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1.
Monaldi Arch Chest Dis ; 90(3)2020 Sep 02.
Artigo em Inglês | MEDLINE | ID: mdl-32875776

RESUMO

Lung Ultrasound (LUS) is regarded to be potentially useful to diagnose lung injury in older adults living in nursing homes with suspected COVID-19 pneumonia. We aimed at evaluating presence lung injury among senior nursing home residents by LUS performed with portable wireless scanner echography. The study population consisted of 150 residents with a mean age of 88 years (85% female) residing in 12 nursing homes in Northern Italy. Subjects had to have a history of recent onset of symptoms compatible with COVID-19 pneumonia or have been exposed to the contagion of patients carrying the disease. COVID-19 testing was performed with SARS-CoV-2 nasal-pharyngeal (NP) swabs. Positive subjects to LUS scanning were considered those with non-coascelent B-lines in >3 zones, coalescent B-lines in >3 zones and with iperdensed patchy non-consolidated lungs. Sixty-three percent had positive NP testing and 65% had LUS signs of pulmonary injury. LUS had a sensitivity of 79% in predicting positive NP testing. Sixteen percent of residents tested negative for SARSCoV-2 carried the signs of COVID-19 lung injury at LUS. There were 92 patients (61%) with current or recent symptoms.Positivity to LUS scanning was reported in 73% of residents with symptoms, while it was 53% in those without (P=0.016). A positive NP testing was observed in 66% of residents with symptoms and in 57% of those without (P=0.27). We conclude that assessment of LUS by portable wireless scanner echography can be profitability utilized to diagnose lung injury among senior nursing home residents with or without symptoms compatible with COVID-19 pneumonia.


Assuntos
Infecções por Coronavirus , Lesão Pulmonar/diagnóstico por imagem , Pandemias , Pneumonia Viral/diagnóstico , Testes Imediatos , Ultrassonografia , Idoso de 80 Anos ou mais , Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/fisiopatologia , Feminino , Instituição de Longa Permanência para Idosos/estatística & dados numéricos , Humanos , Itália/epidemiologia , Masculino , Casas de Saúde/estatística & dados numéricos , Pneumonia Viral/epidemiologia , Pneumonia Viral/etiologia , Pneumonia Viral/fisiopatologia , Valor Preditivo dos Testes , Sensibilidade e Especificidade , Ultrassonografia/instrumentação , Ultrassonografia/métodos , Tecnologia sem Fio
2.
Dtsch Arztebl Int ; 117(29-30): 500-506, 2020 07 20.
Artigo em Inglês | MEDLINE | ID: mdl-32865490

RESUMO

BACKGROUND: The histomorphological changes of lung damage in severe coronavirus disease 2019 (COVID-19) have not yet been adequately characterized. In this article, we describe the sequence of pathological changes in COVID-19 and discuss the implications for approaches to treatment. METHODS: Standardized autopsies were performed on thirteen patients who had died of COVID-19. The findings were analyzed together with clinical data from the patients' medical records. RESULTS: Most (77%) of the deceased patients were men. Their median age at death was 78 years (range, 41-90). Most of them had major pre-existing chronic diseases, most commonly arterial hypertension. The autopsies revealed characteristic COVID-19-induced pathological changes in the lungs, which were regarded as the cause of death in most patients. The main histological finding was sequential alveolar damage, apparently due in large measure to focal capillary microthrombus formation. Alveolar damage leads to the death of the patient either directly or by the induction of pulmonary parenchymal fibrosis. Diffuse lung damage was seen exclusively in invasively ventilated patients. CONCLUSION: Autopsies are crucial for the systematic assessment of new diseases such as COVID-19: they provide a basis for further investigations of disease mechanisms and for the devising of potentially effective modes of treatment. The autopsy findings suggest that focal damage of the microvascular pulmonary circulation is a main mechanism of lethal lung disease due to the SARS-CoV-2 virus. It may also be a cause of persistent lung damage in patients who recover from severe COVID-19.


