SAP deficiency aggravates periodontitis possibly via C5a-C5aR signaling-mediated defective macrophage phagocytosis of Porphyromonas gingivalis

Wang, Liping; Liang, Dongliang; Huang, Yufan; Chen, Yunxin; Yang, Xiaobo; Huang, Zhijun; Jiang, Yiqin; Su, Haibo; Wang, Lijing; Pathak, Janak L.; Ge, Linhu

doi:10.1016/j.jare.2022.10.003

Cited by 8 publications

(2 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oral microbiome diversities are lower in patients experiencing cognitive decline when compared to cognitively healthy individuals, suggesting an overgrowth of specific microbiota in patients with cognitive decline [29]. The impact of P. gingivalis on CNS pathogenesis related to AD has been revealed through in vitro and in vivo studies using animal models [23,[30][31][32][33][34]. In one study, the human neuroblastoma cell line SH-SY5Y produced Aβ40 and Aβ42 in response to P. gingivalis, which occurred through the cleavage of the amyloid-β protein precursor in vitro [30].…”

Section: Porphyromonas Gingivalismentioning

confidence: 99%

Oral Microbiome and Alzheimer’s Disease

Wan,

Fan

2023

Microorganisms

View full text Add to dashboard Cite

The accumulation of amyloid-beta plaques in the brain is a central pathological feature of Alzheimer’s disease. It is believed that amyloid responses may be a result of the host immune response to pathogens in both the central nervous system and peripheral systems. Oral microbial dysbiosis is a chronic condition affecting more than 50% of older adults. Recent studies have linked oral microbial dysbiosis to a higher brain Aβ load and the development of Alzheimer’s disease in humans. Moreover, the presence of an oral-derived and predominant microbiome has been identified in the brains of patients with Alzheimer’s disease and other neurodegenerative diseases. Therefore, in this opinion article, we aim to provide a summary of studies on oral microbiomes that may contribute to the pathogenesis of the central nervous system in Alzheimer’s disease.

show abstract

Section: Porphyromonas Gingivalismentioning

confidence: 99%

Oral Microbiome and Alzheimer’s Disease

Wan,

Fan

2023

Microorganisms

View full text Add to dashboard Cite

show abstract

“…The distances from the cementum enamel junction to the alveolar bone crest (CEJ-ABC) distances were measured at 6 xed palatal sites. Each site was measured three times, and the average of 6 sites represented the bone resorption height [24].…”

Section: Micro Ct Analysismentioning

confidence: 99%

Glipizide alleviates periodontitis pathogenicity via inhibition of angiogenesis, osteoclastogenesis, and M1/M2 macrophage ratio in periodontal tissue

Guo

Yang

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

New consensus indicates type 2 diabetes mellitus (T2DM) and periodontitis as comorbidity and may share common pathways of disease progression. Sulfonylureas have been reported to improve the periodontal status in periodontitis patients. Glipizide, a sulfonylurea widely used in the treatment of T2DM, has also been reported to inhibit inflammation and angiogenesis. However, the effect of Glipizide on periodontitis pathogenicity has not been investigated yet. We developed ligature-induced periodontitis in mice and treated with different concentrations of glipizide. Periodontal tissue status, alveolar bone loss, and osteoclast numbers were analyzed. Immunohistochemistry, RT-qPCR, and ELISA analyzed the inflammatory cells' infiltration and angiogenesis. Transwell assay and Western bolt analyzed macrophage migration and polarization. 16S rRNA sequencing analyzed the effect of glipizide on the oral microbial flora. mRNA sequencing of bone marrow-derived macrophages (BMMs) stimulated by P. gingivalis lipopolysaccharide (Pg-LPS) after treatment with glipizide was analyzed. Glipizide reduced alveolar bone resorption, periodontal tissue degeneration, and the number of osteoclasts in periodontitis-affected periodontal tissue (PAPT). Glipizide-treated periodontitis mice showed reduced micro-vessel density and leukocyte/macrophage infiltration in PAPT. Glipizide significantly inhibited osteoclast differentiation in vitro experiments. Glipizide treatment did not affect the oral microbiome of periodontitis mice. mRNA sequencing and KEGG analysis showed that glipizide activated PI3K/AKT signaling in LPS-stimulated BMMs. Glipizide inhibited the LPS-induced migration of BMMs but promoted M2/M1 macrophage ratio in LPS-induced BMMs via activation of PI3K/AKT signaling. In conclusion, glipizide inhibits angiogenesis, macrophage inflammatory phenotype, and osteoclastogenesis to alleviate periodontitis pathogenicity suggesting its’ possible application in the treatment of periodontitis and diabetes comorbidity.

show abstract

Glipizide Alleviates Periodontitis Pathogenicity via Inhibition of Angiogenesis, Osteoclastogenesis and M1/M2 Macrophage Ratio in Periodontal Tissue

Guo

Huang

et al. 2023

Inflammation

View full text Add to dashboard Cite

SAP deficiency aggravates periodontitis possibly via C5a-C5aR signaling-mediated defective macrophage phagocytosis of Porphyromonas gingivalis

Cited by 8 publications

References 60 publications

Oral Microbiome and Alzheimer’s Disease

Oral Microbiome and Alzheimer’s Disease

Glipizide alleviates periodontitis pathogenicity via inhibition of angiogenesis, osteoclastogenesis, and M1/M2 macrophage ratio in periodontal tissue

Glipizide Alleviates Periodontitis Pathogenicity via Inhibition of Angiogenesis, Osteoclastogenesis and M1/M2 Macrophage Ratio in Periodontal Tissue

Contact Info

Product

Resources

About