Effect of temperature modulation and bvg mutation of Bordetella bronchiseptica on adhesion, intracellular survival and cytotoxicity for swine alveolar macrophages

Citation
Sl. Brockmeier et Kb. Register, Effect of temperature modulation and bvg mutation of Bordetella bronchiseptica on adhesion, intracellular survival and cytotoxicity for swine alveolar macrophages, VET MICROB, 73(1), 2000, pp. 1-12
Citations number
42
Categorie Soggetti
Veterinary Medicine/Animal Health",Microbiology
Journal title
VETERINARY MICROBIOLOGY
ISSN journal
03781135 → ACNP
Volume
73
Issue
1
Year of publication
2000
Pages
1 - 12
Database
ISI
SICI code
0378-1135(20000404)73:1<1:EOTMAB>2.0.ZU;2-R
Abstract
Bordetella bronchiseptica causes respiratory disease in swine, yet there ar e no studies examining the interaction of B. bronchiseptica with swine alve olar macrophages. A swine isolate of B. bronchiseptica was able to adhere t o, and survive intracellularly in, swine alveolar macrophages, but the rela tive ability of the bacteria to accomplish these functions was dependent on its phenotypic phase and culture conditions. More bacteria were observed e xtracellularly as well as intracellularly by immunofluorescent staining whe n B. bronchiseptica was cultured at 23 degrees C as compared to 37 degrees C. However, more bacteria cultured at 37 degrees C were found surviving int racellularly after the macrophages were cultured with polymyxin B to kill e xtracellular bacteria. Similar results were seen in experiments performed w ith an isogenic Bvg(-) phase-locked mutant of B. bronchiseptica cultured at 37 or 2.3 degrees C, indicating that another temperature dependent mechani sm in addition to bVg may play a role in adhesion and intracellular surviva l. B. bronchiseptica was cytotoxic for swine alveolar macrophages in the Bv g(+) phase only. The cytotoxicity of B. bronchiseptica for alveolar macroph ages, and its ability to survive phagocytosis, are no doubt important to es cape from immune clearance mechanisms and establish infection, and could le ave the host susceptible to secondary respiratory pathogens. Published by E lsevier Science B.V.