Assuntos
Infecções por Coronavirus/complicações , Lesão Pulmonar/patologia , Lesão Pulmonar/virologia , Pneumonia Viral/complicações , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Pandemias , Índice de Gravidade de Doença
3.
Medicine (Baltimore) ; 99(33): e21685, 2020 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-32872040

RESUMO

Chest injuries are common and inevitable complications of chest compressions during cardiopulmonary resuscitation (CPR). This study aimed to investigate lung parenchymal and thoracic skeletal injuries after CPR by using computed tomography (CT) and to analyze the correlation between the duration of CPR and related complications.We examined 43 non-traumatic cardiac arrest patients who were successfully resuscitated after CPR and had chest CT scans within 24 hours of CPR. Lung parenchymal injuries were assessed by quantifying the lung contusion score (LCS) on the CT images, and each skeletal injury was investigated by classifying the location and the distribution. Other CPR-related chest injuries were also described, such as pleural effusion/hemothorax, pneumothorax, and retrosternal hematoma. Statistical analysis was conducted to determine whether the duration of CPR was correlated with each complication.Lung contusions were found in all of the patients (mean LCS: 22, range: 5-47). The distribution of lung contusions were predominantly in the bilateral dependent portions of the lungs (41 patients). All of the rib fractures occurred in the anterior arc (43 patients), and the sternal fractures occurred predominantly in the mid-sternal body (31 patients). In patients younger than 70 years old, the number of rib fractures significantly increased among those who underwent CPR for more than 25 minutes compared to those who received CPR for less than 25 minutes (median 4.5 vs 9; mean 8.3 vs 5.6 per person, respectively; P = .035). The risk of sternal fracture tended to be higher for patients who received CPR for more than 10 minutes compared to those who received CPR for less than 10 minutes (odds ratio: 3.60; 95% confidence interval: 0.86-15.06; P = .079). However, there was no statistically significant correlation between the duration of CPR and LCS or other CPR-related chest injuries.The duration of CPR was associated with the number of rib fractures and the occurrence of sternal fractures, but it did not affect the extent of CPR-related lung contusions or other CPR-related chest injuries. All of the rib fractures occurred in the anterior arc, while the sternal fractures occurred predominantly in the mid-sternal body. However, since this study was conducted in a single institution, the number of patients included was relatively small, thus limiting the statistical analysis.


Assuntos
Reanimação Cardiopulmonar/efeitos adversos , Lesão Pulmonar/diagnóstico por imagem , Fraturas das Costelas/diagnóstico por imagem , Esterno/diagnóstico por imagem , Adolescente , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Reanimação Cardiopulmonar/métodos , Criança , Feminino , Humanos , Lesão Pulmonar/etiologia , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada Multidetectores , Estudos Retrospectivos , Fraturas das Costelas/etiologia , Esterno/lesões , Fatores de Tempo , Adulto Jovem
4.
Monaldi Arch Chest Dis ; 90(3)2020 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-32885626

RESUMO

'Tree-in-bud' (TIB) appearance in computed tomography (CT) chest is most commonly a manifestation of infection. We here describe an unusual cause of TIB during the COVID-19 pandemic. A young male patient who had a history of fever, cough, and respiratory distress presented in the emergency department. As these symptoms matched with coronavirus infection, the COVID-19 test was done, which was found negative. He was then moved to the intensive care unit where he developed severe acute respiratory distress syndrome and was put on mechanical ventilation. Further workup did not reveal any source of infection, as all his cultures were negative, but his CT chest showed a tree-in-bud appearance. After obtaining a detailed history from his friends, the patient was found a chronic abuser of inhaled cocaine and treated with intravenous steroids. Subsequently, he was weaned from the ventilator and discharged from the intensive care unit after becoming asymptomatic.


