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1.
Int J Biol Macromol ; 198: 101-110, 2022 Feb 15.
Article in English | MEDLINE | ID: covidwho-1587672

ABSTRACT

Respiratory infected by COVID-19 represents a major global health problem at moment even after recovery from virus corona. Since, the lung lesions for infected patients are still sufferings from acute respiratory distress syndrome including alveolar septal edema, pneumonia, hyperplasia, and hyaline membranes Therefore, there is an urgent need to identify additional candidates having ability to overcome inflammatory process and can enhance efficacy in the treatment of COVID-19. The polypenolic extracts were integrated into moeties of bovine serum albumin (BSA) and then were coated by chitosan as a mucoadhesion polymer. The results of interleukin-6, and c-reactive protein showed significant reduction in group treated by Encap. SIL + CUR (64 ± 0.8 Pg/µL & 6 ± 0.5 µg/µL) compared to group treated by Cham. + CUR (102 ± 0.8 Pg/µL & 7 ± 0.5 µg/µL) respectively and free capsules (with no any drug inside) (148 ± 0.6 Pg/µL & 10 ± 0.6 µg/µL) respectively. Histopathology profile was improved completely. Additionally, encapsulating silymarin showed anti-viral activity in vitro COVID-19 experiment. It can be summarized that muco-inhalable delivery system (MIDS) loaded by silymarin can be used to overcome inflammation induced by oleic acid and to overcome COVID-19.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Antiviral Agents/pharmacology , COVID-19/drug therapy , Curcumin/pharmacology , Lung Injury/drug therapy , Nanoparticles/chemistry , Silymarin/pharmacology , Administration, Inhalation , Animals , Anti-Inflammatory Agents/administration & dosage , Antiviral Agents/administration & dosage , C-Reactive Protein/metabolism , Chamomile/chemistry , Chitosan/chemistry , Chlorocebus aethiops , Curcumin/administration & dosage , Drug Delivery Systems/methods , Flavonoids/analysis , Flavonoids/chemistry , Interleukin-6/metabolism , Lung Injury/blood , Lung Injury/chemically induced , Lung Injury/pathology , Male , Mice , Milk Thistle/chemistry , Nanoparticles/administration & dosage , Oleic Acid/toxicity , Silymarin/administration & dosage , Vero Cells , Viral Plaque Assay
2.
Mol Med Rep ; 24(4)2021 Oct.
Article in English | MEDLINE | ID: covidwho-1395036

ABSTRACT

Chronic alcohol abuse increases the risk of mortality and poor outcomes in patients with acute respiratory distress syndrome. However, the underlying mechanisms remain to be elucidated. The present study aimed to investigate the effects of chronic alcohol consumption on lung injury and clarify the signaling pathways involved in the inhibition of alveolar fluid clearance (AFC). In order to produce rodent models with chronic alcohol consumption, wild­type C57BL/6 mice were treated with alcohol. A2a adenosine receptor (AR) small interfering (si)RNA or A2bAR siRNA were transfected into the lung tissue of mice and primary rat alveolar type II (ATII) cells. The rate of AFC in lung tissue was measured during exposure to lipopolysaccharide (LPS). Epithelial sodium channel (ENaC) expression was determined to investigate the mechanisms underlying alcohol­induced regulation of AFC. In the present study, exposure to alcohol reduced AFC, exacerbated pulmonary edema and worsened LPS­induced lung injury. Alcohol caused a decrease in cyclic adenosine monophosphate (cAMP) levels and inhibited α­ENaC, ß­ENaC and γ­ENaC expression levels in the lung tissue of mice and ATII cells. Furthermore, alcohol decreased α­ENaC, ß­ENaC and γ­ENaC expression levels via the A2aAR or A2bAR­cAMP signaling pathways in vitro. In conclusion, the results of the present study demonstrated that chronic alcohol consumption worsened lung injury by aggravating pulmonary edema and impairing AFC. An alcohol­induced decrease of α­ENaC, ß­ENaC and γ­ENaC expression levels by the A2AR­mediated cAMP pathway may be responsible for the exacerbated effects of chronic alcohol consumption in lung injury.


