SARS-CoV-2 Infection of Airway Epithelial Cells

Ryu, Gwanghui; Shin, Hyun–Woo

doi:10.4110/in.2021.21.e3

Cited by 56 publications

(57 citation statements)

References 113 publications

(129 reference statements)

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“…Tuning of the immune response is needed to have the target cell eliminated but FIGURE 3 | A cascade of events after SARS-CoV-2 infection starts with a few days time lag in which the virus replicates using a set of open frame genes in airway epithelial cells (70). Then pneumocytes are invaded and huge amount of DAMPS are released (71). After that innate immunity receptors recognize viral RNA and proinflammatory cytokines are produced using the NFkappaB signaling pathway.…”

Section: The Impact Of Chronic CMV Infection On Blood Lymphocyte Subpopulationsmentioning

confidence: 99%

Cytokine Overproduction and Immune System Dysregulation in alloHSCT and COVID-19 Patients

Lange

Lange²,

Jaskuła

2021

Front. Immunol.

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The COVID-19 pathomechanism depends on (i) the pathogenicity of the virus, (ii) ability of the immune system to respond to the cytopathic effect of the virus infection, (iii) co-morbidities. Inflammatory cytokine production constitutes a hallmark of COVID-19 that is facilitated by inability of adaptive immunity to control virus invasion. The effect of cytokine release syndrome is deleterious, but the severity of it depends on other confounding factors: age and comorbidities. In this study, we analyze the literature data on the post-transplant course of allogeneic hematopoietic stem cell transplanted (alloHSCT) patients, which is affected by generated inflammatory cytokines. The sequence of events boosting cytokine production was analyzed in relation to clinical and laboratory data highlighting the impact of cytokine generation on the post-transplant course. The collected data were compared to those from studies on COVID-19 patients. The similarities are: (i) the damage/pathogen-associated molecular pattern (DAMP/PAMP) stage is similar except for the initiation hit being sterile in alloHSCT (toxic damage of conditioning regimen) and viral in COVID-19; (ii) genetic host-derived factors play a role; (iii) adaptive immunity fails, DAMP signal(s) increases, over-production of cytokines occurs; (iv) monocytes lacking HLADR expression emerge, being suppressor cells hampering adaptive immunity; (v) immune system homeostasis is broken, the patient’s status deteriorates to bed dependency, leading to hypo-oxygenation and malnutrition, which in turn stimulates the intracellular alert pathways with vigorous transcription of cytokine genes. All starts with the interaction between DAMPs with appropriate receptors, which leads to the production of pro-inflammatory cytokines, the inflammatory process spreads, tissue is damaged, DAMPs are released and a vicious cycle occurs. Attempts to modify intracellular signaling pathways in patients with post-alloHSCT graft vs host disease have already been undertaken. The similarities documented in this study show that this approach may also be used in COVID-19 patients for tuning signal transduction processes to interrupt the cycle that powers the cytokine overproduction.

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Section: The Impact Of Chronic CMV Infection On Blood Lymphocyte Subpopulationsmentioning

confidence: 99%

Cytokine Overproduction and Immune System Dysregulation in alloHSCT and COVID-19 Patients

Lange

Lange²,

Jaskuła

2021

Front. Immunol.

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“…SARS-CoV-2 targets alveolar epithelial cells and enterocytes, leading to Covid-19 [ 12 , 13 ]. The disease is predominantly characterized by respiratory symptoms and may progress to bilateral interstitial pneumonia, respiratory failure, or acute respiratory distress syndrome (ARDS) [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 diagnosis: a single-centre experience

et al. 2021

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The coronavirus disease 2019 (COVID-19) was declared a pandemic by the World Health Organization (WHO) on the 11th of March 2020. In Romania, there have been 983,217 confirmed cases and 24,386 deaths. We aim to show our experience at the Fundeni Clinical Institute in the diagnosis of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection in both patients and health care personnel. Swab samples were collected for extraction of the SARS-CoV-2 RNA from 29380 patients and health care personnel. We have combined three real-time reverse transcription-polymerase chain reaction (RT-PCR) assays for the qualitative detection of SARS-CoV-2. Also, the presence of IgG against SARS-CoV-2 nucleoprotein was analyzed in 1068 patients and clinical staff using the chemiluminescence method. Other 50 people were screened post-vaccination for the presence of SARS-CoV-2 antibodies against the spike (S) protein, using the chemiluminescence method as well. The majority of confirmed cases were in adults, 71.3% of cases being registered in people aged 30-69 years. Most patients diagnosed with SARS-CoV-2 infection (83%) were admitted to the gastroenterology, hematology, and surgery wards. Our study showed that one-third of people developed antibodies against the nucleocapsid of SARS-CoV-2. SARS-CoV-2 IgG seroprevalence does not vary by gender or age. Also, we noticed the presence of antibodies against the SARS-CoV-2 spike protein in all 50 people post-vaccination that were tested two weeks after the second dose. Due to the increasing number of infected patients with SARS-CoV-2, the new coronavirus pandemic involves a sustained testing effort for an accurate virological diagnosis in both direct and indirect diagnosis.

