Porphyromonasï¿½gingivalis induced inflammatory responses and promoted apoptosis in lung epithelial cells infected with H1N1 via the Bcl‑2/Bax/Caspase‑3 signaling pathway

Chen, Yongju; Zhou, Rui; Zhou, Yi; Li, Yonggang; Fu, Ying; Zhang, Hongjie; Li, Ping; Li, Xin; Pan, Yaping

doi:10.3892/mmr.2018.8983

Cited by 33 publications

(34 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…5c). As mentioned in the literature review, the Bcl2/ Bax/caspase3 pathway is an important apoptosis pathway 54 , and our results confirmed that ASF1B disruption mediated by shRNA caused cervical cancer cell apoptosis in this way. Subsequently, we further confirmed that ASF1B and CDK9 are the factors of a nuclear complex to promote cervical cancer progression by co-IP and colocalization of ASF1B and CDK9 in the nucleus (Fig.…”

Section: Discussionsupporting

confidence: 87%

ASF1B promotes cervical cancer progression through stabilization of CDK9

et al. 2020

View full text Add to dashboard Cite

Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Recent studies have shown that anti-silencing function 1B (ASF1B) might be used as a new proliferation marker for cancer diagnosis and prognosis. However, the expression and function of ASF1B in cervical cancer remain unclear. Here, we induced ASF1B knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established two murine models using stable ASF1B-shRNA HeLa cells or normal HeLa cells following AAV-shRNA-ASF1B administration to evaluate how suppression of ASF1B affects tumor growth. We showed that ASF1B functions as an oncogene in cervical cancer cells. Silence of ASF1B suppressed cervical cancer cell growth in vitro and in vivo, while, ASF1B overexpression accelerated cancer cell proliferation. Furthermore, ASF1B deficiency induced cell cycle arrest and apoptosis. Mechanistically, we found that ASF1B formed stable complexes with cyclin-dependent kinase 9 (CDK9), and positively regulated CDK9 stabilization. Taken together, tumorigenic ASF1B could be targeted to suppress cervical cancer tumor growth by inducing apoptotic cell death.

show abstract

Section: Discussionsupporting

confidence: 87%

ASF1B promotes cervical cancer progression through stabilization of CDK9

et al. 2020

View full text Add to dashboard Cite

show abstract

“…As an opportunistic pathogen, P. gingivalis cannot be completely eliminated by host cells. An in vitro study suggested that during co-infection of P. gingivalis and influenza virus, significant apoptosis and necrosis can be observed in lung epithelial cells within a short timeframe ( Connolly et al, 2017 ) as the Bcl2/Bax/Caspase3 signaling pathway was activated ( Chen et al, 2018 ). Cytotoxic products of P. gingivalis (e.g., lipopolysaccharide) can induce host cells release of inflammatory cytokines such as TNF-α, IL-1β, and IL-6 ( Ke et al, 2016 ), which in turn increase NO production leading to lung epithelial cell damage ( Alayan et al, 2006 ; Wu et al, 2016 ; Ahamed et al, 2017 ).…”

Section: Interaction Between Oral Microbiome and Virus Infectionmentioning

confidence: 99%

Oral Microbiome and SARS-CoV-2: Beware of Lung Co-infection

et al. 2020

View full text Add to dashboard Cite

The new coronavirus SARS-CoV-2, the cause of COVID-19, has become a public health emergency of global concern. Like the SARS and influenza pandemics, there have been a large number of cases coinfected with other viruses, fungi, and bacteria, some of which originate from the oral cavity. Capnocytophaga , Veillonella , and other oral opportunistic pathogens were found in the BALF of the COVID-19 patients by mNGS. Risk factors such as poor oral hygiene, cough, increased inhalation under normal or abnormal conditions, and mechanical ventilation provide a pathway for oral microorganisms to enter the lower respiratory tract and thus cause respiratory disease. Lung hypoxia, typical symptoms of COVID-19, would favor the growth of anaerobes and facultative anaerobes originating from the oral microbiota. SARS-CoV-2 may aggravate lung disease by interacting with the lung or oral microbiota via mechanisms involving changes in cytokines, T cell responses, and the effects of host conditions such as aging and the oral microbiome changes due to systemic diseases. Because the oral microbiome is closely associated with SARS-CoV-2 co-infections in the lungs, effective oral health care measures are necessary to reduce these infections, especially in severe COVID-19 patients. We hope this review will draw attention from both the scientific and clinical communities on the role of the oral microbiome in the current global pandemic.

show abstract

“…Furthermore, P. gingivalis might affect pneumonia progression through interactions with other respiratory pathogens. Co-infection of P. gingivalis and H1N1 in lung epithelial cells promoted the production of inflammatory CKs and NO, resulting in increased levels of apoptosis via the Bcl-2/Bax/caspase-3 pathway [ 111 ]. P. gingivalis can modulate Pseudomonas aeruginosa -induced respiratory epithelial cell apoptosis via the STAT3 signaling pathway by causing transient inhibition and, ultimately, exerting promoting effects [ 112 ].…”

Section: Respirologymentioning

confidence: 99%

Porphyromonas gingivalis and Its Systemic Impact: Current Status

et al. 2020

View full text Add to dashboard Cite

The relationship between periodontitis and systemic diseases, notably including atherosclerosis and diabetes, has been studied for several years. Porphyromonas gingivalis, a prominent component of oral microorganism communities, is the main pathogen that causes periodontitis. As a result of the extensive analysis of this organism, the evidence of its connection to systemic diseases has become more apparent over the last decade. A significant amount of research has explored the role of Porphyromonas gingivalis in atherosclerosis, Alzheimer’s disease, rheumatoid arthritis, diabetes, and adverse pregnancy outcomes, while relatively few studies have examined its contribution to respiratory diseases, nonalcoholic fatty liver disease, and depression. Here, we provide an overview of the current state of knowledge about Porphyromonas gingivalis and its systemic impact in an aim to inform readers of the existing epidemiological evidence and the most recent preclinical studies. Additionally, the possible mechanisms by which Porphyromonas gingivalis is involved in the onset or exacerbation of diseases, together with its effects on systemic health, are covered. Although a few results remain controversial, it is now evident that Porphyromonas gingivalis should be regarded as a modifiable factor for several diseases.

show abstract

Porphyromonasï¿½gingivalis induced inflammatory responses and promoted apoptosis in lung epithelial cells infected with H1N1 via the Bcl‑2/Bax/Caspase‑3 signaling pathway

Cited by 33 publications

References 35 publications

ASF1B promotes cervical cancer progression through stabilization of CDK9

ASF1B promotes cervical cancer progression through stabilization of CDK9

Oral Microbiome and SARS-CoV-2: Beware of Lung Co-infection

Porphyromonas gingivalis and Its Systemic Impact: Current Status

Contact Info

Product

Resources

About