Oral Presentation MedVetPATHOGENS 2018

A new perspective on the pathogenesis of bovine pneumonic pasteurellosis: Mannheimia haemolytica serotype A1 invades differentiated bovine bronchial epithelial cells (#47)

Daniel Cozens 1 , Erin Sutherland 1 , Miquel Lauder 1 , Geraldine Taylor 2 , Catherine C Berry 3 , Robert L Davies 1
  1. Institute of Infection, Immunity and Inflammation, Univeristy of Glasgow, Glasgow, United Kingdom
  2. The Pirbright Institute, Pirbright, United Kingdom
  3. Institute of Molecular, Cell and Systems Biology, University of Glasgow, Glasgow, United Kingdom

Bovine pneumonic pasteurellosis is an economically significant infection of cattle caused by the Gram-negative bacterium Mannheimia haemolytica.  Healthy cattle are often colonised by commensal serotype A2 strains but, for reasons which are not completely understood, disease is usually caused by a sudden explosive proliferation of serotype A1 strains within the upper respiratory tract (URT).  In the present study, we have used a previously-optimised differentiated bronchial epithelial cell (DBEC) model of the bovine respiratory tract to compare the host-pathogen interactions of serotype A1 and A2 strains.  The infection process was followed at various time-points for five days by bacterial enumeration, immunofluorescence and scanning electron microscopy of cultures, and light microscopy of histological sections.  The innate pro-inflammatory immune response of the epithelial cells was also assessed by measuring the production of IL-1b, IL-6, CXCL8 (Il-8) and TNFa.  The serotype A1 and A2 isolates behaved very differently and there was a strong correlation between events in vitro and typical behaviour in vivo.  Bacterial numbers of the serotype A1 isolate increased significantly over the first 24 h of infection and microscopy demonstrated that this was due to invasion, rapid intracellular replication and subsequent spread of bacteria through the epithelial layer; tissue damage increased significantly from 24 h onwards.  In contrast, bacterial numbers of the serotype A2 isolate did not increase and there were no signs of invasion; indeed, the epithelium remained healthy at day 5 and bacteria were mostly completely eliminated.  Isolates of both serotypes stimulated the production of all four cytokines/chemokines in a manner that mimicked published in vivo data; notably, production of IL-1b and TNFa varied for the two strains.  In conclusion, use of our DBEC model has identified a previously unknown invasion mechanism of M. haemolytica serotype A1 which provides a possible explanation for its sudden proliferation within the bovine URT.