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Related Concept Videos

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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Defense Against Bacterial Pathogens

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Among the three main modes of HGT—transformation, conjugation, and transduction—transduction is unique in that it is mediated by bacteriophages, or bacterial viruses.Transduction occurs in two ways. Generalized transduction occurs during the lytic cycle of a bacteriophage infection. In this process, bacteriophages infect bacterial cells, replicate within them, and ultimately cause cell lysis, releasing newly assembled virions. Occasionally, random fragments of the bacterial genome are...
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Investigation of Microbial Cooperation via Imaging Mass Spectrometry Analysis of Bacterial Colonies Grown on Agar and in Tissue During Infection
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Microbial hijacking of complement-toll-like receptor crosstalk.

Min Wang1, Jennifer L Krauss, Hisanori Domon

  • 1Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, KY 40292, USA.

Science Signaling
|February 18, 2010
PubMed
Summary

Pathogens like Porphyromonas gingivalis exploit immune crosstalk between complement and Toll-like receptors (TLRs). This interaction suppresses macrophage function via cAMP, aiding pathogen survival and suggesting new therapeutic targets.

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Area of Science:

  • Immunology
  • Microbiology

Background:

  • Crosstalk between complement and Toll-like receptors (TLRs) is crucial for innate immunity.
  • Porphyromonas gingivalis is an oral and systemic pathogen implicated in periodontitis and atherosclerosis.

Purpose of the Study:

  • To investigate a novel immune subversion mechanism where P. gingivalis exploits complement-TLR crosstalk.
  • To elucidate the signaling pathway involved in P. gingivalis-mediated immune suppression.

Main Methods:

  • Investigated the synergy between P. gingivalis and C5a in modulating immune responses.
  • Utilized TLR2 signaling, pertussis toxin, thapsigargin, and downstream effectors (PKA, GSK-3β) to define the pathway.
  • Assessed the impact of C5a receptor blockade on pathogen survival.

Main Results:

  • P. gingivalis synergizes with C5a to increase cAMP concentrations, suppressing macrophage immune function.
  • This immunosuppression requires TLR2 signaling and involves a C5a receptor pathway with PKA and GSK-3β as effectors.
  • Blocking the C5a receptor abrogated the immune evasion strategy.

Conclusions:

  • P. gingivalis exploits complement-TLR crosstalk for immune evasion by inducing immunosuppressive cAMP signaling.
  • This mechanism enhances pathogen survival both in vitro and in vivo.
  • Targeting the C5a receptor offers potential therapeutic strategies for P. gingivalis-associated diseases.