Airway epithelial immunoproteasome subunit LMP7 protects against rhinovirus infection

Kris Genelyn Dimasuay
National Jewish Health
January 1, 2022
Sci Rep
https://pubmed.ncbi.nlm.nih.gov/36008456

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36008456

Research summary

This study investigates the role of the immunoproteasome subunit LMP7 in airway epithelial cells during rhinovirus (RV) infection. Using a tamoxifen-inducible, airway epithelial-specific LMP7 conditional Knockout (CKO) mouse model, the researchers demonstrated that LMP7 deficiency led to increased viral load, heightened neutrophilic inflammation, and reduced expression of the negative immune regulator A20/TNFAIP3. Additionally, induction of LMP7 via low-dose polyinosinic:polycytidylic acid (PI:C) treatment reduced RV-mediated inflammation, highlighting LMP7's protective role in antiviral and anti-inflammatory responses.

Key outcome of the study

LMP7 in airway epithelial cells is crucial for resolving RV-induced lung inflammation and controlling viral replication. Its deficiency exacerbates inflammation and viral load, while its induction mitigates these effects, suggesting potential therapeutic avenues for RV infections.

Mouse model

Tamoxifen-inducible, airway epithelial-specific LMP7 conditional Knockout (CKO) mouse model, generated using Cre-loxP technology with Sox2-CreERT2 driver for targeted deletion of LMP7 in airway epithelial cells.

TARGET:
Psmb8
LMP7, β5i, Proteasome subunit beta type-8

Keywords

Rhinovirus infection, Airway inflammation, Immunoproteasome, LMP7, Antiviral immunity

Technical specifications

Conditional Knockout model, Tamoxifen-inducible Cre-loxP system, Sox2-CreERT2 driver, Airway epithelial-specific gene deletion

Related products

Catalogue product

No items found.

Customized product

Tissue-specific KO mouse

Use tissue- or cell-specific conditional Knockout mouse models to bypass embryonic lethality, compensatory mechanisms, complex phenotypes, etc.