The influence of adhesin protein from Aggregatibacter actinomycetemcomitans on IL-8 and MMP-8 titre in aggressive periodontitis

Background: Adhesion can actually be considered as a part of both a powerful survival mechanism and a virulence mechanism for bacterial pathogens. Bacterial adhesin is an instrument for bacteria to do invasion to host. Bacterial adhesin depends on ligand interaction as a signaling mediator that will influence invasion and increase pro and anti-inflammatory because of the influence of the receptors of innate immune response. Aggregatibacter actimycetemcomitans has fimbriae included in type IV pili containing mostly with protein weighed 6.5 kDa and at least with protein weighed 54 kDa. Purpose: The purpose of this research is to analyze the influence of the induction of adhesin protein derived from A. actinomycetemcomitans on IL-8 and MMP-8 titre of Wistar rats. Methods: Adhesin protein derived from A. actinomycetemcomitans weighed 24 kDa was induced on the maxillary first molar sulcus of Wistar rats to prove that adhesin protein could affect IL-8 and MMP-8 titre. Next, to determine its influence, Elisa technique was conducted. Results: It is known that the levels of IL-8 and MMP-8 titre were increased in the group induced with adhesin protein derived from A. actinomycetemcomitans compared with the control group. Conclusion: It can be concluded that adhesin protein derived from A. actinomycetemcomitans can cause alveolar bone damage through the increasing levels of IL-8 and MMP-8 in aggressive periodontitis

The toxicity test of Streptococcus mutans 1 (c) 67 kDa monoclonal antibodies in cell culture with MTT assay = Uji toksisitas antibodi monoklonal Streptococcus mutans 1 (c) 67 kDa pada kultur sel dengan MTT assay

Dental caries is infectious disease in hard tissue of tooth which cause dental structural disorder and chronic. From several the result of the study in Jakarta and Surabaya showed that the prevalency of dental caries was high. Therefore prevention of dental caries is still continuing, because the prevalency caries is high. There were many method to prevent dental caries, i.e. dental education, oral hygiene, special method on tooth brushing, water fluoridation, fissure sealant and later on the passive immunization with monoclonal antibodies. The material qualifications in dentistry must be non toxic, non iritation in tissue and have biocompatibility. The purpose of this study was to investigate about monoclonal antibodies toxicity of IgA, IgG1 and IgG3 in BHK-21 cell culture with MTT assay. A laboratory experimental study has been carried out. BHK-21 cell was included in microplate well with density 2×105 in 100 μl culture media, included for every well with IgA, IgG1 or IgG3 about 50 μl, appropriate with sample group. The cell control and media control were prepared too. Cell control was cell and culture media. Media control was only culture media. Replication for each monoclonal antibodies (with IgA, IgG1 and IgG3) was 10 times. Microplate with PBS (25 μl) and MTT 5 mg/ml was incubated for 24 hours in 37oC. Optical density formazan read by spectrophotometer with λ 540 nm. The data obtained in this study was analyzed with one way Anova and LSD. The result of this study showed that there was a significant difference of toxicity between IgA and IgG3 so IgG1 and IgG3. There wasn’t a significant difference of toxicity between IgA and IgG1 so between IgA with the control group, but there was a significant difference of toxicity between IgG1 and IgG3 with control group. The conclusion of this study showed that monoclonal antibodies of S. mutans 1 (c) 67 kDa wasn’t toxic and the material was safe to use with the lowest percentage level of the dead cell were IgA, IgG1 and IgG3