Assuntos
Fumar Cocaína/efeitos adversos , Transtornos Relacionados ao Uso de Cocaína/diagnóstico , Infecções por Coronavirus/diagnóstico , Lesão Pulmonar/diagnóstico por imagem , Pulmão/diagnóstico por imagem , Pneumonia Viral/diagnóstico , Síndrome do Desconforto Respiratório do Adulto/diagnóstico por imagem , Adulto , Betacoronavirus , Transtornos Relacionados ao Uso de Cocaína/complicações , Diagnóstico Diferencial , Glucocorticoides/uso terapêutico , Humanos , Lesão Pulmonar/etiologia , Lesão Pulmonar/terapia , Masculino , Metilprednisolona/uso terapêutico , Pandemias , Respiração Artificial , Síndrome do Desconforto Respiratório do Adulto/etiologia , Síndrome do Desconforto Respiratório do Adulto/terapia , Tomografia Computadorizada por Raios X
5.
Zhonghua Jie He He Hu Xi Za Zhi ; 43(9): 772-777, 2020 Sep 12.
Artigo em Chinês | MEDLINE | ID: mdl-32894911

RESUMO

Objective: To explore the therapeutic effect of carnosine and dexamethasone in lung injury caused by seawater drowning. Methods: The in vitro experiments with A549 cells were divided into 5 groups: blank control group (C), seawater injury group (S), seawater injury+dexamethasone treatment group (S+D), seawater injury+carnosine treatment group (S+C), seawater injury dexamethasone and carnosine combined therapy(S+D+C) group. The optimal therapeutic dose of drugs for the treatment of seawater drowning lung injury was tested in vitro. Based on the optimal dose, the levels of TNF-α and IL-6 in each group at different time points were detected at the cell level by ELISA. The level of apoptosis was detected by flow cytometry. The in vivo experiments with SD rats were randomly divided into 5 groups (n=8 each): blank control group (RC),seawater drowning injury group (RS),seawater drowning injury+dexamethasone treatment group (RSD),seawater drowning injury+carnosine treatment group (RSC),seawater drowning injury+dexamethasone+carnosine combined treatment group (RSDC). The animal model with seawater inhalation acute lung injury was made by intratracheal infusion (4 ml/kg). The pathological changes of the lungs were observed. The expression of superoxide dismutase (SOD) in each group was detected by Western blot. Results: The results of in vitro experiments showed significant increase of apoptosis after seawater injury. The normal cell rate in group C was 98.3% while the apoptosis rate was 1.7%. The normal cell in group S was 18.8%, and the apoptosis rate was 81% (P<0.01). TNF-α and IL-6 levels in group S increased to 180.25 ng/L and 61.56 ng/L, respectively, which were statistically significant compared with group C (P<0.01). After drug protection, apoptosis was reduced in S+D group, S+C group and S+D+C group, with apoptosis rates of 65.4%, 70.9% and 42.6%, respectively. The contents of TNF-α and IL-6 also decreased in the S+D+C group (P<0.01). The results of in vivo experiments showed obvious lung injury and disordered lung tissue structures in the RS group at 4 h after modeling. There was hemorrhage in the pulmonary interstitium and a large number of inflammatory cells. Results of western blot showed that the expression of SOD increased in the RS group. Compared with RS group, the treatment alleviated acute lung injury and decreased the expression level of SOD in RSD, RSC and RSDC groups (P<0.01). Conclusion: Dexamethasone and carnosine reduced the influence of seawater inhalation on the lung in the rat model. The positive effect of combination of these two drugs on lung injury caused by seawater inhalation was stronger than a single drug.


Assuntos
Afogamento , Lesão Pulmonar , Animais , Carnosina , Dexametasona , Pulmão , Ratos , Ratos Sprague-Dawley , Água do Mar , Fator de Necrose Tumoral alfa
6.
Nan Fang Yi Ke Da Xue Xue Bao ; 40(7): 930-935, 2020 Jul 30.
Artigo em Chinês | MEDLINE | ID: mdl-32895152

