Cytokine milieu modulates release of thymic stromal lymphopoietin from human keratinocytes stimulated with double-stranded RNA

Kinoshita, Hirokazu; Takai, Toshiro; Lê, Tuấn Anh; Kamijo, Seiji; Wang, Xiao Ling; Ushio, Hiroko; Hara, Mutsuko; Kawasaki, Junko; Vu, Anh Tuan; Ogawa, Takasuke; Gunawan, Hendra; Ikeda, Shigaku; Okumura, Ko; Ogawa, Hideoki

doi:10.1016/j.jaci.2008.10.008

Cited by 117 publications

(137 citation statements)

References 45 publications

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“…Furthermore, the observation that neutralizing Abs against TSLP slightly downregulated Th2 skewing, even in the PBS-treated KCM, indicated that basal production of periostin from untreated fibroblasts can cause induction of TSLP in keratinocytes, followed by Th2 skewing via DCs to a small extent. It has been reported that synergistic stimuli of Th2 cytokines (IL-4 or IL-13) and proinflammatory cytokines (TNF-α or IL-1α), or extrinsic stimuli via several TLRs, induce TSLP production in keratinocytes (48)(49)(50). In addition to these factors, we demonstrated that periostin was an intrinsic inducer of TSLP from keratinocytes, a finding we believe to be novel.…”

Section: Discussionsupporting

confidence: 64%

Periostin promotes chronic allergic inflammation in response to Th2 cytokines

et al. 2012

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Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with α v integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or α v integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation.

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Section: Discussionsupporting

confidence: 64%

Periostin promotes chronic allergic inflammation in response to Th2 cytokines

et al. 2012

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“…Pollen grains contain various releasable or insoluble substances including lipids (12-18), proteases (13, 19, 30), NADPH oxidase (8 -11), subpollen particles (10), and starch granules (55), which could be involved in the pathogenesis of allergic diseases. Mechanisms of the induction of DC responses by pollen and induction of Th2-inducing cytokines in other types of cells (22,56,57) by pollen-derived substances should be addressed in future studies.…”

Section: Discussionmentioning

confidence: 99%

Cupressaceae Pollen Grains Modulate Dendritic Cell Response and Exhibit IgE-Inducing Adjuvant Activity In Vivo

Kamijo¹,

Takai²,

Kuhara³

et al. 2009

The Journal of Immunology

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Pollen is considered a source of not only allergens but also immunomodulatory substances, which could play crucial roles in sensitization and/or the exacerbation of allergies. We investigated how allergenic pollens from different plant species (Japanese cedar and Japanese cypress, which belong to the Cupressaceae family, and birch, ragweed, and grass) modulate murine bone marrow-derived dendritic cell (DC) responses and examined the effect of Cupressaceae pollen in vivo using mice. DCs were stimulated with pollen extracts or grains in the presence or absence of LPS. Cell maturation and cytokine production in DCs were analyzed by flow cytometry, ELISA, and/or quantitative PCR. Pollen extracts suppressed LPS-induced IL-12 production and the effect was greatest for birch and grass. Without LPS, pollen grains induced DC maturation and cytokine production without IL-12 secretion and the response, for which TLR 4 was dispensable, was greatest for the Cupressaceae family. Intranasal administration of Cupressaceae pollen in mice induced an elevation of serum IgE levels and airway eosinophil infiltration. Coadministration of ovalbumin with Cupressaceae pollen grains induced ovalbumin-specific IgE responses associated with eosinophil infiltration. The results suggest that modulation of DC responses by pollen differs among the plant families via (1) the promotion of DC maturation and cytokine production by direct contact and/or (2) the inhibition of IL-12 production by soluble factors. The strong DC stimulatory activity in vitro and IgE-inducing activity in mice support the clinical relevance of Cupressaceae pollen to allergies in humans.