The Role of Actinobacillus actinomycetemcomitans fimbrial adhesin against MMP-8 activity in aggressive periodontitis pathogenesis

abstract Background: Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is Gram negative and a major bacterial agent associated with aggressive periodontitis in young adult, this bacteria was an important factor in pathogenesis of aggressive periodontitis. A. actinomycetemcomitans possesses fimbriae with an adhesin protein that was the first bacterial molecules to make physical contact with host. Purpose: The objective of this research was to analyzed the influence of A. actinomycetemcomitans fimbrial adhesin protein induction on MMP-8 activity. Methods: The research was an experimental laboratory study, the step in this study were isolation and identification A. actinomycetemcomitans, characterize A. actinomycetemcomitans adhesin and study the role of A. actinomycetemcomitans adhesin in Wistar rats. Results: The result of this research on the role of adhesin in Wistar rats after analysis with Analysis of Variance (ANOVA) showed significant differences in the control group with group induction with A. actinomycetemcomitans, A. actinomycetemcomitans plus adhesin and adhesin. MMP-8 activity increased with induction A. actinomycetemcomitans and 24 kDa A. actinomycetemcomitans adhesin. This fimbrial adhesin protein showed that A. actinomycetemcomitans has the ability to adhesion, colonization and invasion for host in aggressive periodontitis pathogenesis. Conclusion: A. actinomycetemcomitans fimbrial adhesin protein induction increasing MMP-8 activity for aggressive periodontitis pathogenesis

A.actinomycetemcomitans adhesi protein increasing IL-8 titre in heart of wistar rat with aggressive periodontitis

Cardiovascular and periodontal diseases are common inflammatory conditions in the human population. Tlymphocytes participate in the pathogenesis and inflammatory events of atherosclerosis. These immune cells enter the inflamed artery wall and join macrophages via a number of interferon-c-inducible chemokines. Chemokines (IL-8), cytokines, and growth factors also participate in this process. The interaction between interleukin- 8 and its receptor, CXCR2, can also contribute to lesion formation in mice. The main causes of aggressive periodontitis is Actinobacillus actinomycetemcomitans. Previous studies have proven that adhesin protein with 24 kDa molecular weight from A.actinomycetemcomitans is a specific adhesin, this adhesin proteins play a role in the adhesion process on host. this kind adhesion in the epithelial attachment would lead to colonization and invasion of A.actinomycetemcomitans that will stimulate the host immune response. This study aimed to analyze the influence of induction 24 kDa A.actinomycetemcomitans adhesin protein to the titre of IL-8 in heart of Wistar rat with aggressive periodontitis using Elisa method to measure and analyze the titre of IL-8. After analyzed with analysis of variance, showed significant differences of IL-8 titre in the control group and the group with the induction by A.actinomycetemcomitans, A.actinomycetemcomitans plus 24 kDa A.actinomycetemcomitans adhesin protein, and only with 24 kDa A.actinomycetemcomitans adhesin protein. It can be concluded that A.actinomycetemcomitans adhesin protein with 24 kDa molecular weight has a role in increasing of IL-8 titre in heart wistar rat with aggressive periodontitis

Effect of lipopolysaccharide derived from surabaya isolates of Actinobacillus actinomycetemcomitans on alveolar bone destruction

Background: Actinobacillus actinomycetemcomitans’ lipopolysaccharide (LPS) has a high virulence factor. It interacts with serum protein through receptors on the epithelial cell surface, thereby increasing both interleukin (IL)-1β, and IL-6 which results in damage to periodontal tissue. Aim: The aim of the study was to identify and evaluate the effect of LPS derived from local isolates (A.actinomycetemcomitans) on the destruction of alveolar bone by means of several biomarkers, including; the number of osteoblasts and osteoclasts, the expression of IL-6, matrix metallopeptidase 1 (MMP-1), and receptor activator of nuclear factor kappa-Β ligand (RANKL). Materials and Methods: The isolation of LPS from A. actinomycetemcomitans was calculated using phenol, while purification was performed using Sephadex C-18 column chromatography. 40 Wistar rats were divided into four groups of 10. Each treatment was divided into two groups which were 0.9% NaCl and LPS induced for 7 and 14 days, respectively. Gingival and alveolar bones were further introduced into the induction area, followed by the measuring of osteoblast and osteoclast with hematoxylin-eosin staining, IL-6, MMP-1 and RANKL expression with immunohistochemical. Results: Reduced numbers of osteoblasts at the 7th and 14th day of treatment were detected, while those of osteoclasts increased. There was an increased expression of IL-6, MMP-1, and RANKL in the 7th and 14th-day treatment group. Treatment of LPS from A. actinomycetemcomitans over 7 and 14 days resulted in damage to periodontal tissue and alveolar bone in Wistar rats. Conclusion: LPS of A. actinomycetemcomitans administration for 7 and 14 days causes periodontal and alveolar tissue destruction in Wistar rats