RESUMO

OBJECTIVE: To assess the effect of neutralizing CD96 on natural killer (NK) cell functions in mice with pulmonary Chlamydia muridarum infection and explore the possible mechanism. METHODS: Male BALB/c mice were randomly divided into infection group (Cm group), anti-CD96 treatment group (anti-CD96 group) and control group (n=5). In the former two groups, C. muridarum was inoculated via intranasal administration to establish mouse models of pulmonary C. muridarum infection, and the mice in the control group received intranasal administration of the inhalation buffer. In anti-CD96 group, the mice were injected with anti-CD96 antibody intraperitoneally at the dose of 250 µg every 3 days after the infection; the mice in Cm group received intraperitoneal injections of saline. The body weight of the mice was recorded daily. The mice were sacrificed 5 days after C. muridarum infection, and CD96 expression was detected by quantitative real-time PCR and Western blotting. HE staining and pathological scores were used to evaluate pneumonia of the mice. The inclusion body forming units (IFUs) were detected in the lung tissue homogenates to assess lung tissue chlamydia load. Flow cytometry and ELISA were used to assess the capacity of the lung NK cells to produce interferon-γ (IFN-γ) and regulate macrophages and Th1 cells. RESULTS: C. muridarum infection inhibited CD96 expression in NK cells of the mice. Compared with those in Cm group, the mice in antiCD96 mice showed significantly milder lung inflammation (P < 0.05) and reduced chlamydia load in the lung tissue (P < 0.05). Neutralizing CD96 with anti-CD96 significantly enhanced IFN-γ secretion by the NK cells (P < 0.05) and augmented the immunoregulatory effect of the NK cells shown by enhanced responses of the lung macrophages (P < 0.05) and Th1 cells (P < 0.05). CONCLUSIONS: Inhibition of CD96 alleviates pneumonia in C. muridarum-infected mice possibly by enhancing IFN-γ secretion by NK cells and augmenting the immunoregulatory effect of the NK cells on innate and adaptive immunity.


Assuntos
Infecções por Chlamydia , Chlamydia muridarum , Células Matadoras Naturais , Lesão Pulmonar , Animais , Antígenos CD , Interferon gama , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL
7.
Ann Am Thorac Soc ; 17(8): 918-921, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32735170

RESUMO

Amid efforts to care for the large number of patients with coronavirus disease (COVID-19), there has been considerable speculation about whether the lung injury seen in these patients is different than acute respiratory distress syndrome from other causes. One idea that has garnered considerable attention, particularly on social media and in free open-access medicine, is the notion that lung injury due to COVID-19 is more similar to high-altitude pulmonary edema (HAPE). Drawing on this concept, it has also been proposed that treatments typically employed in the management of HAPE and other forms of acute altitude illness-pulmonary vasodilators and acetazolamide-should be considered for COVID-19. Despite some similarities in clinical features between the two entities, such as hypoxemia, radiographic opacities, and altered lung compliance, the pathophysiological mechanisms of HAPE and lung injury due to COVID-19 are fundamentally different, and the entities cannot be viewed as equivalent. Although of high utility in the management of HAPE and acute mountain sickness, systemically delivered pulmonary vasodilators and acetazolamide should not be used in the treatment of COVID-19, as they carry the risk of multiple adverse consequences, including worsened ventilation-perfusion matching, impaired carbon dioxide transport, systemic hypotension, and increased work of breathing.


Assuntos
Doença da Altitude , Infecções por Coronavirus , Hipertensão Pulmonar , Pandemias , Pneumonia Viral , Síndrome do Desconforto Respiratório do Adulto , Acetazolamida/farmacologia , Doença da Altitude/fisiopatologia , Doença da Altitude/terapia , Betacoronavirus/isolamento & purificação , Inibidores da Anidrase Carbônica/farmacologia , Infecções por Coronavirus/complicações , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/terapia , Humanos , Hipertensão Pulmonar/fisiopatologia , Hipertensão Pulmonar/terapia , Lesão Pulmonar/etiologia , Lesão Pulmonar/fisiopatologia , Lesão Pulmonar/terapia , Nifedipino/farmacologia , Pneumonia Viral/fisiopatologia , Pneumonia Viral/terapia , Síndrome do Desconforto Respiratório do Adulto/etiologia , Síndrome do Desconforto Respiratório do Adulto/fisiopatologia , Síndrome do Desconforto Respiratório do Adulto/terapia , Vasodilatadores/farmacologia
8.
Rev Med Suisse ; 16(703): 1511-1517, 2020 Aug 26.
Artigo em Francês | MEDLINE | ID: mdl-32852174

