Oral Microbiota from Periodontitis Promote Oral Squamous Cell Carcinoma Development via γδ T Cell Activation

Wei, Wei; Li, Jia; Shen, Xin; Lyu, Jinglu; Yan, Caixia; Tang, Boyu; Ma, Wenjuan; Xie, Huixu; Жао, Леи; Cheng, Lei; Deng, Ye; Li, Yan

doi:10.1128/msystems.00469-22

Cited by 13 publications

(17 citation statements)

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“…In lung tissue, IL 17 expressed by activated γδ T cells could induce macrophage proliferation and M2 polarization, thus further affect disease progression ( 30 , 38 , 39 ). This procedure had been demonstrated in both pulmonary inflammation and lung fibrosis ( 38 , 39 ) as well as in OSCC with periodontitis models ( 35 ). Therefore, does such an immune regulatory mechanism also exist in the COPD disease model and can periodontitis further promote COPD progression by regulating this mechanism?…”

Section: Discussionmentioning

confidence: 99%

“…For the bacteria-cell co-culture experiments, the bacteria were centrifuged and resuspended in 10% fetal bovine serum (FBS) containing DMEM. The bacteria were then co-cultured with cells at a multiplicity of infection (MOI) of 100 ( 35 , 73 ).…”

Section: Methodsmentioning

confidence: 99%

“…The correlation between M2 polarization and COPD is controversial, and the mechanism of M2 polarization in periodontitis-promoted COPD remains unclear and needs further study. Through chemokines, cytokines, and cell surface receptors, γδ T cells and macrophages may undergo some inter-regulation ( 35 – 37 ). IL 17 and IFN γ produced by γδ T cells can play an inflammatory role; meanwhile, IL 17 can also promote the M2 polarization of lung macrophages ( 38 , 39 ).…”

Section: Introductionmentioning

confidence: 99%

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Periodontitis aggravates COPD through the activation of γδ T cell and M2 macrophage

Xiong,

Ao,

Wei

et al. 2024

mSystems

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Chronic obstructive pulmonary disease (COPD) is a chronic systemic inflammatory disease with high morbidity and mortality. Periodontitis exacerbates COPD progression; however, the immune mechanisms by which periodontitis affects COPD remain unclear. Here, by constructing periodontitis and COPD mouse models, we demonstrated that periodontitis and COPD could mutually aggravate disease progression. For the first time, we found that the progression was associated with the activation of γδ T cells and M2 macrophages, and M2 polarization of macrophages was affected by γδ T cells activation. In the lung tissues of COPD with periodontitis, the activation of γδ T cells finally led to the increase of IL 17 and IFN γ expression and M2 macrophage polarization. Furthermore, we found that the periodontitis-associated bacteria Porphyromonas gingivalis ( P. gingivalis ) promoted the activation of γδ T cells and M2 macrophages ex vivo . The data from clinical bronchoalveolar lavage fluid (BALF) samples were consistent with the in vivo and ex vivo experiments. For the first time, our results identified the crucial role of γδ T-M2 immune mechanism in mediating periodontitis-promoted COPD progression. Therefore, targeting at periodontitis treatment and the γδ T-M2 immune mechanism might provide a new practical strategy for COPD prevention or control. IMPORTANCE Periodontitis exacerbates chronic obstructive pulmonary disease (COPD) progression. For the first time, the current study identified that the impact of periodontitis on COPD progression was associated with the activation of γδ T cells and M2 macrophages and that M2 polarization of macrophages was affected by γδ T cells activation. The results indicated that targeting at periodontitis treatment and the γδ T-M2 immune mechanism might provide a new practical strategy for COPD prevention or control.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Periodontitis aggravates COPD through the activation of γδ T cell and M2 macrophage

Xiong,

Ao,

Wei

et al. 2024

mSystems

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“…A recent study revealed that C. albicans promoted OSCC development via the IL-17A/IL-17RA-macrophage axis, and the tumor-associated macrophages (TAMs) attracted by C. albicans infection polarized into the M2 phenotype with high expression of PD-L1 [ 11 ]. Another study demonstrated that periodontitis-associated oral microbiota could activate IL-17-positive δγ T cells and promote OSCC development and that activated δγT cells were necessary for the IL-17/signal transducer and promoted M2 macrophage infiltration in OSCC proliferation [ 21 ]. Researchers have reported that Prevotella activates TLR2, leading to the production of Th17-polarizing cytokines, including IL-23 and IL-1.…”

Section: Discussionmentioning

confidence: 99%

Heat-killed Prevotella intermedia promotes the progression of oral squamous cell carcinoma by inhibiting the expression of tumor suppressors and affecting the tumor microenvironment

Zhou,

Qin,

et al. 2024

Exp Hematol Oncol

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Background Oral microbial dysbiosis contributes to the development of oral squamous cell carcinoma (OSCC). Our previous study showed that Prevotella intermedia (P. intermedia) were enriched in the oral mucosal surface, plaque, and saliva of patients with OSCC. Intratumoral microbiome could reshape the immune system and influence the development of various tumors. However, the invasion status of human OSCC tissues by P. intermedia and the pathway through which intratumoral P. intermedia potentiates tumor progression remain unexplored. Methods P. intermedia in human OSCC or normal tissues was detected by FISH. A mouse OSCC cell line SCC7 was adopted to investigate the effects of heat-killed P. intermedia treatment on cell proliferation, invasion, and cytokine release by using CCK-8 assay, transwell invasion assay and ELISA. Moreover, we established a mouse transplanted tumor model by using SCC7 cells, injected heat-killed P. intermedia into tumor tissues, and investigated the effects of heat-killed P. intermedia on tumor growth, invasion, cytokine levels, immune cell infiltrations, and expression levels by using gross observation, H&E staining, ELISA, immunohistochemistry, mRNA sequencing, and transcriptomic analysis. Results Our results indicated that P. intermedia were abundant in OSCC and surrounding muscle tissues. Heat-killed P. intermedia promoted SCC7 cell proliferation, invasion and proinflammatory cytokine secretions, accelerated transplanted tumor growth in mice, exacerbate muscle and perineural invasion of OSCC, elevated the serum levels of IL-17A, IL-6, TNF-α, IFN-γ, and PD-L1, induced Treg cells M2 type macrophages in mouse transplanted tumors. The data of transcriptomic analysis revealed that heat-killed P. intermedia increased the expression levels of inflammatory cytokines and chemokines while reduced the expression levels of some tumor suppressor genes in mouse transplanted tumors. Additionally, IL-17 signaling pathway was upregulated whereas GABAergic system was downregulated by heat-killed P. intermedia treatment. Conclusions Taken together, our results suggest that P. intermedia could inhibit the expression of tumor suppressors, alter the tumor microenvironment, and promote the progression of OSCC.

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“…However, the neutralisation of γδT cells further boosted the overgrowth of Ascomycota in the gut. It is worth mentioning that microbiota-related IL-17A producing γδT cells were reported to promote OC and colorectal cancers (Reis et al 2022 ; Wei et al 2022 ). That’s to say, γδT cells may be important parts in maintaining microbial homoeostasis, the abnormality of which may promote cancer development.…”

Section: Discussionmentioning

confidence: 99%

Candida albicans overgrowth disrupts the gut microbiota in mice bearing oral cancer

Wang,

Wu,

et al. 2023

Mycology

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Candida albicans is one of the most common opportunistic fungi in cancer patients. This study explored the influence of C. albicans on gut microbiota in oral tumour-bearing mice by means of 16S rRNA sequencing and ITS sequencing. It was found that C. albicans infection induced the decrease of alpha diversity of bacteria and fungi in the gut microbiome. For the bacteria, C. albicans caused the reduction of Ralstonia , Alistipes , Clostridia UCG-014 , Ruminococcus , and Lachnospiraceae NK4A136 group . For the fungi, C. albicans inhibited the growth of other fungi including Aspergillus , Cladosporium , and Bipolaris . The neutralisation of γδT cells partly alleviated the out-of-balance of Firmicutes / Bacteroidota (F/B) ratio in the gut caused by C. albicans infection. However, γδT cell neutralisation boosted the overgrowth of C. albicans . Additionally, IL-17A neutralisation aggravated the microbial dysbiosis of bacteria and fungi caused by C. albicans infection. Further analysis indicated that C. albicans overgrowth might influence the correlations between fungal and bacterial kingdoms. In conclusion, C. albicans infection disturbed the gut microbiota of both bacteria and fungi in oral tumour-bearing mice, which may be associated with the intestinal immune components including γδT cells and IL-17A.

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Oral Microbiota from Periodontitis Promote Oral Squamous Cell Carcinoma Development via γδ T Cell Activation

Cited by 13 publications

References 50 publications

Periodontitis aggravates COPD through the activation of γδ T cell and M2 macrophage

Periodontitis aggravates COPD through the activation of γδ T cell and M2 macrophage

Heat-killed Prevotella intermedia promotes the progression of oral squamous cell carcinoma by inhibiting the expression of tumor suppressors and affecting the tumor microenvironment

Candida albicans overgrowth disrupts the gut microbiota in mice bearing oral cancer

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