Employing classically activated (M1) and alternatively activated (M2) murine bone-marrow-derived macrophage (BMDMø), we observed that immunologic activation of macrophages before P. gingivalis challenge dictated phenotype-specific changes in the expression of inflammation-associated molecules important to sensing and tuning host response to bacterial infection including Toll-like receptors 2 and 4, CD14, CD18 and CD11b (together comprising CR3), major histocompatibility complex class II, CD80, and CD86.
The adoptive transfer of CD11b+ macrophages from LPS-primed mice to control mice increased survival after bacterial infection and reduced the elevation of plasma TNF.
Neonatal and adult neutrophils were evaluated for their ability to combat bacterial infection by examining their functional activity (CD11b and reactive oxygen intermediates) and their persistence at inflammatory sites (apoptosis).
The number of lymphocytes, CD3+ gammadelta+, CD8+ CD11b-, CD8+ HLA-DR+, and CD4+ CD29+ cells was higher in patients with bacterial infection than in those without bacterial infection, and interestingly, macrolide therapy reduced the number of lymphocytes, CD3+ gammadelta+, CD8+ CD11b- and CD8+ HLA-DR+ cells, irrespective of bacterial infection.