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Immunologic environment influences macrophage response to Porphyromonas gingivalis
Author(s) -
Papadopoulos G.,
ShaikDasthagirisaheb Y.B.,
Huang N.,
Viglianti G.A.,
Henderson A.J.,
Kantarci A.,
Gibson F.C.
Publication year - 2017
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12168
Subject(s) - porphyromonas gingivalis , macrophage , biology , macrophage inflammatory protein , immune system , monocyte , immunology , inflammation , tumor necrosis factor alpha , cytokine , microbiology and biotechnology , interleukin , in vitro , bacteria , biochemistry , genetics
Summary Macrophages adapt both phenotypically and functionally to the cytokine balance in host tissue microenvironments. Recent studies established that macrophages contribute an important yet poorly understood role in the development of infection‐elicited oral bone loss. We hypothesized that macrophage adaptation to inflammatory signals encountered before pathogen interaction would significantly influence the subsequent immune response of these cells to the keystone oral pathobiont Porphyromonas gingivalis . Employing classically activated (M1) and alternatively activated (M2) murine bone‐marrow‐derived macrophage ( BMDM ø), 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, CD 14, CD 18 and CD 11b (together comprising CR 3), major histocompatibility complex class II , CD 80, and CD 86. M2 cells responded to P. gingivalis with higher expression of tumor necrosis factor‐α, interleukin‐6, monocyte chemoattractant protein‐1, macrophage inflammatory protein‐1α, regulated on activation normal T cell expressed and secreted, and KC than M1 cells. M1 BMDM ø expressed higher levels of interleukin‐10 to P. gingivalis than M2 BMDM ø. Functionally, we observed that M2 BMDM ø bound P. gingivalis more robustly than M1 BMDM ø. These data describe an important contribution of macrophage skewing in the subsequent development of the cellular immune response to P. gingivalis .