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“…However, many viruses, including SARS-CoV-2 [20] , antagonize MAVS activation and evade IFN I-dependent immune responses [26] . It is now understood that SARS-CoV-2, in fact, does not primarily induce immune response through IFNs, but rather leads to expression of chemokines and cytokines, such as IL-6, TNF, IL-8, MCP-1 and MIG, resulting in cytokine storm or hypercytokinemia [ 9 , 27 ]. Similar to SARS-CoV-2, here we found that coronavirus CoV-229E appears not to induce an immune response through IFNs (IFN-α2 and IFN-γ), but rather activates the expression of chemokines and cytokines including IL-6, TNF, IL-8, MCP-1, MIG, and at a later stage, IP-10.…”

Section: Discussionmentioning

confidence: 99%

“…The term “cytokine storm” [6] describes surging levels of cytokines produced by airway epithelial cells in response to SARS-CoV-2. These cytokines include interleukin (IL)-6, tumor necrosis factor (TNF), interferon gamma-induced protein 10 (IP-10, also known as C-X-C motif chemokine ligand 10 (CXCL10)), and macrophage inflammatory protein (MIP)-1α and 1β 7 , 8 , 9 . Excessive elevation of these cytokines and hyperactivation of immune cells is associated with poor patient outcomes and death in COVID-19 patients [10] .…”

Section: Introductionmentioning

confidence: 99%

Ultraviolet-A light reduces cellular cytokine release from human endotracheal cells infected with Coronavirus

Leite¹,

Pimentel²,

Mathur

et al. 2021

Photodiagnosis and Photodynamic Therapy

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Background An important clinical feature of coronavirus disease 2019 (COVID-19) is hypercytokinemia (cytokine storm). We previously showed that narrow band ultraviolet-A (NB-UVA) treatment salvages coronavirus (CoV)-229E-infected human tracheal cells, and that daily endotracheal NB-UVA therapy reduced severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) levels in human subjects, with improved clinical outcomes. Here, we examined NB-UVA effects on cytokine release during CoV-229E infection. Methods Primary human tracheal epithelial cells were transfected with CoV-229E, then exposed to 2 mW/cm 2 NB-UVA for 20 minutes every 24h, either 3 or 4 times. Secreted cytokine/chemokine levels were analyzed in supernatants harvested from CoV-229E-infected/UVA-exposed cells 24h after the last UVA treatment, and from matched non-infected/UVA-exposed controls, CoV-229E-infected/non-exposed controls, and non-infected/non-exposed (naïve) controls. Metabolic pathway/downstream prediction analyses were also performed. Results Pro-inflammatory cytokines interleukin(IL)-6 and tumor necrosis factor (TNF), and chemokines IL-8, monocyte chemoattractant protein-1 (MCP1), and interferon gamma-induced protein 10 (IP-10), were significantly increased in CoV-229E-infected cells, and significantly decreased following NB-UVA treatment. Interferon(IFN)-α2, IFN-γ, and IL-10 were not upregulated in response to CoV-229E. Metabolic pathway predictions indicated hypercytokinemia as the top inflammatory response in CoV-229E-infected cells, whereas the top predicted pathway in CoV-229E-infected/UVA-exposed cells was the recovery stage of severe acute respiratory syndrome. Conclusions Human tracheal epithelial cells infected with CoV-229E showed reduced cytokine secretions including IL-6, TNF, IL-8, and MCP-1, following NB-UVA exposure. This reduction of cytokine levels in vitro , coupled with previously identified reduced cell death in CoV-229E-infected/UVA-exposed cells, suggests that determining UVA effects on cytokine storm in human SARS-Co-V2 patients is warranted.

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SARS-CoV-2 Infection of Airway Epithelial Cells

Cited by 56 publications

References 113 publications

Cytokine Overproduction and Immune System Dysregulation in alloHSCT and COVID-19 Patients

Cytokine Overproduction and Immune System Dysregulation in alloHSCT and COVID-19 Patients

SARS-CoV-2 diagnosis: a single-centre experience

Ultraviolet-A light reduces cellular cytokine release from human endotracheal cells infected with Coronavirus

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