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Infection and Immunity, April 2009, p. 1426-1441, Vol. 77, No. 4
0019-9567/09/$08.00+0     doi:10.1128/IAI.00297-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Host-Pathogen Interactions of Actinobacillus pleuropneumoniae with Porcine Lung and Tracheal Epithelial Cells{triangledown} ,{dagger}

Eliane Auger,1 Vincent Deslandes,1 Mahendrasingh Ramjeet,1 Irazù Contreras,2 John H. E. Nash,3,{ddagger} Josée Harel,1 Marcelo Gottschalk,1 Martin Olivier,2 and Mario Jacques1*

Groupe de Recherche sur les Maladies Infectieuses du Porc et Centre de Recherche en Infectiologie Porcine, Faculté de Médecine Vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec J2S 7C6, Canada,1 Department of Microbiology and Immunology, McGill University, Montréal, Québec H3A 2B4, Canada,2 Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada3

Received 5 March 2008/ Returned for modification 28 April 2008/ Accepted 6 January 2009

Host-pathogen interactions are of great importance in understanding the pathogenesis of infectious microorganisms. We developed in vitro models to study the host-pathogen interactions of porcine respiratory tract pathogens using two immortalized epithelial cell lines, namely, the newborn pig trachea (NPTr) and St. Jude porcine lung (SJPL) cell lines. We first studied the interactions of Actinobacillus pleuropneumoniae, an important swine pathogen, using these models. Under conditions where cytotoxicity was absent or low, we showed that A. pleuropneumoniae adheres to both cell lines, stimulating the induction of NF-{kappa}B. The NPTr cells consequently secrete interleukin 8, while the SJPL cells do not, since they are deprived of the NF-{kappa}B p65 subunit. Cell death ultimately occurs by necrosis, not apoptosis. The transcriptomic profile of A. pleuropneumoniae was determined after contact with the porcine lung epithelial cells by using DNA microarrays. Genes such as tadB and rcpA, members of a putative adhesin locus, and a gene whose product has high homology to the Hsf autotransporter adhesin of Haemophilus influenzae were upregulated, as were the genes pgaBC, involved in biofilm biosynthesis, while capsular polysaccharide-associated genes were downregulated. The in vitro models also proved to be efficient with other swine pathogens, such as Actinobacillus suis, Haemophilus parasuis, and Pasteurella multocida. Our results demonstrate that interactions of A. pleuropneumoniae with host epithelial cells seem to involve complex cross talk which results in regulation of various bacterial genes, including some coding for putative adhesins. Furthermore, our data demonstrate the potential of these in vitro models in studying the host-pathogen interactions of other porcine respiratory tract pathogens.

* Corresponding author. Mailing address: Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, Québec J2S 7C6, Canada. Phone: (450) 773-8521, ext. 8348. Fax: (450) 778-8105. E-mail: mario.jacques{at}umontreal.ca

{triangledown} Published ahead of print on 12 January 2009.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: V. J. DiRita

{ddagger} Present address: Office of Biotechnology, Genomics and Population Health, Public Health Agency of Canada, Ottawa, Ontario K1A 0K9, Canada.

Infection and Immunity, April 2009, p. 1426-1441, Vol. 77, No. 4
0019-9567/09/$08.00+0     doi:10.1128/IAI.00297-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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