Mac-1-mediated uptake and killing of Bordetella bronchiseptica by porcine alveolar macrophages.

Jong keuk Lee, Lawrence B. Schook, Mark S. Rutherford

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)41-49
Number of pages9
JournalJournal of veterinary science (Suwon-si, Korea)
Issue number1
StatePublished - Apr 2003
Externally publishedYes

ASJC Scopus subject areas

  • veterinary(all)


Dive into the research topics of 'Mac-1-mediated uptake and killing of Bordetella bronchiseptica by porcine alveolar macrophages.'. Together they form a unique fingerprint.

Cite this