본 연구에서는 유산균에 의한 검은콩의 최적 발효조건을 확립하고 발효된 검은콩의 품질특성을 평가하였다. 가정에서 제조된 배추김치로부터 분리한 Lactobacillus plantarum SU22는 병원성 세균에 대해 강한 항균 활성을 보였고 생체 아민과 발암성 효소인 β-glucuronidase를 생성하지 않았기 때문에 검은콩 발효의 스타터로 선정되었다. 검은콩은 5 kgf/cm2, 150oC로 조절된 팽화기에서 10분 동안 팽화 처리한 것과 처리하지 않은 것으로 각각 10- 30% 혼합액을 만들고 L. plantarum SU22를 1%(v/v) 접종하여 37oC로 48시간 동안 진탕 배양하면서 유산균의 생육 특성을 비교하였다. 유산균의 생균수는 L. plantarum SU22 로 발효된 팽화 검은콩(20%) 배양액에서 9 Log CFU/mL 이상이었다. 20% 팽화 검은콩 배양액을 alcalase로 가수분 해한 후 L. plantarum SU22로 발효하는 것이 최적 조건인 것으로 밝혀졌으며 유산균의 생균수가 10.30 Log CFU/ mL까지 증가하였다. 최적 조건에서 총 폴리페놀 함량(94.02 mg GAE/g)과 DPPH 라디칼 소거능(92.50%)이 비 발효 대조군(87.74 mg GAE/g, 83.14%)에 비해 현저하게 증가하였다(P<0.05). 결론적으로 검은콩을 팽화한 후 alcalase 처리와 L. plantarum SU22를 병행하여 발효할 때 바이오제닉 아민이 없는 검은콩 발효액을 효과적으로 제조할 수 있으며, 총 폴리페놀과 DPPH 라디칼 소거능을 유의적으로 증가시킬 수 있다는 것을 알 수 있었다.

본 연구는 아로니아 천연 발효종을 사용하여 sourdough starter를 만들고, sourdough starter 첨가량을 0%, 15%, 25%, 35%로 증가하며 모닝빵을 제조할 때 starter 첨가량에 따른 품질특성, 항산화력, 소비자 선호도를 비교하기 위해 수행하였다. 아로니아 sourdough starter 함량이 증가할수록 모닝빵의 pH는 감소하였고, 총산도와 수분함량은 증가하였다. 비용적과 굽기 손실율 또한 sourdough starter 첨가량에 따라 유의적으로 증가하여 35% 첨가군(AS3)에서 가장 큰 굽기 손실율을 나타내었으나(P<0.05), 높이는 25% 첨가군(AS2)이 가장 높고 35% 첨가군에서 급격히 감소하였다. 발효 팽창력의 경우 0-25% 첨가군(AS0, AS1, AS2) 모두 45분까지 유의적으로 증가하였으나(P<0.05), 35% 첨가군은 30분까지만 팽창력이 증가하다가 30분 이후에는 급격히 감소하는 것으로 나타났다. 모닝빵의 총 페놀 함량과 DPPH 라디칼 소거능은 아로니아 sourdough starter 첨가량이 증가함에 따라 유의적으로 향상되었으며 (P<0.05), 색도는 첨가량이 증가할수록 밝기(L*)와 황색도 (b*)는 감소하고, 적색도는(a*) 증가하였다(P<0.05). 모닝빵의 조직감 측정 결과 응집성(cohesiveness)은 25% 첨가군이 가장 높고, 경도(hardness), 검성(gumminess), 씹힘성 (chewiness)은 아로니아 sourdough starter 첨가량이 증가할수록 유의적으로 낮게 측정되었다(P<0.05). 소비자 선호도 조사에서는 35% 첨가군의 색에 대한 선호도가 가장 낮았고, 15%와 25% 첨가군이 조직감과 전반적인 기호도가 좋은 것으로 나타났다(P<0.05). 이상의 결과에서 아로니아 sourdough starter를 첨가한 모닝빵의 품질특성, 항산화 활성, 소비자 선호도를 모두 고려할 때에 sourdough starter 는 밀가루 대비 25%를 첨가하는 것이 가장 우수하다는 것을 알 수 있었다.

