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Virus-Induced Type I Interferon Deteriorates Control of Systemic Pseudomonas Aeruginosa Infection.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Merches Katja, Khairnar Vishal, Knuschke Torben, Shaabani Namir, Honke Nadine, Duhan Vikas, Recher Mike, Navarini Alexander A, Hardt Cornelia, Häussinger Dieter, Tümmler Burkhard, Gulbins Erich, Futerman Anthony H, Hoffmann Daniel, Lang Florian, Lang Philipp A, Westendorf Astrid M, Lang Karl S,
Project Analysis of RAG-dependent immunodeficiency and autoimmunity
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Original article (peer-reviewed)

Journal Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
Volume (Issue) 36(6)
Page(s) 2379 - 92
Title of proceedings Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
DOI 10.1159/000430200

Abstract

Type I interferon (IFN-I) predisposes to bacterial superinfections, an important problem during viral infection or treatment with interferon-alpha (IFN-α). IFN-I-induced neutropenia is one reason for the impaired bacterial control; however there is evidence that more frequent bacterial infections during IFN-α-treatment occur independently of neutropenia. We analyzed in a mouse model, whether Pseudomonas aeruginosa control is influenced by co-infection with the lymphocytic choriomeningitis virus (LCMV). Bacterial titers, numbers of neutrophils and the gene-expression of liver-lysozyme-2 were determined during a 24 hours systemic infection with P. aeruginosa in wild-type and Ifnar(-/-) mice under the influence of LCMV or poly(I:C). Virus-induced IFN-I impaired the control of Pseudomonas aeruginosa. This was associated with neutropenia and loss of lysozyme-2-expression in the liver, which had captured P. aeruginosa. A lower release of IFN-I by poly(I:C)-injection also impaired the bacterial control in the liver and reduced the expression of liver-lysozyme-2. Low concentration of IFN-I after infection with a virulent strain of P. aeruginosa alone impaired the bacterial control and reduced lysozyme-2-expression in the liver as well. We found that during systemic infection with P. aeruginosa Kupffer cells quickly controlled the bacteria in cooperation with neutrophils. Upon LCMV-infection this cooperation was disturbed.
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