Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Pfeffer, Paul; Lu, Haw; Mann, Elizabeth H.; Chen, Yin-Huai; Ho, Tzer-Ren; Cousins, David J.; Corrigan, Christopher; Kelly, Frank J.; Mudway, Ian; Hawrylowicz, Catherine M.

doi:10.1371/journal.pone.0200040

Cited by 68 publications

(45 citation statements)

References 72 publications

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“…As an antecedent at the respiratory level, vitamin D stimulated the activation of the glucose-6-phosphate dehydrogenase signaling pathway and the production of oxidized glutathione as antioxidant mechanisms against oxidative stress induced by pollutant particulate matter in human bronchial epithelial cells. Therefore, vitamin D may exert a protective antioxidant effect on lungs and airways under oxidative stress conditions such as asthma or chronic obstructive pulmonary disease in smoking patients [162,163]. In this regard, it was observed that patients with pulmonary pathologies usually have lowered vitamin D serum levels, which would indicate a possible correlation between an impaired antioxidant defense and a susceptibility to suffer lung disease [164].…”

Section: Vitamin D Antioxidative Actions Against Sars-cov-2 Infectionmentioning

confidence: 99%

Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D

et al. 2020

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Due to its high degree of contagiousness and like almost no other virus, SARS-CoV-2 has put the health of the world population on alert. COVID-19 can provoke an acute inflammatory process and uncontrolled oxidative stress, which predisposes one to respiratory syndrome, and in the worst case, death. Recent evidence suggests the mechanistic role of mitochondria and vitamin D in the development of COVID-19. Indeed, mitochondrial dynamics contribute to the maintenance of cellular homeostasis, and its uncoupling involves pathological situations. SARS-CoV-2 infection is associated with altered mitochondrial dynamics with consequent oxidative stress, pro-inflammatory state, cytokine production, and cell death. Furthermore, vitamin D deficiency seems to be associated with increased COVID-19 risk. In contrast, vitamin D can normalize mitochondrial dynamics, which would improve oxidative stress, pro-inflammatory state, and cytokine production. Furthermore, vitamin D reduces renin–angiotensin–aldosterone system activation and, consequently, decreases ROS generation and improves the prognosis of SARS-CoV-2 infection. Thus, the purpose of this review is to deepen the knowledge about the role of mitochondria and vitamin D directly involved in the regulation of oxidative stress and the inflammatory state in SARS-CoV-2 infection. As future prospects, evidence suggests enhancing the vitamin D levels of the world population, especially of those individuals with additional risk factors that predispose to the lethal consequences of SARS-CoV-2 infection.

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Section: Vitamin D Antioxidative Actions Against Sars-cov-2 Infectionmentioning

confidence: 99%

Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D

et al. 2020

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“…In addition, it was suggested that S. pneumoniae produces hydrogen peroxide that damages the DNA and induces apoptosis in lung epithelial cells (Rai et al, 2015). Similarly, the toxicity of ASD is attributed to oxidative stress and apoptosis (Go et al, 2015;Chang et al, 2016;Pfeffer et al, 2018). Therefore, it appears that the additive effects of ASD and S. pneumoniae enhance apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Asian Sand Dust Particles Increased Pneumococcal Biofilm Formation in vitro and Colonization in Human Middle Ear Epithelial Cells and Rat Middle Ear Mucosa

Yadav

Chae

et al. 2020

Front. Genet.

