Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury

Yoshida, Kaya; Fujiwara, Naofumi; Seyama, Mariko; Ono, Koji; Kawai, Hiroki; Guo, Jiajie; Wang, Ziyi; Weng, Yao; Yu, Yaqiong; Uchida-Fukuhara, Yoko; Ikegame, Mika; Sasaki, Akira; Nagatsuka, Hitoshi; Kamioka, Hiroshi; Okamura, Hirohiko; Ozaki, Kazumi

doi:10.1016/j.bbadis.2021.166236

Cited by 8 publications

(5 citation statements)

References 41 publications

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“…2-piperidone, which was significantly decreased in PAH-LTRS, was significantly positively correlated with Moraxella and Porphyromonas, which were decreased in abundance in PAH-LTRS. Porphyromonas was one of the most important genera of the phylum of Bacteroidetes and was reported involved in inflammatory diseases (66)(67)(68) and other human diseases (69,70). Bacteroidetes might play a role in prohibiting PAH progression in patients with LTRS by Porphyromonas through related metabolites, such as 2piperidone.…”

Section: Discussionmentioning

confidence: 99%

Altered Lung Microbiome and Metabolome Profile in Children With Pulmonary Arterial Hypertension Associated With Congenital Heart Disease

Cheng²,

Song³

et al. 2022

Front. Med.

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BackgroundsPulmonary arterial hypertension (PAH) is characterized by progressive pulmonary vascular functional and structural changes, resulting in increased pulmonary vascular resistance and eventually right heart failure and death. Congenital Left-to-Right shunts (LTRS) is one type of congenital heart disease (CHD) and PAH associated with the congenital Left-to-Right shunt (PAH-LTRS) is a severe disease in children. However, changes in the lung microbiome and their potential impact on PAH-LTRS have not been not fully studied. We hypothesized that lung microbiota and their derived metabolites have been disturbed in children with PAH-LTRS, which might contribute to the progression and outcomes of PAH-LTRS.MethodsIn this study, 68 age- and sex-matched children of three different groups (patients with PAH-LTRS cohort, patients with LTRS but have no pathologic features of PAH cohort, and healthy reference cohort) were enrolled in the current study. Bronchoalveolar lavage fluid samples from these participants were conducted for multi-omics analysis, including 16S rRNA sequencing and metabolomic profiling. Data progressing and integration analysis were performed to identify pulmonary microbial and metabolic characteristics of PAH-LTRS in children.ResultsWe found that microbial community density was not significantly altered in PAH-LTRS based on α-diversity analysis. Microbial composition analysis indicated phylum of Bacteroidetes was that less abundant while Lactobacillus, Alicycliphilus, and Parapusillimonas were significantly altered and might contribute to PAH in children with LTRS. Moreover, metabolome profiling data showed that metabolites involved in Purine metabolism, Glycerophospholipid metabolism, Galactose metabolism, and Pyrimidine metabolism were also significantly disturbed in the PAH-LTRS cohort. Correlation analysis between microbes and metabolites indicated that alterations in the microbial composition from the lung microbiota could eventually result in the disturbance in certain metabolites, and might finally contribute to the pathology of PAH-LTRS.ConclusionLung microbial density was not significantly altered in patients with PAH-LTRS. Composition analysis results showed that the relative microbiome abundance was different between groups. Metabolome profiling and correlation analysis with microbiota showed that metabolome also altered in children with PAH-LTRS. This study indicated that pulmonary microbes and metabolites disturbed in PAH-LTRS could be potentially effective biomarkers and provides valuable perspectives on clinical diagnosis, treatment, and prognosis of pediatric PAH-LTRS.

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Section: Discussionmentioning

confidence: 99%

Altered Lung Microbiome and Metabolome Profile in Children With Pulmonary Arterial Hypertension Associated With Congenital Heart Disease

Cheng²,

Song³

et al. 2022

Front. Med.

