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Article Dans Une Revue ImmunoHorizons Année : 2021

Chronic Pseudomonas aeruginosa Lung Infection Is IL-1R Independent, but Relies on MyD88 Signaling

Louis Fauconnier
  • Fonction : Auteur
Thomas Secher
Alessandra Bragonzi
Francois Huaux
Tobias Stoeger
Herbert B Schiller
  • Fonction : Auteur
Jean-Claude Sirard
Dieudonnée Togbe

Résumé

Cystic fibrosis is associated with chronic Pseudomonas aeruginosa colonization and inflammation. The role of MyD88, the shared adapter protein of the proinflammatory TLR and IL-1R families, in chronic P. aeruginosa biofilm lung infection is unknown. We report that chronic lung infection with the clinical P. aeruginosa RP73 strain is associated with uncontrolled lung infection in complete MyD88-deficient mice with epithelial damage, inflammation, and rapid death. Then, we investigated whether alveolar or myeloid cells contribute to heightened sensitivity to infection. Using cell-specific, MyD88-deficient mice, we uncover that the MyD88 pathway in myeloid or alveolar epithelial cells is dispensable, suggesting that other cell types may control the high sensitivity of MyD88-deficient mice. By contrast, IL-1R1-deficient mice control chronic P. aeruginosa RP73 infection and IL-1b Ab blockade did not reduce host resistance. Therefore, the IL-1R1/MyD88 pathway is not involved, but other IL-1R or TLR family members need to be investigated. Our data strongly suggest that IL-1 targeted neutralizing therapies used to treat inflammatory diseases in patients unlikely reduce host resistance to chronic P. aeruginosa infection. ImmunoHorizons, 2021, 5: 273-283.
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Dates et versions

hal-03429701 , version 1 (15-11-2021)

Identifiants

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Claire Mackowiak, Tiffany Marchiol, Hana Cipcic Paljetak, Louis Fauconnier, Jennifer Palomo, et al.. Chronic Pseudomonas aeruginosa Lung Infection Is IL-1R Independent, but Relies on MyD88 Signaling. ImmunoHorizons , 2021, 5 (5), pp.273 - 283. ⟨10.4049/immunohorizons.2000095⟩. ⟨hal-03429701⟩

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