Mac-1-mediated uptake and killing of Bordetella bronchiseptica by porcine alveolar macrophages.
The role of Mac-1 as a receptor for Bordetella bronchiseptica infection of alveolar macrophages (AMphi) was examined using 6 strains (2 ATCC and 4 pathogenic field isolates) to assess B. bronchiseptica binding, uptake and replication in primary porcine AMphi. All B. bronchiseptica strains were rapidly killed by porcine serum in a dose- and time-dependent manner. However, heat-inactivated porcine serum (HIS) did not demonstrate any bacterial-killing activity, suggesting that complement may have a direct killing activity. All field isolates were more resistant to direct complement-mediated B. bronchiseptica killing. The uptake of B. bronchiseptica into AMphi was inhibited approximately 50% by anti-Mac-1 monoclonal antibodies in the medium. However, B. bronchiseptica phagocytosed in the presence of serum or HIS was not altered by anti-Mac-1 antibodies although more bacteria were internalized by addition of serum or HIS. These data suggest that Mac-1 is a target for direct uptake of B. bronchiseptica via opsonin-independent binding. The phagocytosed B. bronchiseptica, either via direct or serum-mediated binding, were efficiently killed by AMphi within 10 hr postinfection. This demonstrates that Mac-1-mediated B. bronchiseptica uptake is a bacterial killing pathway not leading to productive infections in AMphi.
Lee
Jong-keuk
JK
National Genome Research Institute, National Institute of Health, Seoul, Korea. cookie_jklee@hotmail.com
Schook
Lawrence B
LB
Rutherford
Mark S
MS
D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D016950:Bordetella bronchiseptica / Q000276:immunology*; D016177:Macrophage-1 Antigen / Q000276:immunology*; D016676:Macrophages, Alveolar / Q000276:immunology*; D010587:Phagocytosis; D011485:Protein Binding; D013552:Swine / Q000276:immunology* / Q000382:microbiology*
D000907:Antibodies, Bacterial; D016177:Macrophage-1 Antigen