ILC1s and ILC3s Exhibit Inflammatory Phenotype in Periodontal Ligament of Periodontitis Patients

Li, Changyi; Liu, Jianyue; Pan, Jie; Wang, Yuhui; Shen, Lei; Xu, Yan

doi:10.3389/fimmu.2021.708678

Cited by 9 publications

(3 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both protective and deleterious roles of ILCs in diabetes have been emerging (Miani et al, 2018). Recently, it was reported that ILC3s are the predominant subset in the periodontal tissue of periodontitis in comparison with the healthy people (Li et al, 2021). And our data showed that periodontitis microbiota helped the ILC3s to overexpress in the small intestine and spleen and the intestinal IL22 from ILCs, which might be critical to promote inflammatory immune regulation in the progression of T1D.…”

Section: Discussionmentioning

confidence: 63%

Ectopic Colonization and Immune Landscapes of Periodontitis Microbiota in Germ-Free Mice With Streptozotocin-Induced Type 1 Diabetes Mellitus

Shen

Wei

et al. 2022

Front. Microbiol.

View full text Add to dashboard Cite

A two-way relationship between diabetes and periodontitis has been discussed recently. Periodontitis microbiota might affect the immune homeostasis of diabetes, but the molecular mechanism of their interactions is still not clear. The aims of this study were to clarify the possible immune regulatory effects of periodontitis microbiota on diabetes and the correlation between immunomodulation and ectopic colonization. A model of germ-free mice with streptozotocin-induced type 1 diabetes mellitus (T1D), which was orally inoculated with mixed saliva samples for 2 weeks, was used in this study. Those mice were randomly divided into two groups, namely, SP (where the T1D mice were orally inoculated with mixed saliva samples from periodontitis patients) and SH (where the T1D mice were orally inoculated with mixed saliva samples from healthy subjects). Ectopic colonization of saliva microbiota was assessed using culture-dependent method and Sanger sequencing, and the composition of gut microbiota was analyzed using 16S rRNA gene sequencing. Changes in 15 types of immune cells and six cytokines either from the small intestine or spleen were detected by multicolor flow cytometry. The correlation between gut microbiota and immune cells was evaluated by redundancy analysis. Although periodontitis microbiota minorly colonized the lungs, spleens, and blood system, they predominantly colonized the gut, which was mainly invaded by Klebsiella. SH and SP differed in beta diversity of the gut bacterial community. Compared to SH, microbial alteration in small intestine occurred with an increase of Lacticaseibacillus, Bacillus, Agathobacter, Bacteroides, and a decrease of Raoultella in SP. More types of immune cells were disordered in the spleen than in the small intestine by periodontitis microbiota, mainly with a dramatical increase in the proportion of macrophages, plasmacytoid dendritic cells (pDCs), monocytes, group 3 innate lymphoid cells, CD4-CD8- T cells and Th17 cells, as well as a decline of αβT cells in SP. Cytokines of IFNγ, IL17, and IL22 produced by CD4 + T cells as well as IL22 produced by ILCs of small intestine rose in numbers, and the intestinal and splenic pDCs were positively regulated by gut bacterial community in SP. In conclusion, periodontitis microbiota invasion leads to ectopic colonization of the extra-oral sites and immune cells infiltration, which might cause local or systemic inflammation. Those cells are considered to act as a “bridge” between T1D and periodontitis.

show abstract

Section: Discussionmentioning

confidence: 63%

Ectopic Colonization and Immune Landscapes of Periodontitis Microbiota in Germ-Free Mice With Streptozotocin-Induced Type 1 Diabetes Mellitus

Shen

Wei

et al. 2022

Front. Microbiol.