Peran andhesin fimbriae actinobacillus actinomycetemcomitans terhadap aktivitas MMP-8 pada patogenesis periodontitis agersif

A.actinomycetemcomitans merupakan salah satu bakteri yang dihubungkan dengan periodontitis agresif yang menyerang pada penderita usia muda dan merupakan faktor penting pada patogenesis periodontitis agresif karena merupakan penyebab utama dari penyakit inL A.actimycetemcomitans mempunyai fimbriae dan macam koloni yang membuat bakteri ini bertahan hidup, beberapa macam koloni A.actinomycetemcomitans adalah koloni transparan kasar, transparan hal us dan opaque halus, banya pada koloni transparan kasar mempunyai fimbriae dengan protein terbanyak pada 6,5 kDa dan sedikit pada 54 kDa

Potensi Imunogenik dari Aggregatibacter actinomycetemcomitans local dan ATCC 43718 ( serotype B) pada tikus wistar

Aggregotibocteroctinomycetemcomitans(A.actinomycetemcomitans) merupakan bakteri patosen yang terlibat dalam periodontitis agresil. Rongga mulut merupakan habitat alami dari A.actinomycetemcomitans. Bakteri A.acrinomycetemcomitans serotipe b merupakan serotipe bakteri dominan yang ditemukan pada lesi lokal periodontitis agresif. Reaksi adaptif terjadi karena adanya respons imun humoral vang diperantarai oleh sel bakteri dan dirangsang oleh antigennva. Imunoglobulin mempunyai perjalanan pada host karena berpengaruh pada kondisi dan metabolisme bakteri, keadaan ini ditunjukkan dengan tingginya kadar slgA, IgG, IgM pada pasien dengan penyakit periodontal dibandingkan dengan pasien yang sehat. Tujuan: Untuk menentukan dan menganalisis kemungkinan heterogenitas dalam respons Imun terhadap bakteri A. actinomycetemcomitons, maka dilakukan penghitungan kadar antibodi IgA dan IgG. Metode: Tikus Wistar diimunisasi dengan A. octinomycetemcomitans isolat lokal dan ATCC 43718 (serotipe b). Tikus Wistar diimunisasl secara intraperitoneal dengan sel A.actinomycetemcomitans ISolat lokal dan ATCC 43718 (serotipe b) yang telah ditambahkan PBS dengan pH 7,2 dan diemulsikan menggunakan Freund adjuvant complete dan incomplete. Kadar serum IgA dan IgG terhadap A.actinomycelemcomitans diukur menggunakan EliSA. Hasil penelitian menunjukkan peningkatan kadar IgA dan IgG dalam serum pada tikus Wistar yang telah diinduksi dengan A.actinomycetemcomitans isolat lokal dan ATCC 43718 (serotipe b) dibandingkan dengan kelompok kontrol. Kesimpulan: A.actinomycetemcomitans isolat lokal dan ATCC 43718 (serotipe b) mempunyai peran penting dalam interaksi dengan sistim kekebalan tubuh dari host dan bakteri ini menyebabkan peningkatan kadar IgA dan IgG dalam serum tlkus Wistar. Kata kunci: Aggregotibacrer octinomycetemcomitans, isolat lokal, serotipe b, IgA, Ig

Sucrose, Lactose, and Xylitol Exposures Affect Biofilm Formation of Streptococcus mutans

