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Published on: August 8, 2014
Porphyromonas gingivalis peptidoglycans induce excessive activation of the innate immune system in silkworm larvae
Kenichi Ishii1, Hiroshi Hamamoto1, Katsutoshi Imamura1
1From the Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan.
Abstract:
Porphyromonas gingivalis, a pathogen that causes inflammation in human periodontal tissue, killed silkworm (Bombyx mori, Lepidoptera) larvae when injected into the blood (hemolymph). Silkworm lethality was not rescued by antibiotic treatment, and heat-killed bacteria were also lethal. Heat-killed bacteria of mutant P. gingivalis strains lacking virulence factors also killed silkworms. Silkworms died after injection of peptidoglycans purified from P. gingivalis (pPG), and pPG toxicity was blocked by treatment with mutanolysin, a peptidoglycan-degrading enzyme. pPG induced silkworm hemolymph melanization at the same dose as that required to kill the animal. pPG injection increased caspase activity in silkworm tissues. pPG-induced silkworm death was delayed by injecting melanization-inhibiting reagents (a serine protease inhibitor and 1-phenyl-2-thiourea), antioxidants (N-acetyl-l-cysteine, glutathione, and catalase), and a caspase inhibitor (Ac-DEVD-CHO). Thus, pPG induces excessive activation of the innate immune response, which leads to the generation of reactive oxygen species and apoptotic cell death in the host tissue.
Insights
Porphyromonas gingivalis peptidoglycans (pPG) trigger a lethal innate immune response in silkworms. This immune overactivation, involving melanization and apoptosis, causes silkworm death, highlighting a conserved toxicity mechanism.
Area of Science:
- Microbiology
- Immunology
- Toxicology
Background:
- Porphyromonas gingivalis is a key pathogen in human periodontal disease.
- Its role in host immune response and toxicity is not fully understood.
- Silkworm larvae (Bombyx mori) serve as a model organism for studying innate immunity.
Purpose of the Study:
- To investigate the lethal effects of P. gingivalis and its components in silkworm larvae.
- To elucidate the mechanisms underlying P. gingivalis-induced toxicity in a model organism.
Main Methods:
- Injection of live and heat-killed P. gingivalis, including mutant strains, into silkworm hemolymph.
- Purification and injection of P. gingivalis peptidoglycans (pPG).
- Treatment with antibiotics, mutanolysin, melanization inhibitors, antioxidants, and caspase inhibitors.
Main Results:
- P. gingivalis, live or heat-killed, caused significant lethality in silkworms.
- Purified pPG was lethal to silkworms, inducing hemolymph melanization and increasing caspase activity.
- pPG toxicity was mitigated by mutanolysin, melanization inhibitors, antioxidants, and a caspase inhibitor.
Conclusions:
- P. gingivalis peptidoglycans induce excessive activation of the silkworm innate immune response.
- This overactivation leads to reactive oxygen species generation and apoptotic cell death, causing host lethality.
- The silkworm model effectively demonstrates conserved mechanisms of P. gingivalis-induced toxicity.
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