RESUMO

Vaping associated lung injury is defined by a compatible clinical and radiological picture in a patient who smoked an electronic cigarette in the previous 90 days and after exclusion of other conditions, -notably infections. The severity varies from mild symptoms to -hypoxemic respiratory failure eventually leading to death. The clinical presentation includes general, respiratory and gastrointestinal symptoms. Laboratory findings show leukocytosis with elevated -inflammatory markers. Radiological features consist of bilateral ground-glass opacities with or without consolidation. Broncho-alveolar lavage can be used to refine the diagnosis and exclude an infection. Corticosteroids are at the center of therapy. Antibiotics are often given because of the initial suspicion of infection.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Pneumopatias , Lesão Pulmonar , Vaping , Humanos , Lesão Pulmonar/etiologia , Tomografia Computadorizada por Raios X , Vaping/efeitos adversos
10.
Virol J ; 17(1): 125, 2020 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-32811514

RESUMO

We recently reported the development of the first African green monkey (AGM) model for COVID-19 based on a combined liquid intranasal (i.n.) and intratracheal (i.t.) exposure to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we followed up on this work by assessing an i.n. particle only route of exposure using the LMA mucosal atomization device (MAD). Six AGMs were infected with SARS-CoV-2; three animals were euthanized near the peak stage of virus replication (day 5) and three animals were euthanized during the early convalescence period (day 34). All six AGMs supported robust SARS-CoV-2 replication and developed respiratory disease. Evidence of coagulation dysfunction as noted by a transient increases in aPTT and circulating levels of fibrinogen was observed in all AGMs. The level of SARS-CoV-2 replication and lung pathology was not quite as pronounced as previously reported with AGMs exposed by the combined i.n. and i.t. routes; however, SARS-CoV-2 RNA was detected in nasal swabs of some animals as late as day 15 and rectal swabs as late as day 28 after virus challenge. Of particular importance to this study, all three AGMs that were followed until the early convalescence stage of COVID-19 showed substantial lung pathology at necropsy as evidenced by multifocal chronic interstitial pneumonia and increased collagen deposition in alveolar walls despite the absence of detectable SARS-CoV-2 in any of the lungs of these animals. These findings are consistent with human COVID-19 further demonstrating that the AGM faithfully reproduces the human condition.


Assuntos
Betacoronavirus/patogenicidade , Infecções por Coronavirus/patologia , Infecções por Coronavirus/virologia , Pneumonia Viral/patologia , Pneumonia Viral/virologia , Animais , Betacoronavirus/imunologia , Chlorocebus aethiops , Convalescença , Infecções por Coronavirus/sangue , Modelos Animais de Doenças , Feminino , Lesão Pulmonar/patologia , Lesão Pulmonar/virologia , Mucosa Nasal/virologia , Pandemias , Pneumonia Viral/sangue , Soroconversão , Carga Viral , Eliminação de Partículas Virais
11.
Nursing ; 50(9): 55-59, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32826679

RESUMO

Youth e-cigarette use was declared a national epidemic in 2018. This article discusses e-cigarette- or vaping-associated lung injury (EVALI) and highlights the unique role nurses can have as advocates, patient educators, and champions of health promotion and disease prevention for their patients and families.


Assuntos
Epidemias , Papel do Profissional de Enfermagem , Vaping/epidemiologia , Adolescente , Promoção da Saúde , Humanos , Lesão Pulmonar/epidemiologia , Lesão Pulmonar/prevenção & controle , Estados Unidos/epidemiologia
12.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 32(7): 890-893, 2020 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-32788032

RESUMO

Mechanical ventilation (MV) is a common way of respiratory support during general anesthesia and in critically ill patients. Recently people gradually realize that MV is a double-edged sword, which itself can also induce or aggravate lung injury as a damage factor, that is, ventilator induced lung injury (VILI). Current researches on the mechanisms of VILI have changed from traditional barotrauma/volutrauma/atelectasis to biotrauma. In particular, it should be noted that MV can not only cause damage to the lung, but also to the distant organs. This article reviews current researches on the molecular mechanisms of VILI, updates our understanding of them, and provides a theoretical basis for the prevention and treatment of VILI and distant organ damage.


