Association of Bordetella pertussis with host immune cells in the mouse lung
| Autor: | Paul J.M. Roholl, Sandra M. M. Hellwig, Jolanda P. Vermeulen, Frits R. Mooi, Jan H.G. Hoekman, Jan A. M. A. Dormans, Rob J. Vandebriel |
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| Rok vydání: | 2003 |
| Předmět: |
Lung Diseases
Bordetella pertussis Whooping Cough Phagocytosis Fimbria Filamentous haemagglutinin adhesin Microbiology Bacterial Adhesion Pathogenesis Mice Immune system Immunity Animals Macrophage Adhesins Bacterial Microscopy Confocal biology biology.organism_classification Immunohistochemistry Mice Inbred C57BL Hemagglutinins Infectious Diseases Microscopy Fluorescence Fimbriae Bacterial Immunology Female Bronchoalveolar Lavage Fluid |
| Zdroj: | Microbial Pathogenesis. 35:19-29 |
| ISSN: | 0882-4010 |
| DOI: | 10.1016/s0882-4010(03)00087-1 |
| Popis: | Mouse models are frequently used to study immunity and pathogenesis to Bordetella pertussis infection. To improve the understanding of the mouse infection model, the influx of host cells and B. pertussis localisation in the lungs were evaluated. Furthermore, the roles of filamentous hemagglutinin (FHA) and fimbriae (Fim) in these processes were determined. B. pertussis infection stimulated the recruitment of polymorphonuclear granulocytes (PMN), alveolar macrophages, and lymphocytes. As deterined by double immunofluorescence staining, 2 hr after infection most B. pertussis were free in the alveolar space, some were attached to alveolar epithelia, and some were associated with and phagocytosed by PMN. After 3 days, most bacteria were associated with and phagocytosed by macrophages, some by PMN. B. pertussis was shown not to be ingested by epithelial cells or associated with interstitial macrophages. B. pertussis mutants lacking expression of FHA or Fim were associated with and phagocytosed by the same cell types as parental bacteria. The Fim mutant, however, induced a more severe inflammation, and was cleared faster from the lungs compared to the parental strain and the FHA mutant. These results suggest that Fim does not affect bacterial localisation in the mouse lung, but does influence host immune mechanisms. Possibly, Fim may exert an anti-inflammatory function and thereby inhibit killing by macrophages. |
| Databáze: | OpenAIRE |
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