Subject(s)
Acute Lung Injury/metabolism , Alveolar Epithelial Cells/metabolism , Epithelial Sodium Channels/drug effects , Epithelial Sodium Channels/metabolism , Ethanol/pharmacology , Receptors, Adenosine A2/metabolism , Acute Lung Injury/chemically induced , Acute Lung Injury/pathology , Alveolar Epithelial Cells/pathology , Animals , Cyclic AMP/metabolism , Cytokines , Lipopolysaccharides/adverse effects , Lung/metabolism , Lung Injury/chemically induced , Lung Injury/metabolism , Lung Injury/pathology , Mice , Mice, Inbred C57BL , Pulmonary Alveoli/metabolism , Pulmonary Edema/chemically induced , Pulmonary Edema/metabolism , Pulmonary Edema/pathology , RNA Splicing Factors/genetics , RNA Splicing Factors/metabolism , Rats , Receptor, Adenosine A2A/genetics , Receptor, Adenosine A2A/metabolism , Signal Transduction
3.
BMJ Case Rep ; 14(7)2021 Jul 23.
Article in English | MEDLINE | ID: covidwho-1322781

ABSTRACT

SARS-CoV-2, the novel coronavirus causing COVID-19, has caused a global pandemic resulting in over 4 million deaths globally (data current as of 14 July 2021). E-cigarette or vaping product use-associated lung injury (EVALI) is a type of acute lung injury of unclear pathogenesis. The two pathologies present with overlapping clinical symptoms, laboratory values and imaging, making them difficult to distinguish, especially in the setting of a global COVID-19 pandemic. We present the case of a 32-year-old woman treated for COVID-19 despite multiple negative SARS CoV-2 PCR tests and nucleocapsid antibody test. On further investigation, she endorsed use of E-cigarettes and was subsequently diagnosed with EVALI. The patient was treated with oral and intravenous steroids, resulting in significant improvement in her symptoms. This case highlights the challenge of diagnosing rarer aetiologies of respiratory distress during the COVID-19 pandemic.


Subject(s)
COVID-19 , Electronic Nicotine Delivery Systems , Lung Injury , Vaping , Adult , Female , Humans , Lung Injury/chemically induced , Lung Injury/diagnosis , Pandemics , SARS-CoV-2 , Vaping/adverse effects
4.
Physiol Rep ; 9(13): e14802, 2021 07.
Article in English | MEDLINE | ID: covidwho-1305905

ABSTRACT

In severe acute respiratory distress syndrome (ARDS), extracorporeal membrane oxygenation (ECMO) is a life-prolonging treatment, especially among COVID-19 patients. Evaluation of lung injury progression is challenging with current techniques. Diagnostic imaging or invasive diagnostics are risky given the difficulties of intra-hospital transportation, contraindication of biopsies, and the potential for the spread of infections, such as in COVID-19 patients. We have recently shown that particle flow rate (PFR) from exhaled breath could be a noninvasive, early detection method for ARDS during mechanical ventilation. We hypothesized that PFR could also measure the progress of lung injury during ECMO treatment. Lipopolysaccharide (LPS) was thus used to induce ARDS in pigs under mechanical ventilation. Eight were connected to ECMO, whereas seven animals were not. In addition, six animals received sham treatment with saline. Four human patients with ECMO and ARDS were also monitored. In the pigs, as lung injury ensued, the PFR dramatically increased and a particular spike followed the establishment of ECMO in the LPS-treated animals. PFR remained elevated in all animals with no signs of lung recovery. In the human patients, in the two that recovered, PFR decreased. In the two whose lung function deteriorated while on ECMO, there was increased PFR with no sign of recovery in lung function. The present results indicate that real-time monitoring of PFR may be a new, complementary approach in the clinic for measurement of the extent of lung injury and recovery over time in ECMO patients with ARDS.


Subject(s)
COVID-19/physiopathology , Lipopolysaccharides/toxicity , Lung Injury/physiopathology , Lung/physiopathology , Particulate Matter/analysis , Respiratory Distress Syndrome/physiopathology , Animals , Blood Gas Analysis/methods , COVID-19/chemically induced , Extracorporeal Membrane Oxygenation/methods , Lung/drug effects , Lung Injury/chemically induced , Particulate Matter/adverse effects , Respiration, Artificial/methods , Respiratory Distress Syndrome/chemically induced , Swine
5.
JCI Insight ; 6(12)2021 06 22.
Article in English | MEDLINE | ID: covidwho-1223641

