Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis

C. Moser; M. van Gennip; T. Bjarnsholt; Peter Østrup Jensen; B. Lee; H.P. Hougen; H. Calum; O. Ciofu; M. Givskov; S. Molin; Niels Høiby

doi:10.1111/j.1600-0463.2008.00018.x

Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis

C. Moser, M. van Gennip, T. Bjarnsholt, Peter Østrup Jensen, B. Lee, H.P. Hougen, H. Calum, O. Ciofu, M. Givskov, S. Molin, Niels Høiby

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

43 Citationer (Scopus)

Abstract

Udgivelsesdato: 2009-Feb

Originalsprog	Engelsk
Tidsskrift	Acta Pathologica Microbiologica et Immunologica Scandinavica
Vol/bind	117
Udgave nummer	2
Sider (fra-til)	95-107
Antal sider	13
ISSN	0903-4641
DOI	https://doi.org/10.1111/j.1600-0463.2008.00018.x https://doi.org/10.1111/j.1600-0463.2008.00018.x
Status	Udgivet - 1 feb. 2009

Bibliografisk note

Keywords: Animals; Chemokine CXCL2; Cystic Fibrosis; Disease Models, Animal; Female; Granulocyte Colony-Stimulating Factor; Humans; Lung; Mice; Mice, Inbred BALB C; Pseudomonas Infections; Pseudomonas aeruginosa; Virulence

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Citationsformater

Moser, C., Gennip, M. V., Bjarnsholt, T., Jensen, P. Ø., Lee, B., Hougen, H. P., Calum, H., Ciofu, O., Givskov, M., Molin, S., & Høiby, N. (2009). Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis. Acta Pathologica Microbiologica et Immunologica Scandinavica, 117(2), 95-107. https://doi.org/10.1111/j.1600-0463.2008.00018.x, https://doi.org/10.1111/j.1600-0463.2008.00018.x

Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis. / Moser, C.; Gennip, M. van; Bjarnsholt, T.; Jensen, Peter Østrup; Lee, B.; Hougen, H.P.; Calum, H.; Ciofu, O.; Givskov, M.; Molin, S.; Høiby, Niels.

I: Acta Pathologica Microbiologica et Immunologica Scandinavica, Bind 117, Nr. 2, 01.02.2009, s. 95-107.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Moser, C, Gennip, MV, Bjarnsholt, T , Jensen, PØ, Lee, B, Hougen, HP, Calum, H, Ciofu, O , Givskov, M, Molin, S & Høiby, N 2009, 'Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis', Acta Pathologica Microbiologica et Immunologica Scandinavica, bind 117, nr. 2, s. 95-107. https://doi.org/10.1111/j.1600-0463.2008.00018.x, https://doi.org/10.1111/j.1600-0463.2008.00018.x

Moser C, Gennip MV, Bjarnsholt T , Jensen PØ, Lee B, Hougen HP et al. Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis. Acta Pathologica Microbiologica et Immunologica Scandinavica. 2009 feb. 1;117(2):95-107. https://doi.org/10.1111/j.1600-0463.2008.00018.x, https://doi.org/10.1111/j.1600-0463.2008.00018.x

Moser, C. ; Gennip, M. van ; Bjarnsholt, T. ; Jensen, Peter Østrup ; Lee, B. ; Hougen, H.P. ; Calum, H. ; Ciofu, O. ; Givskov, M. ; Molin, S. ; Høiby, Niels. / Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis. I: Acta Pathologica Microbiologica et Immunologica Scandinavica. 2009 ; Bind 117, Nr. 2. s. 95-107.

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title = "Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis",

abstract = "The dominant cause of premature death in patients suffering from cystic fibrosis (CF) is chronic lung infection with Pseudomonas aeruginosa. The chronic lung infection often lasts for decades with just one clone. However, as a result of inflammation, antibiotic treatment and different niches in the lungs, the clone undergoes significant genetic changes, resulting in diversifying geno- and phenotypes. Such an adaptation may generate different host responses. To experimentally reflect the year-long chronic lung infection in CF, groups of BALB/c mice were infected with clonal isolates from different periods (1980, 1988, 1997, 1999 and 2003) of the chronic lung infection of one CF patient using the seaweed alginate embedment model. The results showed that the non-mucoid clones reduced their virulence over time, resulting in faster clearing of the bacteria from the lungs, improved pathology and reduced pulmonary production of macrophage inflammatory protein-2 (MIP-2) and granulocyte colony-stimulating factor (G-CSF). In contrast, the mucoid clones were more virulent and virulence increased with time, resulting in impaired pulmonary clearing of the latest clone, severe inflammation and increased pulmonary MIP-2 and G-CSF production. In conclusion, adaptation of P. aeruginosa in CF is reflected by changed ability to establish lung infection and results in distinct host responses to mucoid and non-mucoid phenotypes.",