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Introduction: Air pollutants such as Asian sand dust (ASD) and Streptococcus pneumoniae are risk factors for otitis media (OM). In this study, we evaluate the role of ASD in pneumococcal in vitro biofilm growth and colonization on human middle ear epithelium cells (HMEECs) and rat middle ear using the rat OM model. Methods: S. pneumoniae D39 in vitro biofilm growth in the presence of ASD (50-300 µg/ml) was evaluated in metal ion-free BHI medium using CV-microplate assay, colony-forming unit (cfu) counts, resazurin staining, scanning electron microscopy (SEM), and confocal microscopy (CF). Biofilm gene expression analysis was performed using real-time RT-PCR. The effects of ASD or S. pneumoniae individually or on cotreatment on HMEECs were evaluated by detecting HMEEC viability, apoptosis, and reactive oxygen species (ROS) production. In vivo colonization of S. pneumoniae in the presence of ASD was evaluated using the rat OM model, and RNA-Seq was used to evaluate the alterations in gene expression in rat middle ear mucosa. Results: S. pneumoniae biofilm growth was significantly (P < 0.05) elevated in the presence of ASD. SEM and CF analysis revealed thick and organized pneumococcal biofilms in the presence of ASD (300 µg/ml). However, in the absence of ASD, bacteria were unable to form organized biofilms, the cell size was smaller than normal, and long chain-like structures were formed. Biofilms grown in the presence of ASD showed elevated expression levels of genes involved in biofilm formation (luxS), competence (comA, comB, ciaR), and toxin production (lytA and ply). Prior exposure of HMEECs to ASD, followed by treatment for pneumococci, significantly (P < 0.05) decreased cell viability and increased apoptosis, and ROS production. In vivo experiment results showed significantly (P < 0.05) more than 65% increased bacteria colonization in rat middle ear mucosa in the presence of ASD. The apoptosis, cell death, DNA repair,

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“…Cumulative data suggest that vitamin D exerts anti-inflammatory effects via its actions on both innate and adaptive immune responses. Upon viral infection or exposure of pro-inflammatory stimuli such as Poly(I:C) or PM, 1,25(OH) 2 D attenuates induced expression of cytokines and chemokines e.g., via inhibition of nuclear factor (NF)-κB or oxidative stress, respectively, in (airway) epithelial cells (38,59,116). Furthermore, 1,25(OH) 2 D increases expression of the soluble decoy receptor for IL-33 (sST2) by airway epithelial cells, which in turn inhibits the actions of the type 2 alarmin IL-33 (117).…”

Section: Effects Of Vitamin D On Innate and Adaptive Immune Responsesmentioning

confidence: 99%

Impact of the Local Inflammatory Environment on Mucosal Vitamin D Metabolism and Signaling in Chronic Inflammatory Lung Diseases

2020

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Vitamin D plays an active role in the modulation of innate and adaptive immune responses as well as in the protection against respiratory pathogens. Evidence for this immunomodulatory and protective role is derived from observational studies showing an association between vitamin D deficiency, chronic airway diseases and respiratory infections, and is supported by a range of experimental studies using cell culture and animal models. Furthermore, recent intervention studies have now shown that vitamin D supplementation reduces exacerbation rates in vitamin D-deficient patients with chronic obstructive pulmonary disease (COPD) or asthma and decreases the incidence of acute respiratory tract infections. The active vitamin D metabolite, 1,25-dihydroxy-vitamin D (1,25(OH) 2 D), is known to contribute to the integrity of the mucosal barrier, promote killing of pathogens (via the induction of antimicrobial peptides), and to modulate inflammation and immune responses. These mechanisms may partly explain its protective role against infections and exacerbations in COPD and asthma patients. The respiratory mucosa is an important site of local 1,25(OH) 2 D synthesis, degradation and signaling, a process that can be affected by exposure to inflammatory mediators. As a consequence, mucosal inflammation and other disease-associated factors, as observed in e.g., COPD and asthma, may modulate the protective actions of 1,25(OH) 2 D. Here, we discuss the potential consequences of various disease-associated processes such as inflammation and exposure to pathogens and inhaled toxicants on vitamin D metabolism and local responses to 1,25(OH) 2 D in both immune-and epithelial cells. We furthermore discuss potential consequences of disturbed local levels of 25(OH)D and 1,25(OH) 2 D for chronic lung diseases. Additional insight into the relationship between disease-associated mechanisms and local effects of 1,25(OH) 2 D is expected to contribute to the design of future strategies aimed at improving local levels of 1,25(OH) 2 D and signaling in chronic inflammatory lung diseases.

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Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Cited by 68 publications

References 72 publications

Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D

Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D

Asian Sand Dust Particles Increased Pneumococcal Biofilm Formation in vitro and Colonization in Human Middle Ear Epithelial Cells and Rat Middle Ear Mucosa

Impact of the Local Inflammatory Environment on Mucosal Vitamin D Metabolism and Signaling in Chronic Inflammatory Lung Diseases

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