Effect of periodontal treatment on <i>Aggregatibacter actinomycetemcomitans </i>colonization and serum IgG levels against <i>A. actinomycetemcomitans </i>serotypes and Omp29 of aggressive periodontitis patients

Rebeis, Estela Sanches; Albuquerque‐Souza, Emmanuel; Silva, Maike Paulino da; Giudicissi, Marcela; Mayer, Márcia Pinto Alves; Saraiva, Luciana

doi:10.1111/odi.13010

Cited by 13 publications

(16 citation statements)

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“…Moreover, it has been previously underlined the characteristics of A. actinomycetemcomitans IgG titers in the influence the inflammatory response, have previously been underlined and may interfere on the systemic release of hs-CRP [ 51 – 53 ]. On another hand, the association between A. actinomycetemcomitans IgG antibodies, hs-CRP and PT could be explained by a strong influence exerted by PT on systemic inflammation, which could determine a further release of hs-CRP systemically [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Association among serum and salivary A. actinomycetemcomitans specific immunoglobulin antibodies and periodontitis

et al. 2020

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Background The aim of this study was to assess the association between serum and salivary Immunoglobulin (Ig) Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) specific antibodies in healthy controls (HC) and periodontitis (PT) patients. Furthermore, the objectives were to determine whether PT influenced serum A. actinomycetemcomitans specific antibodies and whether serum or salivary antibodies against A. actinomycetemcomitans IgG were mediated by serum high-sensitivity c-reactive protein (hs-CRP). Methods Fifty-three patients with periodontitis and 48 HC were enrolled in the present study. Patients were regularly examined and characterized by clinical, salivary and blood samples analyses. A. actinomycetemcomitans IgA and IgG antibodies and hs-CRP were evaluated using a commercially available kit. The Spearman Correlation Test and Jonckheere-Terpstra Test were applied in order to assess the interdependence between serum A. actinomycetemcomitans IgG antibodies and clinical periodontal parameters. To evaluate the dependence of the serum and salivary A. actinomycetemcomitans IgG levels from possible confounders, univariate and multivariable linear regression analyses were performed. Results Compared to HC, patients with PT had significantly higher IgA [serum: PT, 1.89 (1.2–2.2) EU vs HC, 1.37 (0.9–1.8) EU (p = 0.022); saliva: PT, 1.67 (1.4–2.1) EU vs HC, 1.42 (0.9–1.6) EU (p = 0.019)] and A. actinomycetemcomitans IgG levels [serum: PT, 2.96 (2.1–3.7) EU vs HC, 2.18 (1.8–2.1) EU (p < 0.001); saliva, PT, 2.19 (1.8–2.5) EU vs HC, 1.84 (1.4–2) EU (p = 0.028)]. In PT patients, serum A. actinomycetemcomitans IgG were associated with a proportional extent of PT and tooth loss (P-trend value< 0.001). The univariate regression analysis demonstrated that PT (p = 0.013) and high hs-CRP (p < 0.001) had a significant negative effect on serum and salivary A. actinomycetemcomitans IgG levels. The multivariate regression analysis showed that PT (p = 0.033), hs-CRP (p = 0.014) and BMI (p = 0.017) were significant negative predictors of serum A. actinomycetemcomitans IgG while hs-CRP (p < 0.001) and BMI (P = 0.025) were significant negative predictors of salivary A. actinomycetemcomitans IgG. Conclusions PT patients presented a significantly higher serum and salivary A. actinomycetemcomitans IgA and IgG compared to HC. There was a significant increase in serum A. actinomycetemcomitans IgG when patients presented a progressive extent of PT. Moreover, PT and hs-CRP were significant negative predictors of increased salivary and serum A. actinomycetemcomitans IgG levels. Trial registration The study was retrospectively registered at clinicaltrials.gov (NCT04417322).

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Section: Discussionmentioning

confidence: 99%

Association among serum and salivary A. actinomycetemcomitans specific immunoglobulin antibodies and periodontitis

et al. 2020

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“…The membrane was blocked with 5% skimmed milk in TBS-T (20 mM Tris-HCl pH 7.6, 0.8% NaCl and 0.1% Tween 20). Anti-OMP29 His polyclonal serum obtained in Balb/c mice and serum of aggressive periodontitis patients colonized by Aa [15] were used as primary antibodies at 1:2,000 dilution in separate membranes. Secondary antibodies consisted of goat anti-mice IgG peroxidase conjugated (Amershan Bioscience, Amershan, Little Chalfont, United Kingdom) or goat anti-human IgG peroxidase conjugated (ThermoFisher, Carlsbad, CA, United States) diluted to 1:10,000.…”

Section: Immunoblottingmentioning

confidence: 99%

“…The OMP29 belongs to the OMPA-like family and it is one of the six major OMPs recognized by antibodies in the serum of patients with periodontitis [14]. Furthermore, immunoglobulin G (IgG) titers against OMP29 and Aa serotypes b and c are reduced after successful periodontal treatment in aggressive periodontitis patients [15].…”

Section: Introductionmentioning

confidence: 99%

Aggregatibacter actinomycetemcomitans Outer Membrane Proteins 29 and 29 Paralogue Induce Evasion of Immune Response