author = "C. Moser and Gennip, {M. van} and T. Bjarnsholt and Jensen, {Peter {\O}strup} and B. Lee and H.P. Hougen and H. Calum and O. Ciofu and M. Givskov and S. Molin and Niels H{\o}iby",

note = "Keywords: Animals; Chemokine CXCL2; Cystic Fibrosis; Disease Models, Animal; Female; Granulocyte Colony-Stimulating Factor; Humans; Lung; Mice; Mice, Inbred BALB C; Pseudomonas Infections; Pseudomonas aeruginosa; Virulence",

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doi = "10.1111/j.1600-0463.2008.00018.x",

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T1 - Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis

AU - Moser, C.

AU - Gennip, M. van

AU - Bjarnsholt, T.

AU - Jensen, Peter Østrup

AU - Lee, B.

AU - Hougen, H.P.

AU - Calum, H.

AU - Ciofu, O.

AU - Givskov, M.

AU - Molin, S.

AU - Høiby, Niels

N1 - Keywords: Animals; Chemokine CXCL2; Cystic Fibrosis; Disease Models, Animal; Female; Granulocyte Colony-Stimulating Factor; Humans; Lung; Mice; Mice, Inbred BALB C; Pseudomonas Infections; Pseudomonas aeruginosa; Virulence

PY - 2009/2/1

Y1 - 2009/2/1

N2 - The dominant cause of premature death in patients suffering from cystic fibrosis (CF) is chronic lung infection with Pseudomonas aeruginosa. The chronic lung infection often lasts for decades with just one clone. However, as a result of inflammation, antibiotic treatment and different niches in the lungs, the clone undergoes significant genetic changes, resulting in diversifying geno- and phenotypes. Such an adaptation may generate different host responses. To experimentally reflect the year-long chronic lung infection in CF, groups of BALB/c mice were infected with clonal isolates from different periods (1980, 1988, 1997, 1999 and 2003) of the chronic lung infection of one CF patient using the seaweed alginate embedment model. The results showed that the non-mucoid clones reduced their virulence over time, resulting in faster clearing of the bacteria from the lungs, improved pathology and reduced pulmonary production of macrophage inflammatory protein-2 (MIP-2) and granulocyte colony-stimulating factor (G-CSF). In contrast, the mucoid clones were more virulent and virulence increased with time, resulting in impaired pulmonary clearing of the latest clone, severe inflammation and increased pulmonary MIP-2 and G-CSF production. In conclusion, adaptation of P. aeruginosa in CF is reflected by changed ability to establish lung infection and results in distinct host responses to mucoid and non-mucoid phenotypes.

AB - The dominant cause of premature death in patients suffering from cystic fibrosis (CF) is chronic lung infection with Pseudomonas aeruginosa. The chronic lung infection often lasts for decades with just one clone. However, as a result of inflammation, antibiotic treatment and different niches in the lungs, the clone undergoes significant genetic changes, resulting in diversifying geno- and phenotypes. Such an adaptation may generate different host responses. To experimentally reflect the year-long chronic lung infection in CF, groups of BALB/c mice were infected with clonal isolates from different periods (1980, 1988, 1997, 1999 and 2003) of the chronic lung infection of one CF patient using the seaweed alginate embedment model. The results showed that the non-mucoid clones reduced their virulence over time, resulting in faster clearing of the bacteria from the lungs, improved pathology and reduced pulmonary production of macrophage inflammatory protein-2 (MIP-2) and granulocyte colony-stimulating factor (G-CSF). In contrast, the mucoid clones were more virulent and virulence increased with time, resulting in impaired pulmonary clearing of the latest clone, severe inflammation and increased pulmonary MIP-2 and G-CSF production. In conclusion, adaptation of P. aeruginosa in CF is reflected by changed ability to establish lung infection and results in distinct host responses to mucoid and non-mucoid phenotypes.

U2 - 10.1111/j.1600-0463.2008.00018.x

DO - 10.1111/j.1600-0463.2008.00018.x

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C2 - 19239431

VL - 117

SP - 95

EP - 107

JO - A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica

JF - A P M I S. Acta Pathologica, Microbiologica et Immunologica Scandinavica

SN - 0903-4641

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