ABSTRACT

Mice are normally unaffected by SARS coronavirus 2 (SARS-CoV-2) infection since the virus does not bind effectively to the murine version of the angiotensin-converting enzyme 2 (ACE2) receptor molecule. Here, we report that induced mild pulmonary morbidities rendered SARS-CoV-2-refractive CD-1 mice susceptible to this virus. Specifically, SARS-CoV-2 infection after application of low doses of the acute lung injury stimulants bleomycin or ricin caused severe disease in CD-1 mice, manifested by sustained body weight loss and mortality rates greater than 50%. Further studies revealed markedly higher levels of viral RNA in the lungs, heart, and serum of low-dose ricin-pretreated mice compared with non-pretreated mice. Furthermore, lung extracts prepared 2-3 days after viral infection contained subgenomic mRNA and virus particles capable of replication only when derived from the pretreated mice. The deleterious effects of SARS-CoV-2 infection were effectively alleviated by passive transfer of polyclonal or monoclonal antibodies generated against the SARS-CoV-2 receptor binding domain (RBD). Thus, viral cell entry in the sensitized mice seems to depend on viral RBD binding, albeit by a mechanism other than the canonical ACE2-mediated uptake route. This unique mode of viral entry, observed over a mildly injured tissue background, may contribute to the exacerbation of coronavirus disease 2019 (COVID-19) pathologies in patients with preexisting morbidities.


Subject(s)
Bleomycin/toxicity , COVID-19/pathology , Lung Injury , Ricin/toxicity , Animals , Chlorocebus aethiops , Comorbidity , Disease Models, Animal , Female , Lung Injury/chemically induced , Lung Injury/virology , Mice , Vero Cells , Virus Attachment , Virus Internalization/drug effects
6.
Rinsho Ketsueki ; 62(1): 30-34, 2021.
Article in Japanese | MEDLINE | ID: covidwho-1069962

ABSTRACT

From December 2019, a 71-year-old male underwent three cycles of a combination therapy of pomalidomide, bortezomib, and dexamethasone for relapsed multiple myeloma and a very good partial response was achieved. In March 2020, he developed a fever of 38.9°C and computed tomography revealed bilateral ground-glass opacities. Antibiotic therapy was ineffective. Bronchoscopy was performed and bortezomib-induced lung injury was initially suspected. Due to respiratory exacerbation, high-dose steroid therapy was administered, which resulted in a dramatic improvement of the patient's respiratory failure. Thereafter, reverse transcription polymerase chain reaction performed on a preserved bronchial lavage sample tested positive, and thus his diagnosis was corrected to COVID-19 pneumonia. It is difficult to discriminate COVID-19 pneumonia from drug-induced lung disease, as both disorders can present similar ground-glass opacities on computed tomography. Therefore, with this presented case, we summarize our experience with steroid therapy for COVID-19 associated respiratory distress at our institution.


Subject(s)
Bortezomib/adverse effects , COVID-19 , Lung Injury , Respiratory Insufficiency , Aged , Humans , Lung Injury/chemically induced , Male , Respiratory Insufficiency/chemically induced , Respiratory Insufficiency/diagnosis , SARS-CoV-2 , Steroids
7.
J Emerg Med ; 60(4): 524-530, 2021 04.
Article in English | MEDLINE | ID: covidwho-1042305

ABSTRACT

BACKGROUND: E-cigarette or vaping product use-associated lung injury (EVALI) is a complex inflammatory syndrome predominantly seen in adolescents and young adults. The clinical and laboratory profile can easily mimic infectious and noninfectious conditions. The exclusion of these conditions is essential to establish the diagnosis. Recently, the novel coronavirus disease 2019 (COVID-19) pandemic introduced the multisystem inflammatory syndrome in children (MIS-C). MIS-C knowledge is evolving. The current criteria to establish the diagnosis are not specific and have overlapping features with EVALI, making the accurate diagnosis a clinical challenge during continued COVID-19 transmission within the community. CASE REPORT: Three young adults evaluated at our emergency department for prolonged fever and gastrointestinal and respiratory symptoms were initially assessed for possible MIS-C due to epidemiologic links to COVID-19 and were eventually diagnosed with EVALI. The clinical, laboratory, and radiologic characteristics of both entities are explored, as well as the appropriate medical management. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Physician awareness of overlapping and differentiating EVALI and MIS-C features is essential to direct appropriate diagnostic evaluation and medical management of adolescents and young adults presenting with systemic inflammatory response during the unfolding pandemic of COVID-19.