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“…Again, the production of CCL2, GM-CSF, and CXCL1 was strongly dependent on MyD88 in keratinocytes of solvent-treated mice, whereas IL-1a and TNF-a were only marginally and TSLP secretion was not affected by MyD88 deficiency. Since TLR3/TRIF or IRF3 activation is able to induce TSLP [39,40] and Th2 cytokines boost TLSP expression [41], it might be possible that enhanced TRIF activation in our setting, might lead to increased TLSP levels.Repeated tape-stripping and application of OVA in vivo led to enhanced expression of all cytokines analyzed even from keratinocytes of noninvolved distant skin in vitro in a MyD88-dependent manner (Fig. 5B).…”

mentioning

confidence: 94%

Requirement of MyD88 signaling in keratinocytes for Langerhans cell migration and initiation of atopic dermatitis‐like symptoms in mice

et al. 2016

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Atopic dermatitis (AD) is a chronic inflammatory disease controlled by the innate and adaptive immune system. To elucidate the impact of innate immune signaling in AD, we analyzed MyD88-deficient mice in a murine model of AD-like dermatitis by epicutaneous sensitization with ovalbumin (OVA). Global MyD88 deficiency led to reduced epidermal thickening and diminished accumulation of macrophages within the inflamed skin. In addition, we observed impaired emigration of Langerhans cells (LCs) out of the epidermis of MyD88-deficient mice. These findings indicate that MyD88 deficiency affects various skin-resident cell types in the AD model. Moreover, production of IFN-g, IL-17, and CCL17 was reduced in skin draining lymph node cells and OVA-specific immunoglobulin levels were lower in MyD88-deficient mice. We further investigated the role of MyD88 in keratinocytes, as keratinocytes contribute to AD pathology. Exclusive expression of MyD88 in epidermal keratinocytes partially restored LC emigration after AD induction and expression of CCL17 in skin draining lymph nodes (LNs), but did not promote epidermal thickening nor production of IL-17. Altogether, these data demonstrate that MyD88 signaling in keratinocytes is able to restore LC migration in an otherwise MyD88-deficient background, and significantly contributes to the development of AD-like dermatitis.Keywords: Allergology r Dermatitis r Innate immunity r Langerhans cells r MyD88 signaling r Skin inflammation Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionAtopic dermatitis (AD) is a chronic, inflammatory skin disease [1,2] characterized by pruritic, scaly, and erythematous skin lesions and is caused by genetic, environmental, and immunologic factors Correspondence: Dr. Heike Weighardt e-mail: Heike.weighardt@uni-bonn.de [3]. Activation of the immune system during AD results in a mixed Th1 and Th2 response, but also Th22 and Th17 subsets contribute to the immune response [4]. In the majority of AD patients the disease is associated with the development of allergen-specific IgE titers, however also a non-IgE-associated form exists [2]. * These authors contributed equally to this work.C 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu 982Sonja Didovic et al. Eur. J. Immunol. 2016. 46: 981-992 The development of AD involves barrier defects caused by mutations in structural genes such as filaggrin or disturbed protease activity in the epidermis [5,6] and a dysregulation of the immune system of the skin [6,7]. Impaired barrier function is characterized by enhanced transepidermal water loss (TEWL), which may enhance entry of pathogens, allergens, or toxins and thereby facilitate activation of the skin immune system [6,7]. The skin dendritic cell (DC) network comprises epidermal Langerhans cells (LCs) and different subsets of dermal DCs (dDCs) [8,9]. Upon antigen acquisition both LCs and dDCs get activated and migrate to the draining lymph nodes (LNs) to induce an immune re...

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Cytokine milieu modulates release of thymic stromal lymphopoietin from human keratinocytes stimulated with double-stranded RNA

Cited by 117 publications

References 45 publications

Periostin promotes chronic allergic inflammation in response to Th2 cytokines

Periostin promotes chronic allergic inflammation in response to Th2 cytokines

Cupressaceae Pollen Grains Modulate Dendritic Cell Response and Exhibit IgE-Inducing Adjuvant Activity In Vivo

Requirement of MyD88 signaling in keratinocytes for Langerhans cell migration and initiation of atopic dermatitis‐like symptoms in mice

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