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

Bierne H, Travier L, Mahlakõiv T, Tailleux L, Subtil A, Lebreton A, Paliwal A, Gicquel B, Staeheli P, Lecuit M, Cossart P - PLoS ONE (2012)

Bottom Line: 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.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 addition, the feto-placental tissue was responsive to IFN-λ2.

View Article: PubMed Central - PubMed

Affiliation: Institut Pasteur, Unité des Interactions Bactéries Cellules, Paris, France. hbierne@pasteur.fr

ABSTRACT
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.

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Induction of IFN-III genes by L. monocytogenes in HepG2 hepatocytes and BeWo trophoblastic cells.Quantification of bacterial loads (CFU) and IFN-λ mRNAs levels in Listeria-infected HepG2 or BeWo cells. IFN-λ1 and IFN-λ2 transcript levels were determined by qRT-PCR and normalized to GAPDH transcript levels. Values are expressed as mean ± S.D. of the fold change relative to that in uninfected cells (n = 3). IFN-λ2 levels in uninfected HepG2 cells were below the detection threshold, preventing measures of fold change. L. monocytogenes (L. m.), L. innocua (L. in.), L.innocua expressing inlA (L. in. (inlA)).
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pone-0039080-g003: Induction of IFN-III genes by L. monocytogenes in HepG2 hepatocytes and BeWo trophoblastic cells.Quantification of bacterial loads (CFU) and IFN-λ mRNAs levels in Listeria-infected HepG2 or BeWo cells. IFN-λ1 and IFN-λ2 transcript levels were determined by qRT-PCR and normalized to GAPDH transcript levels. Values are expressed as mean ± S.D. of the fold change relative to that in uninfected cells (n = 3). IFN-λ2 levels in uninfected HepG2 cells were below the detection threshold, preventing measures of fold change. L. monocytogenes (L. m.), L. innocua (L. in.), L.innocua expressing inlA (L. in. (inlA)).

Mentions: During listeriosis, L. monocytogenes targets epithelial cells of the intestine, but also from other organs, such as the placenta and the liver. We found that L. monocytogenes and inlA-expressing L. innocua up-regulated IFN-III genes in human intestinal cells other than LoVo cells (Caco-2 cells, data not shown), as well as in BeWo trophoblastic cells (Fig. 3, Table 1). L. monocytogenes also highly induced IFN-λ1 in HepG2 hepatocytes. In this cell line, IFN-λ2 mRNA levels slightly increased upon infection, but the steady-state IFN-λ2 levels in uninfected cells were below the detection limits, preventing quantitative measurement of a fold change. In contrast, L. monocytogenes infection had no effect on the expression of IFN-III genes in two non-epithelial human cell lines (HEK293 embryonic cells and THP-1 monocytes, data not shown). Thus, L. monocytogenes might specifically trigger the expression of IFN-III genes in its epithelial niches.


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

Bierne H, Travier L, Mahlakõiv T, Tailleux L, Subtil A, Lebreton A, Paliwal A, Gicquel B, Staeheli P, Lecuit M, Cossart P - PLoS ONE (2012)

Induction of IFN-III genes by L. monocytogenes in HepG2 hepatocytes and BeWo trophoblastic cells.Quantification of bacterial loads (CFU) and IFN-λ mRNAs levels in Listeria-infected HepG2 or BeWo cells. IFN-λ1 and IFN-λ2 transcript levels were determined by qRT-PCR and normalized to GAPDH transcript levels. Values are expressed as mean ± S.D. of the fold change relative to that in uninfected cells (n = 3). IFN-λ2 levels in uninfected HepG2 cells were below the detection threshold, preventing measures of fold change. L. monocytogenes (L. m.), L. innocua (L. in.), L.innocua expressing inlA (L. in. (inlA)).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3375250&req=5

pone-0039080-g003: Induction of IFN-III genes by L. monocytogenes in HepG2 hepatocytes and BeWo trophoblastic cells.Quantification of bacterial loads (CFU) and IFN-λ mRNAs levels in Listeria-infected HepG2 or BeWo cells. IFN-λ1 and IFN-λ2 transcript levels were determined by qRT-PCR and normalized to GAPDH transcript levels. Values are expressed as mean ± S.D. of the fold change relative to that in uninfected cells (n = 3). IFN-λ2 levels in uninfected HepG2 cells were below the detection threshold, preventing measures of fold change. L. monocytogenes (L. m.), L. innocua (L. in.), L.innocua expressing inlA (L. in. (inlA)).
Mentions: During listeriosis, L. monocytogenes targets epithelial cells of the intestine, but also from other organs, such as the placenta and the liver. We found that L. monocytogenes and inlA-expressing L. innocua up-regulated IFN-III genes in human intestinal cells other than LoVo cells (Caco-2 cells, data not shown), as well as in BeWo trophoblastic cells (Fig. 3, Table 1). L. monocytogenes also highly induced IFN-λ1 in HepG2 hepatocytes. In this cell line, IFN-λ2 mRNA levels slightly increased upon infection, but the steady-state IFN-λ2 levels in uninfected cells were below the detection limits, preventing quantitative measurement of a fold change. In contrast, L. monocytogenes infection had no effect on the expression of IFN-III genes in two non-epithelial human cell lines (HEK293 embryonic cells and THP-1 monocytes, data not shown). Thus, L. monocytogenes might specifically trigger the expression of IFN-III genes in its epithelial niches.

Bottom Line: 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.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 addition, the feto-placental tissue was responsive to IFN-λ2.

View Article: PubMed Central - PubMed

Affiliation: Institut Pasteur, Unité des Interactions Bactéries Cellules, Paris, France. hbierne@pasteur.fr

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus