Activation of <scp>RANKL</scp>‐induced osteoclasts and memory T lymphocytes by <i>Porphyromonas gingivalis</i> is serotype dependant

Vernal, Rolando; Díaz‐Zúñiga, Jaime; Melgar‐Rodríguez, Samanta; Pujol, Myriam; Díaz-Guerra, Eva; Silva, Augusto; Sanz, Mariano; García‐Sanz, Jose A.

doi:10.1111/jcpe.12236

Cited by 37 publications

(46 citation statements)

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“…It has been shown that Trm cells produce IFN‐γ and that high expression of IFN‐γ is responsible for inflammatory bone loss . A higher frequency of CD4 memory T cells reactive to serotypes K1 and K2 of Porphyromonas gingivalis was detected in periodontitis tissue compared with healthy gingiva, suggesting a role of memory cells in the recurrence of periodontitis …”

Section: Discussionmentioning

confidence: 99%

Resident memory T cells: Possible players in periodontal disease recurrence

Deli

Romano

Gualini

et al. 2019

J of Periodontal Research

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Background/objectives Tissue‐resident memory T cells (Trm) represent a new subset of long‐lived memory T cells that remain in barrier tissues after previous bacterial or viral infection to support early/immediate defense mechanisms, providing site‐specific protection from pathogen challenge. As data on Trm cells in human gingiva are just emerging, the aim of the present study was to explore their presence and distribution in epithelial and connective periodontal tissues in relation to microbial exposure and periodontal damage. Material and methods Periodontitis tissue specimens were collected from 20 generalized chronic periodontitis patients at the time of osseous resective surgery. As a control, 18 healthy tissue specimens were harvested each from both the primary flap and the palatal graft in 18 periodontally healthy patients during mucogingival surgeries. As CD69 and CD103 are phenotypic markers associated with tissue residence, intraepithelial and stromal CD103+ and CD69+ cells per high‐power field were counted in areas with highest expression. Double immunohistochemistry for CD3 and CD69 was performed to identify T cells. Results CD69 +and CD103+ cells showed a lymphocytic morphology, and double CD69 and CD3 staining confirmed the T cell phenotype of these cells. CD103 and CD69 expression was significantly enhanced in epithelial and connective tissues from patients with periodontitis compared with healthy controls (P < .001). Significant positive correlation between PD and both CD103 and CD69 epithelial expression was observed in tissue specimens from periodontitis patients (P < .001). Conclusion Within the limits of the present study, these results indicate that Trm cells are higher in periodontitis lesions. They could orchestrate the host response to microbial challenge, leading to a faster reactivation of periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Resident memory T cells: Possible players in periodontal disease recurrence

Deli

Romano

Gualini

et al. 2019

J of Periodontal Research

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“…Bacterial encapsulation has long been recognized as a way to protect microorganisms from clearance by host immune defenses, by reducing the ability of immune cells to gain access to the bacteria, which leads to withstand bacterial phagocytosis. Encapsulation, however, also has a direct effect on eliciting host adaptive immune response through activation of effector Th1 and Th17 lymphocytes . In this context, this study sought to clarify whether capsular deficiency in P. gingivalis moderates the Th1‐ and Th17‐pattern of immune response during periodontitis and whether this immune attenuation is associated with less alveolar bone resorption.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that capsule of the P. gingivalis W50 strain, belonging to the K1 serotype, is composed of mannuronic acid, glucuronic acid, galacturonic acid, galactose, and N‐acetylglucosamine, composition that differs from that of the other capsular serotypes . Thus, genetic variations in the capsular polysaccharide loci, which could be reflected in the differences in capsular sugar composition and structure, might be associated to differential immunostimulatory capacity between the different capsular serotypes and between the capsulated and non‐encapsulated strains of P. gingivalis , as it has been described in dendritic cells and T lymphocytes and also reported in the present investigation.…”

Section: Discussionmentioning

confidence: 99%

“…The capsule of all serotypes has been analyzed for the induction of immune response in macrophages, dendritic cells, and T lymphocytes, and it has been demonstrated that the capsule of the K1 serotype induces a higher Th1‐ and Th17‐pattern of immune response compared with the other serotypes . In addition, the encapsulated serotype K1 of P. gingivalis triggers a strong RANKL‐induced osteoclast differentiation and activity in vitro, and this increment was significantly higher than that induced by the other capsulated serotypes …”

