Commensal oral bacteria antigens prime human dendritic cells to induce Th1, Th2 or T<sub>reg</sub> differentiation

Kopitar, Andreja Nataša; Hren, Nataša Ihan; Ihan, Alojz

doi:10.1111/j.1399-302x.2005.00237.x

Cited by 38 publications

(40 citation statements)

References 23 publications

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“…In HC subjects the local micro-milieu characterized by this proinflammatory environment and microbiome-derived excess butyrate causes the FoxP3 epigenetic switch toward the more functional (and, therefore, more protective) FL isoform restoring the equilibrium between FoxP3 isoforms (10 [47,48]. The intestinal immune system is known to play an important role in establishing the tolerogenic environment to commensal bacteria [49], and the microbiome itself is fundamental in shaping the immune system [50,51]. We have previously reported the proof of concept that infants genetically predisposed to CD are characterized by increased production of lactate associated with enrichment in Lactobacilli spp.…”

Section: Regulation Of Foxp3 Isoforms In Coeliac Diseasementioning

confidence: 99%

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

Serena

Shu

Camhi

et al. 2017

Clinical and Experimental Immunology

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SummaryCoeliac disease (CD) is an autoimmune enteropathy triggered by gluten and characterized by a strong T helper type 1 (Th1)/Th17 immune response in the small intestine. Regulatory T cells (T reg ) are CD4 1 CD25 11 forkhead box protein 3 ( FoxP3 1 ) cells that regulate the immune response. Conversely to its counterpart, FoxP3 full length (FL), the alternatively spliced isoform FoxP3 D2, cannot properly down-regulate the Th17-driven immune response. As the active state of CD has been associated with impairments in T reg cell function, we aimed at determining whether imbalances between FoxP3 isoforms may be associated with the disease. Intestinal biopsies from patients with active CD showed increased expression of FOXP3 D2 isoform over FL, while both isoforms were expressed similarly in non-coeliac control subjects (HC). Conversely to what we saw in the intestine, peripheral blood mononuclear cells (PBMC) from HC subjects did not show the same balance between isoforms. We therefore hypothesized that the intestinal microenvironment may play a role in modulating alternative splicing. The proinflammatory intestinal microenvironment of active patients has been reported to be enriched in butyrate-producing bacteria, while high concentrations of lactate have been shown to characterize the preclinical stage of the disease. We show that the combination of interferon (IFN)-g and butyrate triggers the balance between FoxP3 isoforms in HC subjects, while the same does not occur in CD patients. Furthermore, we report that lactate increases both isoforms in CD patients. Collectively, these findings highlight the importance of the ratio between FoxP3 isoforms in CD and, for the first time, associate the alternative splicing process mechanistically with microbial-derived metabolites.

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Section: Regulation Of Foxp3 Isoforms In Coeliac Diseasementioning

confidence: 99%

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

Serena

Shu

Camhi

et al. 2017

Clinical and Experimental Immunology

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“…Kopitar et al stimulated Mo-DCs with different oral bacterial antigens (prepared from Streptococcus mitis, Propionibacterium acnes and Bacteroides spp.) and observed an enhanced expression of CD83, CD80 and HLA-DR compared with monocytes at the beginning of the experiment [16]. Cervi et al showed up-regulation of the surface expression of CD80 and MHC II in mice injected with P. acnes [17].…”

Section: Discussionmentioning

confidence: 97%

“…acnes on T cell functions [16,31]. This knowledge is important for better understanding of the immunopathology of acne vulgaris.…”

Section: Discussionmentioning

confidence: 99%

The effect of Propionibacterium acnes on maturation of dendritic cells derived from acne patients' peripherial blood mononuclear cells.

Michalak-Stoma

Tabarkiewicz²,

Olender³

et al. 2009

Folia Histochem Cytobiol.

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Propionibacterium acnes (P. acnes) has been implicated in the pathogenesis of acne vulgaris which is the most common cutaneous disorder. It has a proinflammatory activity and takes part in immune reactions modulating the Th1/Th2 cellular response. The exposure of dendritic cells (DCs) to whole bacteria, their components, cytokines or other inflammatory stimuli and infectious agents induces differentiation from immature DCs into antigen-presenting mature DCs. The aim of the study was to evaluate the capability of P. acnes to induce the maturation of DCs. We stimulated monocyte derived dendritic cells (Mo-DCs) from acne patients with various concetrations of heat-killed P. acnes (10 6 -10 8 bacteria/ml) cultured from acne lesions. The results showed an increase in CD80+/CD86+/DR+ and CD83+/CD1a+/DR+ cells percentage depending on the concetration of P. acnes. The expression of CD83 and CD80 (shown as the mean fluorescence intensity -MFI) increased with higher concetrations of P. acnes. There were also significant correlations between MFI of CD83, CD80, CD86 and concetration of P. acnes. The study showed that P. acnes in the concetration of 10 8 bacteria/ml is most effective in the induction of Mo-DCs maturation. Futher studies concerning the influence on the function of T cells are needed. Short communicationto whole bacteria, their components, cytokines or other inflammatory stimuli and infectious agents induces differentiation of immature DCs into antigen-presenting mature DCs. DCs maturation is a process where major histocompatibility complex (MHC) class I or II and costimulatory molecules (e.g. CD80 and CD86) are upregulated and at the same time specific markers like CD83 and p55 are expressed [5].The aim of the study was to evaluate the capability of P. acnes to induce the maturation of autologous DCs. Patients and methods

