Differences in phagocytosis susceptibility in Haemophilus parasuis strains.

Centre de Recerca en Sanitat Animal (CReSA), UAB-IRTA, Campus de la Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.
Veterinary Research (Impact Factor: 3.43). 03/2009; 40(3):24. DOI: 10.1051/vetres/2009007
Source: PubMed

ABSTRACT Haemophilus parasuis is a colonizer of the upper respiratory tract of healthy pigs, but virulent strains can cause a systemic infection characterized by fibrinous polyserositis, commonly known as Glässer's disease. The variability in virulence that is observed among H. parasuis strains is not completely understood, since the virulence mechanisms of H. parasuis are largely unknown. In the course of infection, H. parasuis has to survive the host pulmonary defences, which include alveolar macrophages, to produce disease. Using strains from different clinical backgrounds, we were able to detect clear differences in susceptibility to phagocytosis. Strains isolated from the nose of healthy animals were efficiently phagocytosed by porcine alveolar macrophages (PAM), while strains isolated from systemic lesions were resistant to this interaction. Phagocytosis of susceptible strains proceeded through mechanisms independent of a specific receptor, which involved actin filaments and microtubules. In all the systemic strains tested in this study, we observed a distinct capsule after interaction with PAM, indicating a role of this surface structure in phagocytosis resistance. However, additional mechanisms of resistance to phagocytosis should be explored, since we detected different effects of microtubule inhibition among systemic strains.

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    ABSTRACT: Haemophilus parasuis colonises healthy pigs and is the aetiological agent of Glässer's disease. The pathogenicity of H. parasuis is poorly characterised, while prevention and control of Glässer's disease continues to be challenging. Understanding the pathogenicity of H. parasuis is essential for determining how this bacterium produces disease and to better distinguish between virulent and non-virulent strains. Infection by H. parasuis requires adhesion to and invasion of host cells, resistance to phagocytosis by macrophages, resistance to serum complement and induction of inflammation. Identification of virulence factors involved in these mechanisms has been limited by difficulties in producing mutants in H. parasuis. Recent advances in understanding the pathogenesis of H. parasuis are due in part to the production of deletion mutants, although most of the potential virulence factors described so far require further characterisation. Data supporting the role of lipooligosaccharide, capsule formation, porin proteins, cytolethal distending toxin and trimeric autotransporters (VtaA), among other molecules, in the virulence of H. parasuis have been described. This review provides an overview of the current knowledge of virulence factors of H. parasuis.
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    ABSTRACT: Haemophilus parasuis is the causative agent of Glässer's disease in pigs, a severe systemic disease that has led to increasing economic losses in the pig industry worldwide. The H. parasuis genome sequence has been completed, but the function and essentiality of the annotated genes remain largely unknown, especially virulence factors. The recent developments in the efficient genetic manipulation of H. parasuis have greatly facilitated the study of gene function, pathogenesis mechanisms and virulence factors. In this review, we provided update information regarding that (i) how the pathogen overcome host immune responses and cell barriers which were tightly associated with the pathogenesis, and (ii) the several recent identification of virulence factors were involved in evading the immune responses and cell barriers in H. parasuis.
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    ABSTRACT: Haemophilus parasuis is a common inhabitant of the upper respiratory tract of pigs and the etiological agent of Glässer's disease. However, the host-pathogen interaction remains to be well understood. In this work, 33 colostrum-deprived pigs were divided in 4 groups and each group was inoculated intranasally with a different H. parasuis strain (non-virulent strains SW114 and F9, and virulent strains Nagasaki and IT29755). Animals were necropsied at different times in order to determine the location of the bacteria in the respiratory tract of the host during infection. An immunohistochemistry method was developed to detect H. parasuis in nasal turbinates, trachea and lung. Also, the co-localization of H. parasuis with macrophages or neutrophils was examined by double immunohistochemistry and double immunofluorescence. Virulent strains showed a biofilm-like growth in nasal turbinates and trachea and were found easily in lung. Some virulent bacteria were detected in association with macrophages and neutrophils, but also inside pneumocyte-like cells. On the other hand, non-virulent strains were seldom detected in nasal turbinates and trachea, where they showed a microcolony pattern. Non-virulent strains were essentially not detected in lung. In conclusion, this work presents data showing differential localization of H. parasuis bacteria depending on their virulence. Interestingly, the intracellular location of virulent H. parasuis bacteria in non-phagocytic cells in lung could allow the persistence of the bacteria and constitute a virulence mechanism.
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