Atopic March from atopic dermatitis to asthma-like lesions in NC/Nga mice is accelerated or aggravated by neutralization of stratum corneum but partially inhibited by acidification

Hae Jin Lee, Noo Ri Lee, Minyoung Jung, Dong Hye Kim, Eung Ho Choi

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Prolonged and/or repeated damage to the skin barrier followed by atopic dermatitis (AD) is an initial step in atopic March that ultimately progresses to respiratory allergy. Maintaining normal stratum corneum (SC) acidity has been suggested as a therapeutic or preventive strategy for barrier impairment caused by skin inflammation. We determined whether a representative AD murine model, NC/Nga mice, develops airway inflammation after repeated epicutaneous application followed by inhalation of house dust mite (HDM), implying atopic March, and whether prolongation of non-proper SC acidity accelerates respiratory allergy. HDM was applied to the skin of NC/Nga mice, accompanied by the application of neutral cream (pH 7.4) or acidic cream (pH 2.8) for 6 weeks. Intranasal inhalation of HDM was administered daily during the last 3 days. Repeated epicutaneous applications followed by inhalation of HDM in NC/Nga mice induced an atopic March-like progression from AD lesions to respiratory allergy. Concurrent neutral cream treatment accelerated or aggravated the allergic inflammation in the skin and respiratory system, whereas an acidic cream partially alleviated these symptoms. Collectively, we developed an atopic March in NC/Nga mice by HDM application, and found that prevention of a neutral environment in the SC may be an interventional method to inhibit the March.

Original languageEnglish
Pages (from-to)3025-3033
Number of pages9
JournalJournal of Investigative Dermatology
Volume135
Issue number12
DOIs
Publication statusPublished - 2015 Dec 1

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Pyroglyphidae
Acidification
Atopic Dermatitis
Cornea
Dust
Allergies
Asthma
Skin
Inhalation
Hypersensitivity
Inflammation
Acidity
Respiratory system
Respiratory System

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

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title = "Atopic March from atopic dermatitis to asthma-like lesions in NC/Nga mice is accelerated or aggravated by neutralization of stratum corneum but partially inhibited by acidification",
abstract = "Prolonged and/or repeated damage to the skin barrier followed by atopic dermatitis (AD) is an initial step in atopic March that ultimately progresses to respiratory allergy. Maintaining normal stratum corneum (SC) acidity has been suggested as a therapeutic or preventive strategy for barrier impairment caused by skin inflammation. We determined whether a representative AD murine model, NC/Nga mice, develops airway inflammation after repeated epicutaneous application followed by inhalation of house dust mite (HDM), implying atopic March, and whether prolongation of non-proper SC acidity accelerates respiratory allergy. HDM was applied to the skin of NC/Nga mice, accompanied by the application of neutral cream (pH 7.4) or acidic cream (pH 2.8) for 6 weeks. Intranasal inhalation of HDM was administered daily during the last 3 days. Repeated epicutaneous applications followed by inhalation of HDM in NC/Nga mice induced an atopic March-like progression from AD lesions to respiratory allergy. Concurrent neutral cream treatment accelerated or aggravated the allergic inflammation in the skin and respiratory system, whereas an acidic cream partially alleviated these symptoms. Collectively, we developed an atopic March in NC/Nga mice by HDM application, and found that prevention of a neutral environment in the SC may be an interventional method to inhibit the March.",
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Atopic March from atopic dermatitis to asthma-like lesions in NC/Nga mice is accelerated or aggravated by neutralization of stratum corneum but partially inhibited by acidification. / Lee, Hae Jin; Lee, Noo Ri; Jung, Minyoung; Kim, Dong Hye; Choi, Eung Ho.

In: Journal of Investigative Dermatology, Vol. 135, No. 12, 01.12.2015, p. 3025-3033.

Research output: Contribution to journalArticle

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