Murdoch University Research Repository

Welcome to the Murdoch University Research Repository

The Murdoch University Research Repository is an open access digital collection of research
created by Murdoch University staff, researchers and postgraduate students.

Learn more

microRNA-146a is linked to the production of IgE in mice but not in atopic dermatitis patients

Carreras-Badosa, G., Runnel, T., Plaas, M., Kärner, J., Rückert, B., Lättekivi, F., Kõks, S., Cezmi, A.A., Kingo, K. and Rebane, A. (2018) microRNA-146a is linked to the production of IgE in mice but not in atopic dermatitis patients. Allergy, 73 . pp. 126-127.

Link to Published Version:
*Subscription may be required


Background: Atopic dermatitis (AD) is a chronic and complex inflammatory skin disease. At least two AD subtypes have been described: allergic (characterized by Type‐2‐cell‐mediated immunity and increased immunoglobulin E [IgE]) and non‐allergic (characterized by both Type‐2‐cell and Type‐1/17‐cell‐mediated immunity and normal IgE levels). MicroRNA (miR) are small non‐coding RNA molecules involved in genetic regulation. MiR‐146a negatively regulates inflammatory responses during chronic skin inflammation, however, its role in the modulation of immune responses in AD is uncovered. As recently miR‐146a was shown to promote IgE class switch in B cells in mice, we aimed to test whether there is association between miR‐ 146a and increased IgE levels in AD.

Method: Serum samples from miR‐146a−/− and wild‐type C57BL/ 6J mice with MC903‐induced AD‐like inflammation were analysed (N = 8 mice/group) for IgE and cytokine levels. Additionally, 32 serum samples from AD patients were also analysed. Subjects were split into allergic (N = 22) and non‐allergic (N = 10) according to IgE threshold of 150 IU/mL. MiR‐146a relative expression was quantified by real‐time PCR, IgE and human IL‐12p40 by ELISA and mouse cytokines by Bioplex.

Results: MiR‐146a−/− mice showed decreased IgE and increased IL‐ 12p40 serum levels (P < 0.001), while there were no changes in other detected cytokines. Human miR‐146a expression was not significantly different between allergic and non‐allergic subgroups divided based on serum IgE level. However, we observed a negative correlation of serum miR‐146a and IgE levels (P < 0.05) in allergic AD patients. In the allergic subgroup, miR‐146a expression remained independently negatively associated with IgE (β = −0.488, P < 0.05) after adjusting for confounding variables as gender.

Conclusion: Low IgE and high IL‐12p40 serum levels in miR‐ 146a−/− mice indicate that miR‐146a is needed for the production of IgE and associated with the regulation of Type‐1/17‐cell‐mediated immune responses in mice. Negative association of miR‐146a with serum IgE in allergic AD patients suggests that miR‐146a might have capacity to limit Type‐2‐cell‐mediated immune responses in AD. Further studies are needed to elucidate the possible mechanisms of miR‐146a in AD etiopathology.

Item Type: Journal Article
Publisher: Wiley-Blackwell
Copyright: © 2018 European Federation of Periodontology
Other Information: Special Issue: Abstracts from the European Academy of Allergy and Clinical Immunology Congress, 26–30 May 2018, Munich, Germany
Item Control Page Item Control Page