Flaky Tail Mouse Denotes Human Atopic Dermatitis in the Steady State and by Topical Application with Dermatophagoides pteronyssinus Extract

Moniaga, Catharina Sagita; Egawa, Gyohei; Kawasaki, Hiroshi; Hara‐Chikuma, Mariko; Honda, Tetsuya; Tanizaki, Hideaki; Nakajima, Saeko; Otsuka, Atsushi; Matsuoka, Hiroyuki; Kubo, Akiharu; Sakabe, Jun‐ichi; Tokura, Y.; Miyachi, Yoshiki; Amagai, Masayuki; Kabashima, Kenji

doi:10.2353/ajpath.2010.090957

Cited by 120 publications

(140 citation statements)

References 40 publications

(61 reference statements)

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“…Therefore, filaggrin is absent from the cornified layers in the epidermis of the Flg ft mouse (Fallon, et al, 2009, Presland, et al, 2000, Scharschmidt, et al, 2009). Consistently, we and others have described that Flg ft mice express a truncated and smaller profilaggrin protein that is not processed to filaggrin (Fallon, et al, 2009, Moniaga, et al, 2010, Presland, et al, 2000 (Fig.1). Fig.…”

Section: Origin Of Flaky Tail Micesupporting

confidence: 55%

“…The first report showed only histological abnormality without clinical manifestation (Fallon, et al, 2009), and the second demonstrated spontaneous eczematous skin lesions after 28 weeks of www.intechopen.com age (Oyoshi, et al, 2009), and the third contained no notice of any spontaneous dermatitis in Flg ft mice (Scharschmidt, et al, 2009). The fourth paper by Moniaga et al have demonstrated that Flg ft mice showed spontaneous dermatitis with skin lesions mimicking human AD as early as 5 weeks of age with mild erythema and fine scales and the cutaneous manifestations advanced with age in a steady state under SPF conditions (Moniaga, et al, 2010) (Fig. 2).…”

Section: Flaky Tail Mouse In a Steady Statementioning

confidence: 99%

“…Later, the lack of filaggrin in the epidermis was proposed in the commercially available strain of Flg ft mice, which has both Flg and ma mutations, as a model of IV, and therefore there was no discussion about the cutaneous inflammatory conditions from the perspective of AD (Presland, et al, 2000). There have been four recent papers of Flg ft mice as a model of filaggrin deficiency: the first paper used Flg ft mice from which the ma mutation had been eliminated with four additional backcrosses to B6 mice (Fallon, et al, 2009), and the others used the commercially available Flg ft mice (Moniaga, et al, 2010, Oyoshi, et al, 2009, Scharschmidt, et al, 2009). The first report showed only histological abnormality without clinical manifestation (Fallon, et al, 2009), and the second demonstrated spontaneous eczematous skin lesions after 28 weeks of www.intechopen.com age (Oyoshi, et al, 2009), and the third contained no notice of any spontaneous dermatitis in Flg ft mice (Scharschmidt, et al, 2009).…”

Section: Flaky Tail Mouse In a Steady Statementioning

confidence: 99%

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Flaky Tail Mouse as a Novel Animal Model of Atopic Dermatitis: Possible Roles of Filaggrin in the Development of Atopic Dermatitis

Moniaga¹,

Kabashima²

2012

Atopic Dermatitis - Disease Etiology and Clinical Management

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Section: Origin Of Flaky Tail Micesupporting

confidence: 55%

Section: Flaky Tail Mouse In a Steady Statementioning

confidence: 99%

Section: Flaky Tail Mouse In a Steady Statementioning

confidence: 99%

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Flaky Tail Mouse as a Novel Animal Model of Atopic Dermatitis: Possible Roles of Filaggrin in the Development of Atopic Dermatitis

Moniaga¹,

Kabashima²

2012

Atopic Dermatitis - Disease Etiology and Clinical Management

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“…Recently, it was shown by Moniaga et al that Flg-deficient mouse skin shows increased susceptibility to Dermatophagoides pteronyssinus-induced dermatitis, a pathogen relevant for human AD pathogenesis. 29 There may be different thresholds for movement of water versus other chemicals through the stratum corneum, eg, depending on lipophilicity.…”

Section: Discussionmentioning

confidence: 99%

Filaggrin Genotype in Ichthyosis Vulgaris Predicts Abnormalities in Epidermal Structure and Function

