Stimulation of epithelial innate response by flagellin of Bordetella Bronchiseptica

MARTIN RUMBO; JULIETA FERNANDEZ; FEDERICO SISTI; MARIA AMANDA REY; DANIELA HOZBOR; JEAN CLAUDE SIRARD

Córdoba

Congreso; VII Latin Congress of Immunology; 2005

ALAI

Whereas flagellins from several species such as Salmonella, Pseudomonas, Escherichia or Legionella have been described to stimulate innate response through their interaction whit Toll Like Receptor 5 (TLR5), other microorganisms such as Campylobacter jejuni or Helicobacter pylori seem to have evolved to avoid this recognition in order to successfully colonize their hosts. Bordetella bronchiseptica, the etiological agent of acute and chronic respiratory diseases in many different mammals also expresses flagellin under specific environmental conditions. Therefore, we aimed to determine if flagellin from B. bronchiseptica could activate innate response either in vitro or in vivo. Although they showed very different immunochemical cross-reactivity, Salmonella typhymurium and B. bronchiseptica flagellins presented similar activity on CCL20- luciferase reporter system on Caco-2 intestinal epithelial cells. This cell line is known to trigger ccl20 expression upon flagellin stimulation in a TLR5-dependent way. The induction of the chemokines CCL20 and IL-8 on the airway epithelium human cell line A549 was measured by RT-qPCR. In all cases similar inductions levels with either S. typhimurium or B. bronchiseptica flagellin were observed. Activity of both types of flagellin was also assessed in vivo upon intranasal challenge of BALB/c and C3H/HeJ mice. Both strains showed a 50 fold induction of the proinflamatory chemokines CCL20 and CXCL2 in lungs 2h after stimulation. Our results indicate that B. bronchiseptica flagellin can trigger host innate response in a similar way than Salmonella`s flagellin. The significance of this recognition on B. bronchiseptica infection process remains to be determined.