IADR Abstract Archives
Genes Control Gingival Crevicular Fluid Responsiveness to Biofilm Lysine Decarboxylase.
Objectives: We previously reported (PMID:22141361, 26110450) that the activity of lysine decarboxylase from Eikenella corrodens (LdcE) induces experimental gingivitis (EG) within a week. During EG, participants develop gingivitis slowly or rapidly (PMID:30412312), and slow responders exhibit depressed levels of cytokines (PMID:31013451). We reported a similar dichotomy of inflammatory responses in our EG study (IADR London 2018, Abstr ID: 2343). The presence or absence of an interleukin-1 (IL-1) genotype consisting of IL-1A-889 and IL-1B+3954, determines the severity of tooth loss in older adults (PMID: 23752171, 25726344). We examined whether the strong or weak inflammatory response phenotype in our EG study can be identified genetically
Methods: We obtained consent from 15 of the 16 participants in our previous study in which gingival crevicular fluid µL/min measured inflammatory response after a week (PMID:22141361). From a buccal cheek scraping we measured the presence or absence of the following gene variants: IL-1A-889, IL-1B+3954, IL-1B-511, IL-6-1363, IL10-1082, IL10-597 CD14-260, COX2-8473, and MMP8-799. Associations were examined using the Fisher exact test for small sample size.
Results: Participants comprised 6 weak and 9 strong responders. 1: IL-1B+3954(T) identified 5 weak and 3 strong responders (p not significant). 2: IL-6-1363(T) identified the 6th weak responder, and one of 3 strong responders already IL-1B+3954(T), (p<0.03). 3: COX2-8473(A/G) was absent from all weak responders, but present in 3 strong responders including an IL-1B+3954(T) responder, who was therefore considered phenotypically strong (p<0.01).
Conclusions: A strong or weak inflammatory response phenotype to LdcE was determined by the genotype IL-1B+3954, supplemented with IL-6-1363 and COX2-8473. IL-1α expression precedes IL-1β expression in EG (PMID:12670080), because IL-1A activation by bacteria is necessary to activate IL-1B. We suggest that, after a week of EG, individuals with alleles IL-1B+3954(T) or IL-6-1363(T) have a weakened acute GCF exudation response to LdcE unless heterozygous for COX2-8473(AG).
Methods: We obtained consent from 15 of the 16 participants in our previous study in which gingival crevicular fluid µL/min measured inflammatory response after a week (PMID:22141361). From a buccal cheek scraping we measured the presence or absence of the following gene variants: IL-1A-889, IL-1B+3954, IL-1B-511, IL-6-1363, IL10-1082, IL10-597 CD14-260, COX2-8473, and MMP8-799. Associations were examined using the Fisher exact test for small sample size.
Results: Participants comprised 6 weak and 9 strong responders. 1: IL-1B+3954(T) identified 5 weak and 3 strong responders (p not significant). 2: IL-6-1363(T) identified the 6th weak responder, and one of 3 strong responders already IL-1B+3954(T), (p<0.03). 3: COX2-8473(A/G) was absent from all weak responders, but present in 3 strong responders including an IL-1B+3954(T) responder, who was therefore considered phenotypically strong (p<0.01).
Conclusions: A strong or weak inflammatory response phenotype to LdcE was determined by the genotype IL-1B+3954, supplemented with IL-6-1363 and COX2-8473. IL-1α expression precedes IL-1β expression in EG (PMID:12670080), because IL-1A activation by bacteria is necessary to activate IL-1B. We suggest that, after a week of EG, individuals with alleles IL-1B+3954(T) or IL-6-1363(T) have a weakened acute GCF exudation response to LdcE unless heterozygous for COX2-8473(AG).