Assuntos
Lesão Pulmonar , Atelectasia Pulmonar , Lesão Pulmonar Induzida por Ventilação Mecânica , Humanos , Pulmão , Respiração Artificial
13.
Cell Transplant ; 29: 963689720952089, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32830527

RESUMO

The coronavirus disease 2019 (COVID-19) pandemic, originating from Wuhan, China, is known to cause severe acute respiratory symptoms. The occurrence of a cytokine storm in the lungs is a critical step in the disease pathogenesis, as it causes pathological lesions, pulmonary edema, and acute respiratory distress syndrome, potentially resulting in death. Currently, there is no effective treatment that targets the cytokine storm and helps regenerate the damaged tissue. Mesenchymal stem cells (MSCs) are known to act as anti-inflammatory/immunomodulatory candidates and activate endogenous regeneration. As a result, MSC therapy is a potential treatment approach for COVID-19. Intravenous injection of clinical-grade MSCs into COVID-19 patients can induce an immunomodulatory response along with improved lung function. Dental pulp stem cells (DPSCs) are considered a potential source of MSCs for immunomodulation, tissue regeneration, and clinical application. Although some current clinical trials have treated COVID-19 patients with DPSCs, this therapy has not been approved. Here, we review the potential use of DPSCs and their significance in the development of a therapy for COVID-19.


Assuntos
Infecções por Coronavirus/terapia , Polpa Dentária/citologia , Imunomodulação , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/imunologia , Pneumonia Viral/terapia , Betacoronavirus/imunologia , Ensaios Clínicos como Assunto , Infecções por Coronavirus/imunologia , Citocinas/imunologia , Polpa Dentária/imunologia , Humanos , Imunoterapia/métodos , Inflamação/imunologia , Inflamação/terapia , Pulmão/imunologia , Pulmão/fisiologia , Lesão Pulmonar/imunologia , Lesão Pulmonar/terapia , Células-Tronco Mesenquimais/citologia , Pandemias , Pneumonia Viral/imunologia , Regeneração
14.
Orv Hetil ; 161(31): 1281-1285, 2020 08.
Artigo em Húngaro | MEDLINE | ID: mdl-32750017

RESUMO

The electronic cigarette and vaping associated lung injury (EVALI) syndrome was first described in the United States (US) and was presumably strongly associated with cannabinoid vaping and exposure to vitamin E acetate, an oily additive used to dilute/cut cannabinoids vape liquids. As the case numbers were relatively low (epidemiologically) and the available data was inconsistent, several assumptions were made to explain the phenomenon. The lack of standardization of sampling, the self-reported, inhomogeneous user habits, the huge number of potential etiologies, and certain trade/legal loopholes (such as online distribution, black market penetration, or the inefficient regulatory control regarding the quantity and/or quality of ingredients/cutting agents) might question the validity of the data and the consequent conclusions. Furthermore, an interesting but by no means negligible question is the fact why no EVALI cases have been registered outside the US when electronic cigarettes and vapes have become increasingly popular worldwide. The present review seeks to answer whether vitamin E acetate is indeed the cause of this complex syndrome, what potentially non-healthcare related factors might have contributed to the rapid increase and decline in EVALI cases, and last but not least the minimum standards of safe vaping (as potential for drug delivery route for cannbinoids). Orv Hetil. 2020; 161(31): 1281-1285.


Assuntos
Canabinoides/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Vaping/efeitos adversos , Canabinoides/administração & dosagem , Humanos , Autorrelato , Estados Unidos , Vitamina E
15.
Crit Care ; 24(1): 494, 2020 08 10.
Artigo em Inglês | MEDLINE | ID: mdl-32778136

RESUMO

Deterioration of lung function during the first week of COVID-19 has been observed when patients remain with insufficient respiratory support. Patient self-inflicted lung injury (P-SILI) is theorized as the responsible, but there is not robust experimental and clinical data to support it. Given the limited understanding of P-SILI, we describe the physiological basis of P-SILI and we show experimental data to comprehend the role of regional strain and heterogeneity in lung injury due to increased work of breathing.In addition, we discuss the current approach to respiratory support for COVID-19 under this point of view.