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“…The same research group has also shown that the administration of F. nucleatum increases the expression of MMP-9, which is involved in the inflammatory response and in the degradation of components of the lung extracellular matrix such as elastin and collagen [90], in an A549 cell culture and in mouse lung and bronchoalveolar lavage fluid [91]. Yoshida et al showed that the extracellular vesicles derived from P. gingivalis-infected macrophages induced pulmonary inflammation and alveoli destruction in mice [92].…”

Section: The Role Of Microorganismsmentioning

confidence: 98%

“…Yoshida et al showed that the extracellular vesicles derived from P . gingivalis -infected macrophages induced pulmonary inflammation and alveoli destruction in mice [ 92 ].…”

Section: Biological Mechanisms Underlying This Relationshipmentioning

confidence: 99%

Putative Bidirectionality of Chronic Obstructive Pulmonary Disease and Periodontal Disease: A Review of the Literature

Tamiya,

Mitani,

Abe

et al. 2023

JCM

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The prevalence of chronic obstructive pulmonary disease (COPD) is increasing worldwide and is currently the third leading cause of death globally. The long-term inhalation of toxic substances, mainly cigarette smoke, deteriorates pulmonary function over time, resulting in the development of COPD in adulthood. Periodontal disease is an inflammatory condition that affects most adults and is caused by the bacteria within dental plaque. These bacteria dissolve the gums around the teeth and the bone that supports them, ultimately leading to tooth loss. Periodontal disease and COPD share common risk factors, such as aging and smoking. Other similarities include local chronic inflammation and links with the onset and progression of systemic diseases such as ischemic heart disease and diabetes mellitus. Understanding whether interventions for periodontal disease improve the disease trajectory of COPD (and vice versa) is important, given our rapidly aging society. This review focuses on the putative relationship between COPD and periodontal disease while exploring current evidence and future research directions.

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“… 77 Extracellular vesicles of P. gingivalis -infected macrophages could induce the expression of TNF-α and IL-6 in lung epithelium cells, further inducing lung injury and inflammation. 78 Moreover, it has been reported that F. nucleatum can trigger COPD by increasing the expression levels of IL-8 and IL-6 in several human respiratory epithelium cells and mouse lung tissue. 79 In the F. nucleatum -exacerbated COPD mouse model, expressions of inflammatory cytokines were also significantly elevated in lung tissue, including expression of IL-6, CXCL-1, CXCL-5, Monocyte chemoattractant protein-2 (CCL-2), and CXCL-10.…”

Section: The Potential Mechanisms By Which Periodontitis Affects Copdmentioning

confidence: 99%

Research on the Association Between Periodontitis and COPD

Xiong,

Yang,

Cui

et al. 2023

COPD

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Periodontitis is a common chronic bacteria-initiated inflammatory disease that is closely associated with various systemic diseases, including chronic obstructive pulmonary disease (COPD). Periodontitis and COPD share similar risk factors, pathology and microorganisms. Epidemiological and clinical research have shown positive correlation between the two diseases. Individuals with severe periodontitis had a higher risk of developing COPD. Moreover, the relative risk of COPD in severe periodontitis was much higher compared to people without periodontal disease and patients with mild to moderate periodontitis. COPD patients with periodontitis had a higher frequency of COPD exacerbation and periodontal treatment demonstrated some control of COPD. However, the nature of periodontitis affecting COPD still needs further exploration. Periodontitis caused microbial and immune imbalances of the lung through several aspects: (I) under periodontitis status, periodontal pathogens directly caused the lung inflammatory reaction after inhalation and colonization on the lung, (II) periodontitis status promoted the oral colonization of pneumonia-associated pathogens, (III) periodontitis status affected the respiratory epithelium structure and (IV) periodontitis status caused imbalances in neutrophils, macrophages and inflammatory cytokines. In this review, we conclude the association between periodontitis and COPD through several aspects and further discuss the potential mechanism by which periodontitis affects COPD.

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Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury

Cited by 8 publications

References 41 publications

Altered Lung Microbiome and Metabolome Profile in Children With Pulmonary Arterial Hypertension Associated With Congenital Heart Disease

Altered Lung Microbiome and Metabolome Profile in Children With Pulmonary Arterial Hypertension Associated With Congenital Heart Disease

Putative Bidirectionality of Chronic Obstructive Pulmonary Disease and Periodontal Disease: A Review of the Literature

Research on the Association Between Periodontitis and COPD

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