Many mammalian cells express a particular receptor, CD11b, on their surfaces. CIDD researchers and their collaborators have now shown that this receptor plays a crucial role in the immune response to respiratory infection with the bacterium Bordetella bronchiseptica: mice lacking CD11b died from bacterial doses that caused few or no symptoms in wild-type mice.
The receptor appears to affect apoptosis (controlled destruction) of infected host cells, as well as an inflammatory response to the bacterial toxin TTSS (which causes some host cells to necrose and die). Mice lacking the CD11b receptor showed reduced apoptosis, and hence increased numbers of cells in the lungs. Mice lacking CD11b were more likely to survive when inoculated with a bacterial strain unable to produce TTSS.
The researchers suggest that reduced apoptosis and TTSS-related inflammation cause neutrophils to accumulate in the lungs. It is this accumulation that appears to be lethal: mice had higher survival when treated with an antibody that blocks migration of neutrophils to the lungs.
Written By: Mylisa R. Pilione, Luis M. Agosto, Mary J. Kennett, & Eric T. Harvill
Journal: 8: 758-768
Journal Reference: 8: 758-768
Paper Id: 10.1111/j.1462-5822.2005.00663.x