Gruber

Elias

Crumrine

et al. 2011

The American Journal of Pathology

218

238

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Although it is widely accepted that filaggrin (FLG) deficiency contributes to an abnormal barrier function in ichthyosis vulgaris and atopic dermatitis, the pathomechanism of how FLG deficiency provokes a barrier abnormality in humans is unknown. We report here that the presence of FLG mutations in Caucasians predicts dose-dependent alterations in epidermal permeability barrier function. Although FLG is an intracellular protein, the barrier abnormality occurred solely via a paracellular route in affected stratum corneum. Abnormal barrier function correlated with alterations in keratin filament organization (perinuclear retraction), impaired loading of lamellar body contents, followed by nonuniform extracellular distribution of secreted organelle contents, and abnormalities in lamellar bilayer architecture. In addition, we observed reductions in corneodesmosome density and tight junction protein expression. Thus, FLG deficiency provokes alterations in keratinocyte architecture that influence epidermal functions localizing to the extracellular matrix.These results clarify how FLG mutations impair epidermal permeability barrier function.

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“…mRNA was isolated using TRIzol (Invitrogen), according to the manufacturer's instructions. Quantitative RT-PCR was performed as described previously, using the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a control 50 .…”

Section: Bone Marrow Transplantation For Bm Transplantation Red Blomentioning

confidence: 99%

Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

Moniaga

Hara‐Chikuma

2016

Journal of Dermatological Science

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1Aquaporin-9 (AQP9), a water/glycerol channel protein, is expressed in several immune cells including neutrophils; however, its role in immune response remains unknown. Here we show the involvement of AQP9 in hapten-induced contact hypersensitivity (CHS), as a murine model of skin allergic contact dermatitis, using AQP9 knockout (AQP9 −/− ) mice. First, the CHS response to hapten dinitrofluorobenzene (DNFB) was impaired in AQP9 −/− mice compared with wild-type (WT) mice. Adoptive transfer of sensitized AQP9 −/− draining lymph node (dLN) cells into WT recipients resulted in a reduced CHS response, indicating impaired sensitization in AQP9 −/− mice. Second, administration of WT neutrophils into AQP9 −/− mice during sensitization rescued the impaired CHS response. Neutrophil recruitment to dLNs upon hapten application was attenuated by AQP9 deficiency. Coincidentally, AQP9 −/− neutrophils showed a reduced CC-chemokine receptor 7 (CCR7) ligand-induced migration efficacy, which was attributed to the attenuated recruitment of neutrophils to dLNs. Furthermore, we found that neutrophil deficiency, observed in AQP9 −/− or neutrophildepleted mice, decreased IL-17A production by dLN cells, which might be responsible for T cell activation during a subsequent CHS response. Taken together, these findings suggest that AQP9 is required for the development of sensitization during cutaneous acquired immune responses via regulating neutrophil function.Allergic contact dermatitis (ACD) is one of the most prevalent skin diseases consisting of sensitization and elicitation phases 1,2 . Advanced studies of hapten-induced contact hypersensitivity (CHS) as a murine model of ACD have expanded our understanding of the mechanism of allergic reactions occurring in the skin, especially the specific roles of a variety of immune cells. During the sensitization phase, hapten-bearing cutaneous dendritic cells (DCs) migrate into skin draining lymph nodes (dLNs), where the presentation of antigens to naïve T cells and subsequent T cell priming occur. During the elicitation phase, re-exposure to cognate hapten results in the recruitment of antigen-specific T cells to the site of allergen challenge and T cell-mediated tissue damage 2 . Increasing evidence shows that several subsets of immune cells, including various types of T cells (Th1, Th17, regulatory, and natural killer), DCs (dermal DCs and Langerhans cells), and mast cells, work synergistically in the skin and its dLNs to exert antigen presentation and T cell activation during the development of sensitization in CHS [3][4][5][6][7] . Neutrophils have long been considered as the final effector cells of an acute inflammatory response. On the other hand, accumulating evidence has extended the function of neutrophils to include activation and regulation during innate and adaptive immune responses 8,9 . Several studies have focused on the

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Flaky Tail Mouse Denotes Human Atopic Dermatitis in the Steady State and by Topical Application with Dermatophagoides pteronyssinus Extract

Cited by 120 publications

References 40 publications

Flaky Tail Mouse as a Novel Animal Model of Atopic Dermatitis: Possible Roles of Filaggrin in the Development of Atopic Dermatitis

Flaky Tail Mouse as a Novel Animal Model of Atopic Dermatitis: Possible Roles of Filaggrin in the Development of Atopic Dermatitis

Filaggrin Genotype in Ichthyosis Vulgaris Predicts Abnormalities in Epidermal Structure and Function

Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity

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