View full text Add to dashboard Cite

show abstract

“…ILC3s are regulated by cytokines, which are produced by mononuclear phagocytes or triggered by intestinal microbiota [ 27 ]. ILC3s are also the predominant subset in the periodontal tissue of periodontitis, and they were activated by producing more IL-17A and IFN-γ in comparison with the healthy ones [ 28 ]. In our study, ILC3s were increased by F. nucleatum , thus we speculated that ILC3s might participate in the progression of periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Immune Responses Regulated by Key Periodontal Bacteria in Germ-Free Mice

Shen

Yang

et al. 2022

Pathogens

View full text Add to dashboard Cite

The immune dysregulation induced by periodontal bacteria has important roles in the development of periodontitis. However, the role of key periodontal bacteria in local and systemic immunity has not been comprehensively studied. Herein, to explore immunoregulation maps of key periodontal bacteria, a mono-colonized germ-free mice model with P. gingivalis, F. nucleatum, and T. denticola for two weeks was designed in this study. The alveolar bone loss was determined by micro-CT. A total of 14 types of innate and adaptive immune cells of the gingiva, spleen, and colon were detected by multi-color flow cytometry. P. gingivalis induced the strongest innate immune response in gingiva and mononuclear phagocytes (MNPs) changed most significantly, compared to F. nucleatum and T. denticola. Immune dysregulation of the colon was widely induced by F. nucleatum. T. denticola mainly induced immune disorder in spleen. ILC3s, Tregs, CD11B+ dendritic cells s, MNPs, macrophages, and plasmacytoid dendritic cells were the main types in response to key periodontal bacteria. However, the alveolar bone loss was not induced by key periodontal bacteria. In conclusion, the overall immunoregulation of monomicrobial stimuli to decipher the complexities of periodontitis was provided in this study. P. gingivalis, F. nucleatum, and T. denticola have different effects on local and systemic immunity in gingiva, colon, and spleen of germ-free mice.

show abstract

“…ILC1s are a heterogeneous mixed-cell population, a class of helper ILC1 (also known as tissue-resident ILC1), characterized as lin − CD127 + CD117 − CRTH2 − NKp44 − , with the ability to express T-bet and produce TNF-α and IFN-γ. It has been determined that human gingival tissue is dominated by the ILC1 subgroup [ 65 ], with the largest number of ILC1s in the periodontium and gingiva (approximately 50% of total ILC1s) [ 66 ]. In addition, a small subset of RANKL-expressing ILC1s was also found, which may play an immune regulatory role in gingivitis and periodontitis lesions [ 65 ].…”

Section: Ilcs In Periodontal Homeostasismentioning

confidence: 99%

Function of Innate Lymphoid Cells in Periodontal Tissue Homeostasis: A Narrative Review

Wang

2023

IJMS

View full text Add to dashboard Cite

Periodontitis is an irreversible inflammatory response that occurs in periodontal tissues. Given the size and diversity of natural flora in the oral mucosa, host immunity must strike a balance between pathogen identification and a complicated system of tolerance. The innate immune system, which includes innate lymphoid cells (ILCs), certainly plays a crucial role in regulating this homeostasis because pathogens are quickly recognized and responded to. ILCs are a recently discovered category of tissue-resident lymphocytes that lack adaptive antigen receptors. ILCs are found in both lymphoid and non-lymphoid organs and are particularly prevalent at mucosal barrier surfaces, where they control inflammatory response and homeostasis. Recent studies have shown that ILCs are important players in periodontitis; however, the mechanisms that govern the innate immune response in periodontitis still require further investigation. This review focuses on the intricate crosstalk between ILCs and the microenvironment in periodontal tissue homeostasis, with the purpose of regulating or improving immune responses in periodontitis prevention and therapy.

show abstract

ILC1s and ILC3s Exhibit Inflammatory Phenotype in Periodontal Ligament of Periodontitis Patients

Cited by 9 publications

References 36 publications

Ectopic Colonization and Immune Landscapes of Periodontitis Microbiota in Germ-Free Mice With Streptozotocin-Induced Type 1 Diabetes Mellitus

Ectopic Colonization and Immune Landscapes of Periodontitis Microbiota in Germ-Free Mice With Streptozotocin-Induced Type 1 Diabetes Mellitus

Immune Responses Regulated by Key Periodontal Bacteria in Germ-Free Mice

Function of Innate Lymphoid Cells in Periodontal Tissue Homeostasis: A Narrative Review

Contact Info

Product

Resources

About