Periodontitis results from the activation of host immune and inflammatory defense responses to subgingival plaque bacteria, most of which are gram-negative rods with lipopolysaccharides (LPSs) in their cell walls. LPSs have been known to induce proinflammatory responses and recently it was reported also that they induce the expression of microRNAs(miRNAs) in host cells. In our current study therefore, we aimed to examine and compare the miRNA expression patterns induced by the LPSs of major periodontopathogens in the human gingival epithelial cell line, Ca9-22. The cells were treated with 1 μg/ml of E. coli (Ec) LPS or 5 μg/ml of an LPS preparations from four periodontopathogens Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Aggregatibacter actinomycetemcomitans (Aa), and Fusobacterium nucleatum (Fn) for 24 h. After small RNA extraction from the treated cells, miRNA microarray analysis was carried out and characteristic expression profiles were observed. Fn LPS most actively induced miRNAs related to inflammation, followed by Aa LPS, Pi LPS, and Ec LPS. In contrast, Pg LPS only weakly activated miRNAs related to inflammation. Among the miRNAs induced by each LPS, miR-875-3p, miR-449b, and miR-520d-3p were found to be commonly up-regulated by all five LPS preparations, although at different levels. When we further compared the miRNA expression patterns induced by each LPS, Ec LPS and Pi LPS were the most similar although Fn LPS and Aa LPS also induced a similar miRNA expression pattern. In contrast, the miRNA profile induced by Pg LPS was quite distinctive compared with the other bacteria. In conclusion, miR-875- 3p, miR-449b, and miR-520d-3p miRNAs are potential targets for the diagnosis and treatment of periodontal inflammation induced by subgingival plaque biofilms. Furthermore, the observations in our current study provide new insights into the inflammatory miRNA response to periodontitis.

Porphyromonas gingivalis lipopolysaccharide (Pg LPS) is an important virulence factor in chronic periodontitis. The aim of this study was to compare the expression of inflammatory cytokine genes in Escherichia coli LPS (Ec LPS) and Pg LPS-stimulated mouse macrophage RAW 264.7 cells. Cells were treated with Ec LPS and Pg LPS for 18 hours, and the cytokine gene expression profile was assessed using microarrays and confirmed by real-time PCR. Microarray analysis showed that both types of LPS induced a significant increase in the expression of IL-17β, IL-2, Ccl4, Cxcl2 and TNFα compared with the control. However, LT-b was up-regulated by Pg LPS but not by Ec LPS. Real-time PCR analysis of these genes showed similar results for LT-b, Ccl4, Cxcl2, and TNF- but found that IL-17β and IL-2 were upregulated by Pg LPS but not by Ec LPS. These data indicate that Pg LPS stimulates the transcription of IL-17β, IL-2, Ccl4, Cxcl2, LT-b, and TNFα, all of which may be involved in the pathogenesis of chronic periodontitis.

Porphyromonas (P.) gingivalis lipopolysaccharide (Pg LPS) is the major pathogenic component of periodontal disease. In this study, we have attempted to determine the expression profiles of the signal transduction pathway genes induced by Pg LPS in comparison with Escherichia (E.) coli LPS (Ec LPS). DC2.4 cells were treated for two hours with 1 μg/mℓ of Pg LPS or 0.5μg/mℓ of Ec LPS. The total RNA from these cells was then isolated and reverse-transcribed. Gene expression profiles were then analyzed with a signal transduction pathway finder GEArray Q series kit and significant changes in expression were confirmed by real-time PCR. The microarray results indicated that several genes, including Tnfrsf10b, Vcam1, Scyb9, Trim25, Klk6, and Stra6 were upregulated in the DC2.4 cells in response to Pg LPS treatment, but were downregulated or unaffected by Ec LPS. Realtime PCR revealed that the expression of Trim25, Scyb9 and Tnfrsf10b was increased over the untreated control. Notably, Trim25 and Tnfrsf10b were more strongly induced by Pg LPS than by Ec LPS. These results provide greater insight into the signal transduction pathways that are altered by P. gingivalis LPS.