In:
The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 1_Supplement ( 2021-05-01), p. 110.13-110.13
Abstract:
Chronic periodontitis (CP) is an inflammatory disease of the tooth supporting tissue developed in response to formation of the dysbiotic biofilm on the subgingival tooth surface. Although exacerbated inflammation leads to the alveolar bone destruction and may cause tooth loss the molecular basis of CP initiation and progression remains elusive. The control over the inflammatory reaction and homeostasis can be efficiently restored by the negative regulators of TLRs signaling pathways, such as MCPIP-1, which is constitutively expressed in gingival keratinocytes and prevents the hyporesponsiveness in the gum. Here we found that inflammophilic periodontal species influence stability of MCPIP-1 leading to aggravated response of the epithelium to proinflammatory stimulation. We identified that among enzymes secreted by those pathogenic species, gingipains – cysteine proteases from Porphyromonas gingivalis play a crucial role. Their proteolytic activity leads to a rapid degradation of MCPIP-1 exacerbating inflammatory response induced by endotoxin. Taken together, we showed the novel mechanism of corruption of inflammatory signaling by periodontal pathogens indicating new possibilities for treatment of this chronic disease.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.206.Supp.110.13
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2021
detail.hit.zdb_id:
1475085-5
Permalink