Inhibition of miR-99a-5p prevents allergen-driven airway exacerbations without compromising type-2 memory responses in the intestine following helminth infection.


Journal

Mucosal immunology
ISSN: 1935-3456
Titre abrégé: Mucosal Immunol
Pays: United States
ID NLM: 101299742

Informations de publication

Date de publication:
07 2021
Historique:
received: 14 09 2020
accepted: 14 03 2021
revised: 16 02 2021
pubmed: 14 4 2021
medline: 28 12 2021
entrez: 13 4 2021
Statut: ppublish

Résumé

Acute exacerbations (AE) of asthma, remain one of the biggest concerns for patients living with asthma. As such, identifying the causes, the molecular mechanisms involved and new therapeutic interventions to prevent AE is a high priority. Immunity to intestinal helminths involves the reactivation of type-2 immune responses leading to smooth muscle contraction and mucus hypersecretion-physiological processes very similar to acute exacerbations in the airways following allergen exposure. In this study, we employed a murine model of intestinal helminth infection, using Heligmosomoides polygyrus, to identify miRNAs during active expulsion, as a system for the identification of miRNAs that may contribute to AE in the airways. Concomitant with type-2 immunity and expulsion of H. polygyrus, we identified miR-99a-5p, miR-148a-3p and miR-155-5p that were differentially regulated. Systemic inhibition of these miRNAs, alone or in combination, had minimal impact on expulsion of H. polygyrus, but inhibition of miR-99a-5p or miR-155-5p significantly reduced house dust mite (HDM)-driven acute inflammation, modelling human acute exacerbations. Immunological, pathological and transcriptional analysis identified that miR-155-5p or miR-99a-5p contribute significantly to HDM-driven AE and that transient inhibition of these miRNAs may provide relief from allergen-driven AE, without compromising anti-helminth immunity in the gut.

Identifiants

pubmed: 33846533
doi: 10.1038/s41385-021-00401-x
pii: S1933-0219(22)00189-1
pmc: PMC8222002
doi:

Substances chimiques

Allergens 0
Biomarkers 0
MicroRNAs 0
Mirn99 microRNA, mouse 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

912-922

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Cancer Research UK
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UP_A253_1028
Pays : United Kingdom

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Auteurs

Lewis Entwistle (L)

Francis Crick Institute, London, UK.

Helena Aegerter (H)

Francis Crick Institute, London, UK.

Stephanie Czieso (S)

Francis Crick Institute, London, UK.

Eleni Amaniti (E)

Francis Crick Institute, London, UK.

Riccardo Guidi (R)

Francis Crick Institute, London, UK.

Abdul Sesay (A)

Francis Crick Institute, London, UK.

Nikolay Nikolov (N)

Francis Crick Institute, London, UK.

Probir Chakravaty (P)

Francis Crick Institute, London, UK.

Alison Huynh (A)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Jessica Mills (J)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Sean Flanagan (S)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Shannon Hambro (S)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Victor Nunez (V)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Yi Cao (Y)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Christine Clarke (C)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Angela Martzall (A)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Laurie Leong (L)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Dennis Wilson (D)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Cary Austin (C)

Immunology, Genentech Inc, South San Francisco, CA, USA.

Mark Wilson (M)

Francis Crick Institute, London, UK. wilson.mark@gene.com.
Immunology, Genentech Inc, South San Francisco, CA, USA. wilson.mark@gene.com.

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