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Virulence Mechanism of Bacteria in Mixed Infection: Attenuation of Cytokine Levels and Evasion of Polymorphonuclear Leukocyte Phagocytosis
Author(s) -
Polak David,
Shapira Lior,
Weiss Ervin I.,
HouriHaddad Yael
Publication year - 2013
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2012.120528
Subject(s) - phagocytosis , fusobacterium nucleatum , porphyromonas gingivalis , microbiology and biotechnology , virulence , bacteria , biology , ex vivo , flow cytometry , in vivo , macrophage , immunology , in vitro , biochemistry , genetics , gene
Background: The objective of the present study is to evaluate the effect of bacterial viability on the virulence of mixed infection. Methods: Expression of pro‐ and anti‐inflammatory cytokines (interleukin [IL]‐1β and IL‐10, respectively) was tested in vivo, following live versus heat‐killed infection (mono or mixed), using the mouse chamber model of infection. Ex vivo, phagocytosis of fluorescently labeled bacteria was tested in primary mouse polymorphonuclear leukocytes by flow cytometry. Results: In monoinfection, heat‐killed Porphyromonas gingivalis led to augmented levels of IL‐1β 2 hours postinfection, whereas IL‐10 levels remained unaffected. Phagocytosis of heat‐killed P. gingivalis was reduced compared with that of the live P. gingivalis , whereas phagocytosis of heat‐killed Fusobacterium nucleatum was augmented compared with that of live F. nucleatum . In mixed infection, both IL‐1β and IL‐10 levels were augmented 24 hours postinfection when the bacteria were heat‐killed. Although the phagocytosis pattern of F. nucleatum in the mixed infection remained similar to that upon monoinfection, phagocytosis of P. gingivalis was reduced following mixed infection. Conclusions: The inflammatory response to live mixed infection is attenuated with reduced phagocytosis, compared with that of heat‐killed mixed infection. The lower response to live mixed infection could stem from a mechanism enabling the bacteria to evade the host response, thereby increasing bacterial survival.