Human periodontitis-associated salivary microbiome affects the immune response of diabetic mice

He, Jinzhi; Shen, Xin; Fu, Di; Yang, Yutao; Xiong, Kaixin; Zhao, Lei; Xie, Huixu; Pelekos, Georege; Li, Yan

doi:10.1080/20002297.2022.2107814

Cited by 6 publications

(4 citation statements)

References 47 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ILC3s are involved in inflammatory bone diseases. Transfer of human periodontitis saliva to diabetic mice impairs IL17 production by ILC3s and increases osteoclasts and TNF‐α and IL‐1β levels [54] (Fig. 2D).…”

Section: Crosstalk Between Ilcs and Bone Cellsmentioning

confidence: 99%

Innate lymphoid cells: New players in osteoimmunology

Wu,

Lin,

Yuan

et al. 2024

Eur J Immunol

View full text Add to dashboard Cite

Innate lymphoid cells (ILCs) are the most recently identified immune cell types existing in lymphoid and nonlymphoid organs. Albeit they lack the expression of antigen receptors, ILCs play vital roles in innate immune responses by producing multiple effector cytokines. The ILC family includes conventional natural killer cells and cytokine‐producing ILCs, which are divided into group 1, group 2, and group 3 ILCs based on their effector cytokines and developmental requirements. Emerging evidence has indicated that ILCs are essential immune regulators of bone homeostasis, playing a critical role in osteoimmunology. In this mini‐review, we discuss recent advances in the understanding of ILC functions in bone homeostasis under physiological and pathological conditions, with an emphasis on the communication between ILCs and bone cells including osteoclasts and osteoblasts, as well as the underlying immunoregulatory networks involving ILC‐derived cytokines and growth factors. This review also discusses future research directions and the potential of targeting ILCs for the treatment of inflammation‐associated bone disorders.

show abstract

Section: Crosstalk Between Ilcs and Bone Cellsmentioning

confidence: 99%

Innate lymphoid cells: New players in osteoimmunology

Wu,

Lin,

Yuan

et al. 2024

Eur J Immunol

View full text Add to dashboard Cite

show abstract

“…gingivalis can manipulate the host immune system by producing virulence factors that can interfere with immune cell signaling pathways or by inducing the production of antiinflammatory cytokines, in order to maintain inflammation, obtain nutrients, and evade host immune killing. e, JZ et al found that P. gingivalis was able to interfere with the immune system and thus induce insulin resistance (He et al, 2022).…”

Section: Immune Escapementioning

confidence: 99%

“…e, JZ et al. found that P. gingivalis was able to interfere with the immune system and thus induce insulin resistance ( He et al., 2022 ).…”

Section: Pathogenesis Of Insulin Resistance Caused By P Gin...mentioning

confidence: 99%

Host insulin resistance caused by Porphyromonas gingivalis-review of recent progresses

Jia

2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Porphyromonas gingivalis (P. gingivalis) is a Gram-negative oral anaerobic bacterium that plays a key role in the pathogenesis of periodontitis. P. gingivalis expresses a variety of virulence factors that disrupt innate and adaptive immunity, allowing P. gingivalis to survive and multiply in the host and destroy periodontal tissue. In addition to periodontal disease, P.gingivalis is also associated with systemic diseases, of which insulin resistance is an important pathological basis. P. gingivalis causes a systemic inflammatory response, disrupts insulin signaling pathways, induces pancreatic β-cell hypofunction and reduced numbers, and causes decreased insulin sensitivity leading to insulin resistance (IR). In this paper, we systematically review the studies on the mechanism of insulin resistance induced by P. gingivalis, discuss the association between P. gingivalis and systemic diseases based on insulin resistance, and finally propose relevant therapeutic approaches. Overall, through a systematic review of the mechanisms related to systemic diseases caused by P. gingivalis through insulin resistance, we hope to provide new insights for future basic research and clinical interventions for related systemic diseases.

show abstract

“…We performed glucose tolerance tests after 4-week oral administration of the probiotics (Figure 1). The mice were fasted overnight and then orally administered with D-glucose by gavage (2 g/kg, n = 3 for each group) [20,21], which was dissolved in 20 mM PBS (10% D-glucose, pH 7.0). Blood glucose levels were measured by using a blood glucose meter (Yicheng, Beijing, China).…”

Section: Oral Glucose Tolerance Test (Ogtt)mentioning

confidence: 99%

Kluyveromyces marxianus Ameliorates High-Fat-Diet-Induced Kidney Injury by Affecting Gut Microbiota and TLR4/NF-κB Pathway in a Mouse Model

Zhao

2023

Cellular Microbiology

View full text Add to dashboard Cite

Objectives. The effects of Kluyveromyces marxianus on high-fat diet- (HFD-) induced kidney injury (KI) were explored. Methods. HFD-induced KI model was established using male C57BL/6 mice and treated with K. marxianus JLU-1016 and acid-resistant (AR) strain JLU-1016A. Glucose tolerance was evaluated via an oral glucose tolerance test (OGTT). KI was measured using Hematoxylin and Eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis. The chemical indexes were analyzed, including lipid profiles, inflammatory cytokines, and creatinine. The levels of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) or phospho-NF-κB p65 (Ser536) and alpha inhibitor of NF-κB (IκBα) were measured using qPCR and Western blot. The gut microbiota was sequenced using high-throughput sequencing. Results. HFD induction increased OGTT value, KI severity, oxidative stress, inflammatory cytokines, oxidative stress, apoptotic rate, creatinine levels, and the expression of TLR4/NF-κB, phospho-NF-κB p65 (Ser536), and IκBα deteriorated lipid profiles ( P < 0.05 ) and reduced gut microbiota abundance. K. marxianus treatment ameliorated HFD-induced metabolic disorders and reversed these parameters ( P < 0.05 ). Compared with the control, HFD induction increased the proportion of Firmicutes but reduced the proportion of Bacteroidetes and Lactobacillus. K. marxianus JLU-1016 and AR strain JLU-1016A treatments improved gut microbiota by reducing the proportion of Firmicutes and increasing the proportion of Bacteroidetes and Lactobacillus in the KI model ( P < 0.0001 ). Helicobacter has been identified with many infectious diseases and was increased after HFD induction and inhibited after K. marxianus JLU-1016 and AR strain JLU-1016A treatments. The strain JLU-1016A exhibited better results possibly with acid-tolerance properties to pass through an acidic environment of the stomach. Conclusions. K. marxianus may have a beneficial effect on KI by improving gut microbiota and inhibiting TLR4/NF-κB pathway activation.

show abstract

Human periodontitis-associated salivary microbiome affects the immune response of diabetic mice

Cited by 6 publications

References 47 publications

Innate lymphoid cells: New players in osteoimmunology

Innate lymphoid cells: New players in osteoimmunology

Host insulin resistance caused by Porphyromonas gingivalis-review of recent progresses

Kluyveromyces marxianus Ameliorates High-Fat-Diet-Induced Kidney Injury by Affecting Gut Microbiota and TLR4/NF-κB Pathway in a Mouse Model

Contact Info

Product

Resources

About