Assuntos
Infecções por Coronavirus/fisiopatologia , Progressão da Doença , Lesão Pulmonar/fisiopatologia , Pneumonia Viral/fisiopatologia , Trabalho Respiratório/fisiologia , Infecções por Coronavirus/terapia , Cuidados Críticos , Humanos , Lesão Pulmonar/etiologia , Pandemias , Pneumonia Viral/terapia , Ensaios Clínicos Controlados Aleatórios como Assunto , Respiração Artificial
16.
Am J Physiol Lung Cell Mol Physiol ; 319(2): L325-L336, 2020 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-32639866

RESUMO

A dysregulation of the renin-angiotensin system (RAS) has been involved in the genesis of lung injury and acute respiratory distress syndrome from different causes, including several viral infections. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of pneumocytes, the hallmark of the pandemic coronavirus disease 2019 (COVID-19) involving both alveolar interstitium and capillaries, is linked to angiotensin-converting enzyme 2 (ACE2) binding and its functional downregulation. ACE2 is a key enzyme for the balance between the two main arms of the RAS: the ACE/angiotensin (Ang) II/Ang II type 1 receptor axis ("classic RAS") and the ACE2/Ang(1-7)/Mas receptor (MasR) axis ("anti-RAS"). The ACE2 downregulation, as a result of SARS-coronaviruses binding, enhances the classic RAS, leading to lung damage and inflammation with leaky pulmonary blood vessels and fibrosis, when the attenuation mediated by the anti-RAS arm is reduced. ACE inhibitors (ACE-I) and Ang II type 1 receptor blockers (ARB), effective in cardiovascular diseases, were found to prevent and counteract acute lung injury in several experimental models by restoring the balance between these two opposing arms. The evidence of RAS arm disequilibrium in COVID-19 and the hypothesis of a beneficial role of RAS modulation supported by preclinical and clinical studies are the focus of the present review. Preclinical and clinical studies on drugs balancing RAS arms might be the right way to counter COVID-19.


Assuntos
Antagonistas de Receptores de Angiotensina/farmacologia , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Infecções por Coronavirus/patologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/patologia , Alvéolos Pulmonares/patologia , Síndrome do Desconforto Respiratório do Adulto/patologia , Células Epiteliais Alveolares/virologia , Betacoronavirus/metabolismo , Infecções por Coronavirus/tratamento farmacológico , Regulação para Baixo , Humanos , Lesão Pulmonar/tratamento farmacológico , Lesão Pulmonar/prevenção & controle , Lesão Pulmonar/virologia , Pandemias , Pneumonia Viral/tratamento farmacológico , Alvéolos Pulmonares/irrigação sanguínea , Alvéolos Pulmonares/virologia , Receptores de Angiotensina/efeitos dos fármacos , Sistema Renina-Angiotensina/efeitos dos fármacos , Síndrome do Desconforto Respiratório do Adulto/virologia
17.
Nat Commun ; 11(1): 3559, 2020 07 16.
Artigo em Inglês | MEDLINE | ID: mdl-32678092

RESUMO

The cell type specific sequences of transcriptional programs during lung regeneration have remained elusive. Using time-series single cell RNA-seq of the bleomycin lung injury model, we resolved transcriptional dynamics for 28 cell types. Trajectory modeling together with lineage tracing revealed that airway and alveolar stem cells converge on a unique Krt8 + transitional stem cell state during alveolar regeneration. These cells have squamous morphology, feature p53 and NFkB activation and display transcriptional features of cellular senescence. The Krt8+ state appears in several independent models of lung injury and persists in human lung fibrosis, creating a distinct cell-cell communication network with mesenchyme and macrophages during repair. We generated a model of gene regulatory programs leading to Krt8+ transitional cells and their terminal differentiation to alveolar type-1 cells. We propose that in lung fibrosis, perturbed molecular checkpoints on the way to terminal differentiation can cause aberrant persistence of regenerative intermediate stem cell states.


