Transcriptomics

Dataset Information

0

Cell-intrinsic regulation of phagocyte function by interferon lambda during pulmonary viral, bacterial super-infection


ABSTRACT: Influenza infections result in a significant number of severe illnesses annually, many of which are complicated by secondary bacterial super-infection. Primary influenza infection has been shown to increase susceptibility to secondary methicillin-resistant Staphylococcus aureus (MRSA) infection by altering the host immune response, leading to significant immunopathology. Type III interferons (IFNs), or IFNλs, have gained traction as potential antiviral therapeutics due to their restriction of viral replication without damaging inflammation. The role of IFNλ in regulating epithelial biology in super-infection has recently been established; however, the impact of IFNλ on immune cells is less defined. In this study, we infected wild-type and IFNLR1-/- mice with influenza A/PR/8/34 followed by S. aureus USA300. We demonstrated that global IFNLR1-/- mice have enhanced bacterial clearance through increased uptake by phagocytes, which was shown to be cell-intrinsic specifically in myeloid cells in mixed bone marrow chimeras. We also showed that depletion of IFNLR1 on CX­3CR1 expressing myeloid immune cells, but not neutrophils, was sufficient to significantly reduce bacterial burden compared to mice with intact IFNLR1. These findings provide insight into how IFNλ in an influenza-infected lung impedes bacterial clearance during super-infection and show a direct cell intrinsic role for IFNλ signaling on myeloid cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE268994 | GEO | 2024/08/15

REPOSITORIES: GEO

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1

Similar Datasets

2022-06-27 | GSE206095 | GEO
2018-12-26 | GSE119029 | GEO
2020-04-02 | MODEL1812040005 | BioModels
2024-08-21 | GSE259429 | GEO
2024-08-21 | GSE243542 | GEO
2018-07-25 | GSE117580 | GEO
2023-01-01 | GSE215195 | GEO
2015-09-20 | E-GEOD-70445 | biostudies-arrayexpress
2017-12-05 | GSE100865 | GEO
2022-11-29 | GSE199708 | GEO