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Jacobsen, H.* ; Walendy-Gnirß, K.* ; Tekin-Bubenheim, N.* ; Kouassi, N.M.* ; Ben-Batalla, I.* ; Berenbrok, N.* ; Wolff, M.* ; dos Reis, V.P.* ; Zickler, M.* ; Scholl, L.* ; Gries, A.* ; Jania, H.* ; Kloetgen, A.* ; Düsedau, A.* ; Pilnitz-Stolze, G.* ; Jeridi, A. ; Yildirim, A.Ö. ; Fuchs, H. ; Gailus-Durner, V. ; Stoeger, C. ; Hrabě de Angelis, M. ; Manuylova, T.* ; Klingel, K.* ; Culley, F.J.* ; Behrends, J.* ; Loges, S.* ; Schneider, B.* ; Krauss-Etschmann, S.* ; Openshaw, P.J.M.* ; Gabriel, G.*

Offspring born to influenza A virus infected pregnant mice have increased susceptibility to viral and bacterial infections in early life.

Nat. Commun. 12:4957 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Influenza during pregnancy can affect the health of offspring in later life, among which neurocognitive disorders are among the best described. Here, we investigate whether maternal influenza infection has adverse effects on immune responses in offspring. We establish a two-hit mouse model to study the effect of maternal influenza A virus infection (first hit) on vulnerability of offspring to heterologous infections (second hit) in later life. Offspring born to influenza A virus infected mothers are stunted in growth and more vulnerable to heterologous infections (influenza B virus and MRSA) than those born to PBS- or poly(I:C)-treated mothers. Enhanced vulnerability to infection in neonates is associated with reduced haematopoetic development and immune responses. In particular, alveolar macrophages of offspring exposed to maternal influenza have reduced capacity to clear second hit pathogens. This impaired pathogen clearance is partially reversed by adoptive transfer of alveolar macrophages from healthy offspring born to uninfected dams. These findings suggest that maternal influenza infection may impair immune ontogeny and increase susceptibility to early life infections of offspring.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Lung-function; Birth-weight; Immune; Exposure; Fetal; Risk; Inflammation; Promotes; Depend; Asthma
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 12, Heft: 1, Seiten: , Artikelnummer: 4957 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Biology (LHI)
Institute of Experimental Genetics (IEG)
Förderungen Department of Health