Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.

Bacterial infections trigger the expression of type I and II interferon genes but little is known about their effect on type III interferon (IFN-λ) genes, whose products play important roles in epithelial innate immunity against viruses. Here, we studied the expression of IFN-λ genes in cultured hum...

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Autores principales: Hélène Bierne, Laetitia Travier, Tanel Mahlakõiv, Ludovic Tailleux, Agathe Subtil, Alice Lebreton, Anupam Paliwal, Brigitte Gicquel, Peter Staeheli, Marc Lecuit, Pascale Cossart
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:1711231359ac456a81ad262309d5a2702021-11-18T07:15:28ZActivation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.1932-620310.1371/journal.pone.0039080https://doaj.org/article/1711231359ac456a81ad262309d5a2702012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22720036/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Bacterial infections trigger the expression of type I and II interferon genes but little is known about their effect on type III interferon (IFN-λ) genes, whose products play important roles in epithelial innate immunity against viruses. Here, we studied the expression of IFN-λ genes in cultured human epithelial cells infected with different pathogenic bacteria and in the mouse placenta infected with Listeria monocytogenes. We first showed that in intestinal LoVo cells, induction of IFN-λ genes by L. monocytogenes required bacterial entry and increased further during the bacterial intracellular phase of infection. Other Gram-positive bacteria, Staphylococcus aureus, Staphylococcus epidermidis and Enterococcus faecalis, also induced IFN-λ genes when internalized by LoVo cells. In contrast, Gram-negative bacteria Salmonella enterica serovar Typhimurium, Shigella flexneri and Chlamydia trachomatis did not substantially induce IFN-λ. We also found that IFN-λ genes were up-regulated in A549 lung epithelial cells infected with Mycobacterium tuberculosis and in HepG2 hepatocytes and BeWo trophoblastic cells infected with L. monocytogenes. In a humanized mouse line permissive to fetoplacental listeriosis, IFN-λ2/λ3 mRNA levels were enhanced in placentas infected with L. monocytogenes. In addition, the feto-placental tissue was responsive to IFN-λ2. Together, these results suggest that IFN-λ may be an important modulator of the immune response to Gram-positive intracellular bacteria in epithelial tissues.Hélène BierneLaetitia TravierTanel MahlakõivLudovic TailleuxAgathe SubtilAlice LebretonAnupam PaliwalBrigitte GicquelPeter StaeheliMarc LecuitPascale CossartPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 6, p e39080 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Hélène Bierne
Laetitia Travier
Tanel Mahlakõiv
Ludovic Tailleux
Agathe Subtil
Alice Lebreton
Anupam Paliwal
Brigitte Gicquel
Peter Staeheli
Marc Lecuit
Pascale Cossart
Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
description Bacterial infections trigger the expression of type I and II interferon genes but little is known about their effect on type III interferon (IFN-λ) genes, whose products play important roles in epithelial innate immunity against viruses. Here, we studied the expression of IFN-λ genes in cultured human epithelial cells infected with different pathogenic bacteria and in the mouse placenta infected with Listeria monocytogenes. We first showed that in intestinal LoVo cells, induction of IFN-λ genes by L. monocytogenes required bacterial entry and increased further during the bacterial intracellular phase of infection. Other Gram-positive bacteria, Staphylococcus aureus, Staphylococcus epidermidis and Enterococcus faecalis, also induced IFN-λ genes when internalized by LoVo cells. In contrast, Gram-negative bacteria Salmonella enterica serovar Typhimurium, Shigella flexneri and Chlamydia trachomatis did not substantially induce IFN-λ. We also found that IFN-λ genes were up-regulated in A549 lung epithelial cells infected with Mycobacterium tuberculosis and in HepG2 hepatocytes and BeWo trophoblastic cells infected with L. monocytogenes. In a humanized mouse line permissive to fetoplacental listeriosis, IFN-λ2/λ3 mRNA levels were enhanced in placentas infected with L. monocytogenes. In addition, the feto-placental tissue was responsive to IFN-λ2. Together, these results suggest that IFN-λ may be an important modulator of the immune response to Gram-positive intracellular bacteria in epithelial tissues.
format article
author Hélène Bierne
Laetitia Travier
Tanel Mahlakõiv
Ludovic Tailleux
Agathe Subtil
Alice Lebreton
Anupam Paliwal
Brigitte Gicquel
Peter Staeheli
Marc Lecuit
Pascale Cossart
author_facet Hélène Bierne
Laetitia Travier
Tanel Mahlakõiv
Ludovic Tailleux
Agathe Subtil
Alice Lebreton
Anupam Paliwal
Brigitte Gicquel
Peter Staeheli
Marc Lecuit
Pascale Cossart
author_sort Hélène Bierne
title Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
title_short Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
title_full Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
title_fullStr Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
title_full_unstemmed Activation of type III interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
title_sort activation of type iii interferon genes by pathogenic bacteria in infected epithelial cells and mouse placenta.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/1711231359ac456a81ad262309d5a270
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