleus, where it acts as a potential transcriptional repressor [16]. Recently, IL-33 has been shown to be released from necrotic cells and may act as an alarmin in a similar manner to IL-1a [17] or high mobility group box1 protein HMGB1 [18,19]. [14]. In accordance with its Th2 functions, administration of IL-33 into naive mice induces severe inflammation in the lung and digestive tract with elevated levels of IL-4, IL-5 and IL-13, splenomegaly and increased serum Ig [10]. In vitro, IL-33 has also been reported to polarize naive CD4 1 T cells to produce IL-5 and IL-13, but not . Polarization of this atypical Th2 population is independent of IL-4, STAT6 and GATA3. On macrophages, IL-33 amplifies IL-13-mediated polarization...

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Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

Cited by 287 publications

References 27 publications

A water extract of Samchulkunbi-tang attenuates airway inflammation by inhibiting inos and MMP-9 activities in an ovalbumin-induced murine asthma model

A water extract of Samchulkunbi-tang attenuates airway inflammation by inhibiting inos and MMP-9 activities in an ovalbumin-induced murine asthma model

Immunity to gastrointestinal nematode infections

IL‐33‐activated dendritic cells are critical for allergic airway inflammation

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