Section: Introductionmentioning

confidence: 99%

“…[11][12][13] In addition, the encapsulated serotype K1 of P. gingivalis triggers a strong RANKL-induced osteoclast differentiation and activity in vitro, and this increment was significantly higher than that induced by the other capsulated serotypes. 14 Identification and characterization of the capsular polysaccharide (K-antigen) locus of P. gingivalis allowed the generation of strain W50 (serotype K1)-based isogenic capsular-deficient mutants. 15 The analysis of such mutants has shown that encapsulation deregulates the production of proinflammatory cytokines by fibroblasts and macrophages, 16,17 thus further demonstrating that encapsulation is a hallmark of virulence heterogeneity of P. gingivalis.…”

Section: Introductionmentioning

confidence: 99%

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Capsular‐defective Porphyromonas gingivalis mutant strains induce less alveolar bone resorption than W50 wild‐type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

Monasterio

Fernández

Castillo

et al. 2018

Journal of Periodontology

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Background Encapsulation of Porphyromonas gingivalis has been demonstrated as responsible of several host immunological changes, which have been associated with the pathogenesis of periodontitis. Using a murine model of periodontitis and two isogenic non‐capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar bone resorption, and whether this bone loss is associated with a T‐helper (Th)1 and Th17‐pattern of immune response. Methods Experimental periodontal infections were generated by oral inoculation with the encapsulated W50 wild‐type strain or isogenic non‐encapsulated ΔPG0116‐PG0120 (GPA) and ΔPG0109‐PG0118 (GPC) mutants of P. gingivalis. Periodontal infections induced with the encapsulated HG184 or non‐encapsulated ATCC 33277 strains of P. gingivalis were used as controls. Alveolar bone resorption was analyzed using microcomputed tomography and scanning electron microscopy. The expression levels of Th1, Th2, Th17, or T regulatory‐associated cytokines and RANKL, as well as the periodontal bacterial load, were quantified by quantitative polymerase chain reaction. The detection of Th1 and Th17 lymphocytes was analyzed by flow cytometry. Results In the periodontal lesions, both capsular‐defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild‐type strain. This decreased bone loss was associated with a dismissed RANKL expression, decreased Th1‐ and Th17‐type of cytokine expression, reduced Th1 and Th17 lymphocyte detection, and low osteoclast finding. Conclusion These data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this bone loss is associated with a Th1‐ and Th17‐pattern of immune response triggered in the periodontal lesions.

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The balance between helper T 17 and regulatory T cells in osteoimmunology and relevant research progress on bone tissue engineering

Zhu,

Zhou,

Xie

2024

Immunity Inflam & Disease

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BackgroundBone regeneration is a well‐regulated dynamic process, of which the prominent role of the immune system on bone homeostasis is more and more revealed by recent research. Before fully activation of the bone remodeling cells, the immune system needs to clean up the microenvironment in facilitating the bone repair initiation. Furthermore, this microenvironment must be maintained properly by various mechanisms over the entire bone regeneration process.ObjectiveThis review aims to summarize the role of the T‐helper 17/Regulatory T cell (Th17/Treg) balance in bone cell remodeling and discuss the relevant progress in bone tissue engineering.ResultsThe role of the immune response in the early stages of bone regeneration is crucial, especially the impact of the Th17/Treg balance on osteoclasts, mesenchymal stem cells (MSCs), and osteoblasts activity. By virtue of these knowledge advancements, innovative approaches in bone tissue engineering, such as nano‐structures, hydrogel, and exosomes, are designed to influence the Th17/Treg balance and thereby augment bone repair and regeneration.ConclusionTargeting the Th17/Treg balance is a promising innovative strategy for developing new treatments to enhance bone regeneration, thus offering potential breakthroughs in bone injury clinics.

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Activation of RANKL‐induced osteoclasts and memory T lymphocytes by Porphyromonas gingivalis is serotype dependant

Cited by 37 publications

References 59 publications

Resident memory T cells: Possible players in periodontal disease recurrence

Resident memory T cells: Possible players in periodontal disease recurrence

Capsular‐defective Porphyromonas gingivalis mutant strains induce less alveolar bone resorption than W50 wild‐type strain due to a decreased Th1/Th17 immune response and less osteoclast activity

The balance between helper T 17 and regulatory T cells in osteoimmunology and relevant research progress on bone tissue engineering

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