Subject(s)
COVID-19/epidemiology , Disease Outbreaks , Electronic Nicotine Delivery Systems , Lung Injury/chemically induced , Systemic Inflammatory Response Syndrome/epidemiology , Vaping/adverse effects , Female , Humans , Lung Injury/epidemiology , Male , SARS-CoV-2 , Young Adult
8.
Am J Physiol Lung Cell Mol Physiol ; 319(4): L585-L595, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-991951

ABSTRACT

In 2019, the United States experienced the emergence of the vaping-associated lung injury (VALI) epidemic. Vaping is now known to result in the development and progression of severe lung disease in the young and healthy. Lack of regulation on electronic cigarettes in the United States has resulted in over 2,000 patients and 68 deaths. We examine the clinical representation of VALI and the delve into the scientific evidence of how deadly exposure to electronic cigarettes can be. E-cigarette vapor is shown to affect numerous cellular processes, cellular metabolism, and cause DNA damage (which has implications for cancer). E-cigarette use is associated with a higher risk of developing crippling lung conditions such as chronic obstructive pulmonary disease (COPD), which would develop several years from now, increasing the already existent smoking-related burden. The role of vaping and virus susceptibility is yet to be determined; however, vaping can increase the virulence and inflammatory potential of several lung pathogens and is also linked to an increased risk of pneumonia. As it has emerged for cigarette smoking, great caution should also be given to vaping in relation to SARS-CoV-2 infection and the COVID-19 pandemic. Sadly, e-cigarettes are continually promoted and perceived as a safer alternative to cigarette smoking. E-cigarettes and their modifiable nature are harmful, as the lungs are not designed for the chronic inhalation of e-cigarette vapor. It is of interest that e-cigarettes have been shown to be of no help with smoking cessation. A true danger lies in vaping, which, if ignored, will lead to disastrous future costs.


Subject(s)
E-Cigarette Vapor/toxicity , Lung Diseases, Interstitial/epidemiology , Lung Injury/epidemiology , Pulmonary Disease, Chronic Obstructive/epidemiology , Vaping/adverse effects , Adolescent , Betacoronavirus , COVID-19 , Coronavirus Infections/pathology , Disease Susceptibility/chemically induced , Electronic Nicotine Delivery Systems/statistics & numerical data , Female , Humans , Lung Diseases, Interstitial/chemically induced , Lung Injury/chemically induced , Lung Injury/mortality , Male , Middle Aged , Pandemics , Pneumonia/epidemiology , Pneumonia, Viral/pathology , Pulmonary Disease, Chronic Obstructive/chemically induced , Pulmonary Disease, Chronic Obstructive/mortality , SARS-CoV-2 , Smoking Cessation/methods , United States/epidemiology , Vaping/epidemiology , Vaping/mortality
10.
J Am Heart Assoc ; 9(18): e017368, 2020 09 15.
Article in English | MEDLINE | ID: covidwho-748837

ABSTRACT

E-cigarette or vaping product use-associated lung injury was recognized in the United States in the summer of 2019 and is typified by acute respiratory distress, shortness of breath, chest pain, cough, and fever, associated with vaping. It can mimic many of the manifestations of coronavirus disease 2019 (COVID-19). Some investigators have suggested that E-cigarette or vaping product use-associated lung injury was due to tetrahydrocannabinol or vitamin E acetate oil mixed with the electronic cigarette liquid. In experimental rodent studies initially designed to study the effect of electronic cigarette use on the cardiovascular system, we observed an E-cigarette or vaping product use-associated lung injury-like condition that occurred acutely after use of a nichrome heating element at high power, without the use of tetrahydrocannabinol, vitamin E, or nicotine. Lung lesions included thickening of the alveolar wall with foci of inflammation, red blood cell congestion, obliteration of alveolar spaces, and pneumonitis in some cases; bronchi showed accumulation of fibrin, inflammatory cells, and mucus plugs. Electronic cigarette users should be cautioned about the potential danger of operating electronic cigarette units at high settings; the possibility that certain heating elements may be deleterious; and that E-cigarette or vaping product use-associated lung injury may not be dependent upon tetrahydrocannabinol, vitamin E, or nicotine.


Subject(s)
Dronabinol/toxicity , E-Cigarette Vapor/toxicity , Electronic Nicotine Delivery Systems , Lung Injury/chemically induced , Lung/drug effects , Pneumonia/chemically induced , Vaping/adverse effects , Vitamin E/toxicity , Animals , Inhalation Exposure , Lung/pathology , Lung Injury/pathology , Models, Animal , Oils , Pneumonia/pathology , Rats , Risk Assessment
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