MUC1 mediates Pneumocystis murina binding to airway epithelial cells.
Pneumocystis
MUC1
adherence
co-localization
pneumocytes
pneumonia
Journal
Cellular microbiology
ISSN: 1462-5822
Titre abrégé: Cell Microbiol
Pays: India
ID NLM: 100883691
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
16
08
2019
revised:
05
12
2019
accepted:
27
01
2020
pubmed:
6
2
2020
medline:
2
6
2021
entrez:
5
2
2020
Statut:
ppublish
Résumé
Previous studies have shown that Pneumocystis binds to pneumocytes, but the proteins responsible for binding have not been well defined. Mucins are the major glycoproteins present in mucus, which serves as the first line of defence during airway infection. MUC1 is the best characterised membrane-tethered mucin and is expressed on the surface of most airway epithelial cells. Although by electron microscopy Pneumocystis primarily binds to type I pneumocytes, it can also bind to type II pneumocytes. We hypothesized that Pneumocystis organisms can bind to MUC1 expressed by type II pneumocytes. Overexpression of MUC1 in human embryonic kidney HEK293 cells increased Pneumocystis binding, while knockdown of MUC1 expression by siRNA in A549 cells, a human adenocarcinoma-derived alveolar type II epithelial cell line, decreased Pneumocystis binding. Immunofluorescence labelling indicated that MUC1 and Pneumocystis were co-localised in infected mouse lung tissue. Incubation of A549 cells with Pneumocystis led to phosphorylation of ERK1/2 that increased with knockdown of MUC1 expression by siRNA. Pneumocystis caused increased IL-6 and IL-8 secretion by A549 cells, and knockdown of MUC1 further increased their secretion in A549 cells. Taken together, these results suggest that binding of Pneumocystis to MUC1 expressed by airway epithelial cells may facilitate establishment of productive infection.
Identifiants
pubmed: 32017380
doi: 10.1111/cmi.13182
pmc: PMC7202957
mid: NIHMS1554495
doi:
Substances chimiques
Interleukin-6
0
Interleukin-8
0
MUC1 protein, human
0
Mucin-1
0
RNA, Small Interfering
0
muc1 protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13182Subventions
Organisme : Intramural NIH HHS
ID : ZIA CL000146
Pays : United States
Informations de copyright
Published 2020. This article is a U.S. Government work and is in the public domain in the USA.
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