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“…Además, estos mayores niveles se asociaron a la presencia de P. gingivalis y A. actinomycetemcomitans en el biofilm subgingival local (64) . Se ha establecido que el perfil de citoquinas sintetizado en respuesta a las bacterias periodontales depende, al menos en parte, del número y del tipo de microorganismos que la desencadena (67)(68)(69)(70) . En este contexto, se ha propuesto que las bacterias podrían definir la polarización de la respuesta efectora Th y consecuentemente la secreción de un patrón de citoquinas bacteria-específico (71,72) .…”

Section: Discussionunclassified

Variabilidad de la síntesis de RANKL por linfocitos T frente a distintos serotipos capsulares de Porphyromonas gingivalis

Navarrete

Silva

Sanz

et al. 2010

Rev. Clin. Periodoncia Implantol. Rehabil. Oral

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RESUMENPropósito: Las periodontitis representan un grupo heterogéneo de infecciones periodontales cuya etiología son las bacterias residentes en el biofilm subgingival. Aunque este biofilm está constituido por una amplia variedad de especies bacterianas, sólo un número limitado de especies, como Porphyromonas gingivalis, se ha asociado a la etiología de la enfermedad. P. gingivalis expresa diversos factores de virulencia que pueden causar daño directo a los tejidos del hospedero; sin embargo, su mayor patogenicidad involucra la inducción de una respuesta inmuno-inflamatoria, durante la cual se secretan una amplia variedad de citoquinas, quimioquinas y mediadores inflamatorios que pueden inducir la destrucción de los tejidos de soporte de los dientes y la pérdida de ellos. Método: En esta investigación, se evaluó si los distintos serotipos capsulares (K) de P. gingivalis pueden determinar los niveles de síntesis de RANKL, citoquina clave en la destrucción del hueso alveolar durante la periodontitis. Para ello, se cuantificaron los niveles de expresión de RANKL mediante PCR cuantitativa y los niveles de secreción mediante ELISA en linfocitos T activados en presencia de los serotipos capsulares K1-K6 de P. gingivalis, y estos se correlacionaron a los niveles de expresión de los factores de transcripción asociados a cada uno de los fenotipos de linfocitos efectores: Th1 (T-bet), Th2 (GATA-3), Th17 (RORC2) y Treg (Foxp3). Resultados: Mayores niveles de expresión y secreción de RANKL fueron detectados en linfocitos T activados en presencia de los serotipos K1 y K2 de P. gingivalis, en comparación a los detectados ante los otros serotipos. Además, estos mayores niveles de RANKL se correlacionaron positivamente con los niveles de expresión de RORC2. Conclusión: Estos datos demuestran que la síntesis de RANKL por linfocitos T se restringe a ciertos serotipos capsulares de P. gingivalis (K1 y K2) y permiten sugerir que los serotipos K1 y K2 de P. gingivalis podrían asociarse a la destrucción del hueso alveolar y a la pérdida de los dientes durante la periodontitis. ABSTRACTAim: Periodontitis represents a heterogenic group of periodontal infections elicited by bacteria residing at the subgingival biofilm. Although this biofilm is constituted by a broad variety of bacterial species, only a limited number has been associated with the periodontitis aetiology, among them Porphyromonas gingivalis. P. gingivalis express a number of virulence factors that contribute to direct tissue damage; however, their pathogenicity relies mainly on the induction of a host immuno-inflammatory response. This leads to the release of a broad array of cytokines, chemokines and inflammatory mediators, which cause destruction of the tooth-supporting alveolar bone and ultimately tooth loss. Method: In the present investigation, in order to determine whether different P. gingivalis serotypes might lead to a differential RANKL synthesis, a key cytokine involved in alveolar bone resorption, the mRNA expression and secretion of RANKL and the expression ...

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Commensal oral bacteria antigens prime human dendritic cells to induce Th1, Th2 or T_reg differentiation

Cited by 38 publications

References 23 publications

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

The effect of Propionibacterium acnes on maturation of dendritic cells derived from acne patients' peripherial blood mononuclear cells.

Variabilidad de la síntesis de RANKL por linfocitos T frente a distintos serotipos capsulares de Porphyromonas gingivalis

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Commensal oral bacteria antigens prime human dendritic cells to induce Th1, Th2 or Treg differentiation

Cited by 38 publications

References 23 publications

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease

The effect of Propionibacterium acnes on maturation of dendritic cells derived from acne patients' peripherial blood mononuclear cells.

Variabilidad de la síntesis de RANKL por linfocitos T frente a distintos serotipos capsulares de Porphyromonas gingivalis

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Commensal oral bacteria antigens prime human dendritic cells to induce Th1, Th2 or T_reg differentiation