Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis

Abstract Cystic fibrosis (CF) involves cycles of bacterial infection and sustained inflammation. IFNγ + Th17 cells are implicated in chronic inflammation, yet their role in CF remains undefined. Here we identify two pathogenic Th17 subsets, Th1/17 + and pro-inflammatory Th17 (pTh17) cells, selectively enriched in CF lungs colonized by Pseudomonas aeruginosa . These pathogenic subsets derive from protective conventional Th17 (cTh17) precursors and, following activation, directly disrupt pulmonary epithelial integrity and trigger exaggerated inflammatory responses. Transcriptomic and T cell receptor profiling reveal in situ reprogramming and clonal selection of Th1/17 + and pTh17 cells in CF lungs. Mechanistically, clinical P. aeruginosa strains persist within dendritic cells and induce a polarizing IL-1β/IL-23 cytokine axis that promotes IFNγ + Th17 differentiation over classical Th1 lineage commitment. P. aeruginosa early isolates, lacking chronic adaptation signatures, still potently reprogramme cTh17 cells, inducing a transcriptional programme that mirrors CF lung-resident Th1/17 + and pTh17 profiles. These findings show that P. aeruginosa subverts mucosal immunity and establishes a self-sustaining immunopathological loop, offering potential targets for CF precision therapies.

Authors

Institutions

Publication Details

Journal
Nature Microbiology
Published
2026-09-24
DOI
https://doi.org/10.1038/s41564-026-02469-2
Primary Topic
Cystic Fibrosis Research Advances
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
article

Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis

Francesco Blasi, Gianmarco Conte, A. Palleschi, Javier Cibella et al.
Nature Microbiology
Cystic Fibrosis Research Advances
article

Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis

Francesco Blasi, Gianmarco Conte, A. Palleschi, Javier Cibella, Daniela Guidone, Helle Krogh Johansen, Diletta Dolfini, Mirko Ronzio, Miriam Ascagni, Enrico Lugli, Paolo Landini, Moira Paroni, Clelia Peano, Simone Puccio, Matteo Chiara, Elio Rossi, Irene Dusetti, Riccardo Orlandi, Luis J. Galietta, Francesco Damarco, Eugenia Ricciardelli, Søren Molin, Andrea Gramegna
article en

Abstract

Abstract Cystic fibrosis (CF) involves cycles of bacterial infection and sustained inflammation. IFNγ + Th17 cells are implicated in chronic inflammation, yet their role in CF remains undefined. Here we identify two pathogenic Th17 subsets, Th1/17 + and pro-inflammatory Th17 (pTh17) cells, selectively enriched in CF lungs colonized by Pseudomonas aeruginosa . These pathogenic subsets derive from protective conventional Th17 (cTh17) precursors and, following activation, directly disrupt pulmonary epithelial integrity and trigger exaggerated inflammatory responses. Transcriptomic and T cell receptor profiling reveal in situ reprogramming and clonal selection of Th1/17 + and pTh17 cells in CF lungs. Mechanistically, clinical P. aeruginosa strains persist within dendritic cells and induce a polarizing IL-1β/IL-23 cytokine axis that promotes IFNγ + Th17 differentiation over classical Th1 lineage commitment. P. aeruginosa early isolates, lacking chronic adaptation signatures, still potently reprogramme cTh17 cells, inducing a transcriptional programme that mirrors CF lung-resident Th1/17 + and pTh17 profiles. These findings show that P. aeruginosa subverts mucosal immunity and establishes a self-sustaining immunopathological loop, offering potential targets for CF precision therapies.

Nature Microbiology
University of Copenhagen (DK), University of Milan (IT), Novo Nordisk Foundation (DK), Rigshospitalet (DK), Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico (IT), Human Technopole (IT), Telethon Institute Of Genetics And Medicine (IT), National Research Council (IT), IRCCS Humanitas Research Hospital (IT), University of Naples Federico II (IT), Technical University of Denmark (DK)
Good health and well-being
Openalex Percentile: Top 12%
Cystic Fibrosis Research Advances
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.