Objective: To determine the level of biofilm formation of S. mutans after being exposed to 5% sucrose, 8% lactose, or 1% xylitol. Material and Methods: This research was a laboratory-based experimental study with post-test only control group design. S. mutans was grown in test tubes containing tryptose soy broth (TSB) medium supplemented with 1% glucose. They were incubated at 37° C for 24 hours to grow the biofilms. The culture was then exposed to 5% sucrose, 8% lactose or 1% xylitol, incubated for 24 hours at 37° C, and examined using ELISA at a wavelength of 625 nm. The statistical analysis was performed using a one-way analysis of variance followed by the least significant difference test (α=0.05). Results: There were some differences in the biofilm formation of S. mutans after exposure to 5% sucrose, 8% lactose, or 1% xylitol (p<0.05). An LSD test indicated significant differences among the biofilm formations after exposure to 5% sucrose and 8% lactose and between 5% sucrose and 1% xylitol. In comparison, there were no significant differences (p>0.05) between 8% lactose and 1% xylitol. Conclusion: Sucrose, lactose and xylitol can form biofilms and the formation of lactose biofilms is the same as xylitol

The activity of polyclonal IgY derived from Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis in inhibiting colonization of Fusobacterium nucleatum and Streptococcus sanguinis

Background: Fusobacterium nucleatum (F. nucleatum) and Streptococcus sanguinis (S. sanguinis) play a role in dental plaque formation which leads to periodontitis. Immunoglobulin Y (IgY) is present in both serum and egg yolk and can bind to the surface components of bacteria. F. nucleatum and S. sanguinis feature the same type of IV pili as Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). Saliva binding protein (SsaB) in S. sanguinis is a FimA homolog. FimA constitutes a surface element of Porphyromonas gingivalis (P. gingivalis). F. nucleatum and P. gingivalis possess the same outer membrane protein (OMP) molecular mass. Purpose: The study aimed to determine the activity of A. actinomycetemcomitans and P. gingivalis polyclonal IgY present in serum and egg yolk that can inhibit colonization of F. nucleatum and S. sanguinis. Methods: IgY samples were diluted with phosphate buffer saline (PBS). Several holes were made in the nutrient medium with 10 μl antigen (F. nucleatum/S. sanguinis) being inserted into the center hole. 10 μl PBS, 1:1, 1:2, 1:4, 1:8, 1:16 A. actinomycetemcomitans or P. gingivalis polyclonal IgY were subsequently introduced into the surrounding holes. The results of incubation at 37°C were observed after 24-48 hours. Kruskal Wallis and Mann-Whitney tests were administered to analyse the data. Results: A. actinomycetemcomitans and P. gingivalis polyclonal IgY groups in serum showed a precipitation line at dilution ratios of 1:1 and 1:2, whereas in egg yolk this occurred only at a 1:1 dilution ratio with F. nucleatum and S. sanguinis bacteria in this study. No significant differences were evident between each dilution (p>0.05) and none existed between serum and egg yolk (p>0.05). Conclusion: IgY polyclonal of A. actinomycetemcomitans and P. gingivalis in both serum and egg yolk initiate activities that can inhibit colonization of F. nucleatum and S. sanguinis

TERAPI PENGGANTIAN STRAIN SEBAGAI ALTERNATIF PENCEGAHAN KARIES GIGI

Dental caries is a unique multifactorial infectious disease. In recent years, the prevalence of dental caries in most western countries has steadily declined. By contrast study done in some developing countries such as Zambia, Nigeria, Thailand and Indonesia showed a marked increase in dental caries. Streptococcus mutans (S. mutans) is the most important agent of human caries. Cariogenic feature of these bacteria include synthesis intracellular polysaccharide, extracellular polysaccharide, lactic acid production and ability to survive in low pH levels. Potentially, caries can be reduced by interfering with transmission of S . mutans, eliminating established S. mutanspopulations from the oral cavity, increasing the acid resistance of the teeth and control and control of the carbohydrate composition of the diet. Oral anti mutans vaccines have been demonstrated in the laboratory, the costs involved in the development for human are relatively high. Studies Strain replacement therapy is a great promise in implantation of benign oral microbial strain capable of successfully competing with S. mutans