Staphylococcal superantigen-like 12 induces the production of interleukin 4 in murine basophils.


Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
05 11 2020
Historique:
received: 09 08 2020
accepted: 11 08 2020
pubmed: 30 8 2020
medline: 19 3 2021
entrez: 30 8 2020
Statut: ppublish

Résumé

S. aureus is associated with atopic dermatitis (AD). Several staphylococcal products including cell wall components, protease, and exotoxins, are thought to be involved in allergic inflammation of AD via activating immune cells such as T cells and mast cells. None of the staphylococcal exotoxins has been reported to activate a primary IL-4 inducer, basophils, that are known to produce large amounts of IL-4 in response to allergens as well as IgE-independent stimuli such as mites and helminth proteases. In this study, we investigated the ability of staphylococcal superantigen-like (SSL) family to activate basophils. SSL12, reported its activity to activate mast cells, induced the production of IL-4 in bone marrow derived basophils. SSL12 also evoked the release of IL-4 in freshly isolated murine basophils in bone marrow cells, as the depletion of basophils by basophils-specific antibodies against high-affinity IgE receptor and CD49b diminished the responsiveness of bone marrow cells for SSL12. These results propose the novel immune regulatory activity of SSL12 by inducing IL-4 in basophils, that contributes to the development of allergic inflammation disorders and the immune evasion of the cocci.

Identifiants

pubmed: 32859377
pii: S0006-291X(20)31589-8
doi: 10.1016/j.bbrc.2020.08.029
pii:
doi:

Substances chimiques

Antigens, Bacterial 0
Il4 protein, mouse 0
Superantigens 0
Interleukin-4 207137-56-2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

200-204

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Saishi Nishiyama (S)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

Ayaka Urabe (A)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

Arisa Morikawa (A)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

Masato Kobayashi (M)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

Kikuo Onozaki (K)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

Saotomo Itoh (S)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan. Electronic address: s-itoh@phar.nagoya-cu.ac.jp.

Shigeaki Hida (S)

Department of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-Dori, Mizuho-ku, Nagoya, 467-8603, Japan.

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Classifications MeSH