PlexinD1 Deficiency in Lung Interstitial Macrophages Exacerbates House Dust Mite-Induced Allergic Asthma.


Journal

Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R

Informations de publication

Date de publication:
01 03 2022
Historique:
received: 28 01 2021
accepted: 17 12 2021
pubmed: 4 2 2022
medline: 8 3 2022
entrez: 3 2 2022
Statut: ppublish

Résumé

Interstitial macrophages (IMs) are key regulators of allergic inflammation. We previously showed that the absence of semaphorin 3E (Sema3E) exacerbates asthma features in both acute and chronic asthma models. However, it has not been studied whether Sema3E, via its receptor plexinD1, regulates IM function in allergic asthma. Therefore, we investigated the role of plexinD1 deficiency on IMs in allergic asthma. We found that the absence of plexinD1 in IMs increased airway hyperresponsiveness, airway leukocyte numbers, allergen-specific IgE, goblet cell hyperplasia, and Th2/Th17 cytokine response in the house dust mite (HDM)-induced allergic asthma model.

Identifiants

pubmed: 35110420
pii: jimmunol.2100089
doi: 10.4049/jimmunol.2100089
doi:

Substances chimiques

Actins 0
IL10 protein, mouse 0
Intracellular Signaling Peptides and Proteins 0
Membrane Glycoproteins 0
Muc5ac protein, mouse 0
Muc5b protein, mouse 0
Mucin 5AC 0
Mucin-5B 0
Plxnd1 protein, mouse 0
RNA, Messenger 0
Sema3e protein, mouse 0
Semaphorins 0
alpha-smooth muscle actin, mouse 0
Interleukin-10 130068-27-8
Immunoglobulin E 37341-29-0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1272-1279

Subventions

Organisme : CIHR
ID : PJT 173291
Pays : Canada

Informations de copyright

Copyright © 2022 by The American Association of Immunologists, Inc.

Auteurs

Amena Aktar (A)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Lianyu Shan (L)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Latifa Koussih (L)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Department of Experimental Biology, Université de Saint-Boniface, Winnipeg, MB, Canada.

Mohamed S Almiski (MS)

Department of Pathology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada; and.

Sujata Basu (S)

Department of Physiology and Physiopathology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Andrew Halayko (A)

Department of Physiology and Physiopathology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Ifeoma Okwor (I)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Jude E Uzonna (JE)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.

Abdelilah S Gounni (AS)

Department of Immunology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada; abdel.gounni@umanitoba.ca.

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Classifications MeSH