Assuntos
Células Epiteliais Alveolares/metabolismo , Queratina-8/metabolismo , Alvéolos Pulmonares/fisiologia , Fibrose Pulmonar/patologia , Regeneração , Células-Tronco/metabolismo , Células Epiteliais Alveolares/citologia , Animais , Comunicação Celular , Modelos Animais de Doenças , Feminino , Perfilação da Expressão Gênica , Humanos , Queratina-8/genética , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Camundongos , Camundongos Endogâmicos C57BL , Alvéolos Pulmonares/citologia , Fibrose Pulmonar/metabolismo , Análise de Célula Única , Células-Tronco/citologia
18.
Respir Res ; 21(1): 201, 2020 Jul 29.
Artigo em Inglês | MEDLINE | ID: mdl-32727465

RESUMO

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a new respiratory and systemic disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The purpose of the present study was to investigate the association between cytokine profiles and lung injury in COVID-19 pneumonia. METHODS: This retrospective study was conducted in COVID-19 patients. Demographic characteristics, symptoms, signs, underlying diseases, and laboratory data were collected. The patients were divided into COVID-19 with pneumonia and without pneumonia. CT severity score and PaO2/FiO2 ratio were used to assess lung injury. RESULTS: 106 patients with 12 COVID-19 without pneumonia and 94 COVID-19 with pneumonia were included. Compared with COVID-19 without pneumonia, COVID-19 with pneumonia had significantly higher serum interleukin (IL)-2R, IL-6, and tumor necrosis factor (TNF)-α. Correlation analysis showed that CT severity score and PaO2/FiO2 were significantly correlated with age, presence of any coexisting disorder, lymphocyte count, procalcitonin, IL-2R, and IL-6. In multivariate analysis, log IL6 was the only independent explanatory variables for CT severity score (ß = 0.397, p < 0.001) and PaO2/FiO2 (ß = - 0.434, p = 0.003). CONCLUSIONS: Elevation of circulating cytokines was significantly associated with presence of pneumonia in COVID-19 and the severity of lung injury in COVID-19 pneumonia. Circulating IL-6 independently predicted the severity of lung injury in COVID-19 pneumonia.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Citocinas/sangue , Lesão Pulmonar/etiologia , Pneumonia Viral/complicações , Adulto , Biomarcadores/sangue , Infecções por Coronavirus/sangue , Infecções por Coronavirus/epidemiologia , Feminino , Humanos , Lesão Pulmonar/sangue , Lesão Pulmonar/diagnóstico , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/sangue , Pneumonia Viral/diagnóstico , Pneumonia Viral/epidemiologia , Estudos Retrospectivos , Tomografia Computadorizada por Raios X
20.
Life Sci ; 257: 118042, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32621926

RESUMO

AIMS: To investigate the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomes in smoke inhalation lung injury. MAIN METHODS: In this study, we initially isolated exosomes from BMSCs and identified them by western blot and transmission electron microscopy. BMSC-derived exosomes were then used to treat in vitro and in vivo models of smoke inhalation lung injury. Pathologic alterations in lung tissue, the levels of inflammatory factors and apoptosis-related factors, and the expression of HMGB1 and NF-κB were determined to evaluate the therapeutic effect of BMSC-derived exosomes. KEY FINDINGS: We found that BMSC-derived exosomes could alleviate the injury caused by smoke inhalation. Smoke inhalation increased the levels of inflammatory factors and apoptosis-related factors and the expression of HMGB1 and NF-κB, and these increases were reversed by BMSC-derived exosomes. HMGB1 overexpression abrogated the exosome-induced decreases in inflammatory factors, apoptosis-related factors and NF-κB. SIGNIFICANCE: Collectively, these results indicate that BMSC-derived exosomes can effectively alleviate smoke inhalation lung injury by inhibiting the HMGB1/NF-κB pathway, suggesting that exosome, a noncellular therapy, is a potential therapeutic strategy for inhalation lung injury.


Assuntos
Exossomos/metabolismo , Células-Tronco Mesenquimais/metabolismo , Lesão por Inalação de Fumaça/metabolismo , Animais , Apoptose/efeitos dos fármacos , Proteína HMGB1/metabolismo , Inflamação/patologia , Lesão Pulmonar/metabolismo , Masculino , Transplante de Células-Tronco Mesenquimais/métodos , NF-kappa B/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais , Fumaça/efeitos adversos , Lesão por Inalação de Fumaça/terapia
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