Silva

Pasetto

et al. 2022

Front. Oral. Health

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Aggregatibacter actinomycetemcomitans (Aa) is abundant within the microbial dysbiotic community of some patients with periodontitis. Aa outer membrane protein 29 (OMP29), a member of the OMPA family, mediates the invasion of Aa to gingival epithelial cells (GECs). This study evaluated the effect of OMP29 and its paralogue OMP29par on the response of GECs to Aa. The omp29 or/and omp29par deletion mutants AaΔ29, AaΔ29P, and AaΔ29Δ29P were constructed, and recombinant Aa OMP29His was obtained. Microarray analysis and the evaluation of cxcl-8 gene expression were performed to examine the response of GECs line OBA-09 to Aa and its mutants. The expression of cxcl-8 and its product CXCL-8 was examined in LPS-stimulated OBA-09 cells with Aa OMP29His. Proteomics analysis showed that the deletion of omp29 led to overexpression of both OMP29par and another membrane protein OMP39, the expression of which was further increased in AaΔ29Δ29P. OBA-09 cells challenged with AaΔ29Δ29P exhibited a higher expression of cxcl-8 in comparison to wildtype Aa strain AaD7S or single-deletion mutants AaΔ29 or AaΔ29P. LPS-stimulated OBA-09 cells challenged with Aa OMP29His showed reduced expressions of cxcl-8 and its product CXCL-8. OBA-09 cells challenged with AaΔ29Δ29P in comparison to Aa strain AaD7S resulted in higher expressions of genes involved in apoptosis and inflammatory response such as bcl2, birc3, casp3, c3, ep300, fas, fosb, grb2, il-1α, il-1β, il-6, cxcl-8, nr3c1, prkcq, socs3, and tnfrsf1β and reduced expressions of cd74, crp, faslg, tlr1, and vcam1. The results suggested a novel strategy of Aa, mediated by OMP29 and OMP29par, to evade host immune response by inhibiting CXCL-8 expression and modulating the genes involved in apoptosis and inflammatory response in GECs. Pending further confirmation, the strategy might interfere with the recruitment of neutrophils and dampen the host inflammatory response, leading to a more permissive subgingival niche for bacterial growth.

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“…actinomycetemcomitans in deep periodontal sites, with the concomitant reduction in levels of commensal bacteria (Amado et al., 2020). Furthermore, periodontal therapy leads to reduction in its abundance in periodontitis sites and in serum antibodies levels against its outer membrane protein OMP29 (Rebeis et al., 2019).…”

Section: Introductionmentioning

confidence: 99%

Lactobacilli postbiotics reduce biofilm formation and alter transcription of virulence genes of Aggregatibacter actinomycetemcomitans

Ishikawa

Bueno

Kawamoto

et al. 2021

Molecular Oral Microbiology

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Periodontitis is characterized by a dysbiotic microbial community and treatment strategies include the reestablishment of symbiosis by reducing pathogens abundance. Aggregatibacter actinomycetemcomitans (Aa) is frequently associated with rapidly progressing periodontitis. Since the oral ecosystem may be affected by metabolic end‐products of bacteria, we evaluated the effect of soluble compounds released by probiotic lactobacilli, known as postbiotics, on Aa biofilm and expression of virulence‐associated genes. Cell‐free pH‐neutralized supernatants (CFS) of Lactobacillus rhamnosus Lr32, L. rhamnosus HN001, Lactobacillus acidophilus LA5, and L. acidophilus NCFM were tested against a fimbriated clinical isolate of Aa JP2 genotype (1 × 107 CFU/well) on biofilm formation for 24 hr, and early and mature preformed biofilms (2 and 24 hr). Lactobacilli CFS partially reduced Aa viable counts and biofilms biomass, but did not affect the number of viable non‐adherent bacteria, except for LA5 CFS. Furthermore, LA5 CFS and, in a lesser extent HN001 CFS, influenced Aa preformed biofilms. Lactobacilli postbiotics altered expression profile of Aa in a strain‐specific fashion. Transcription of cytolethal distending toxin (cdtB) and leukotoxin (ltxA) was downregulated by CFS of LA5 and LR32 CFS. Although all probiotics produced detectable peroxide, transcription of katA was downregulated by lactobacilli CFS. Transcription of dspB was abrogated by LR32 and NCFM CFS, but increased by HN001, whereas expression of pgA was not affected by any postbiotic. Our data indicated the potential of postbiotics from lactobacilli, especially LA5, to reduce colonization levels of Aa and to modulate the expression of virulence factors implicated in evasion of host defenses.

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Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients

Cited by 13 publications

References 57 publications

Association among serum and salivary A. actinomycetemcomitans specific immunoglobulin antibodies and periodontitis

Association among serum and salivary A. actinomycetemcomitans specific immunoglobulin antibodies and periodontitis

Aggregatibacter actinomycetemcomitans Outer Membrane Proteins 29 and 29 Paralogue Induce Evasion of Immune Response

Lactobacilli postbiotics reduce biofilm formation and alter transcription of virulence genes of Aggregatibacter actinomycetemcomitans

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