PuSH - Publikationsserver des Helmholtz Zentrums München: Chronic <em>Pseudomonas aeruginosa</em> lung infection is IL-1R independent, but relies on MyD88 signaling.

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Mackowiak, C.* ; Marchiol, T.* ; Paljetak, H.C.* ; Fauconnier, L.* ; Palomo, J.* ; Secher, T.* ; Panek, C.* ; Sedda, D.* ; Savigny, F.* ; Erard, F.* ; Bragonzi, A.* ; Huaux, F.* ; Stöger, T. ; Schiller, H. B. ; Sirard, J.C.* ; Le Bert, M.* ; Couillin, I.* ; Quesniaux, V.F.J.* ; Togbe, D.* ; Ryffel, B.*

Chronic Pseudomonas aeruginosa lung infection is IL-1R independent, but relies on MyD88 signaling.

Immunohorizons 5, 273-283 (2021)

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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-1β 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.

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