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1.
Medicine (Baltimore) ; 100(31): e26842, 2021 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-34397856

RESUMO

INTRODUCTION: Opportunistic infection with multiple pathogens currently has become less uncommon since the application of immunosuppressant or corticosteroid in non- Human immunodeficiency virus patients. However, the clinical diagnosis of the co-infection remains difficult since the uncertainty and deficiency of the microbiologic testing methods. PATIENT CONCERNS: A 66-year-old male patient was admitted to our hospital with chest stuffiness, shortness of breath and elevated body temperature. DIAGNOSIS: He was diagnosed with the co-infection of Pneumocystis jiroveci and cytomegalovirus by metagenomic next-generation sequencing of bronchoalveolar lavage fluid after bronchoscopy. INTERVENTIONS: The patient was empirically treated with broad-spectrum antibiotics, trimethoprim/ sulfamethoxazole and ganciclovir in the beginning of the admission. OUTCOMES: The condition of this patient was not improved even with the intervention at the early stage of the disease. His family requested discharge after 24 inpatient days. LESSONS: This case highlights the application of metagenomic next-generation sequencing in the clinical diagnosis of pulmonary co-infection. Suitable prophylaxis, necessary clinical awareness and accurate diagnosis are indispensable for immunocompromised patients with pulmonary infection.


Assuntos
Líquido da Lavagem Broncoalveolar/microbiologia , Infecções por Citomegalovirus , Citomegalovirus , Ganciclovir/administração & dosagem , Pneumocystis carinii , Pneumonia por Pneumocystis , Combinação Trimetoprima e Sulfametoxazol/administração & dosagem , Idoso , Anti-Infecciosos/administração & dosagem , Broncoscopia/métodos , Coinfecção/diagnóstico , Coinfecção/microbiologia , Citomegalovirus/genética , Citomegalovirus/isolamento & purificação , Infecções por Citomegalovirus/diagnóstico , Infecções por Citomegalovirus/fisiopatologia , Infecções por Citomegalovirus/terapia , Sequenciamento de Nucleotídeos em Larga Escala/métodos , Humanos , Masculino , Metagenômica/métodos , Metilprednisolona/uso terapêutico , Síndrome Nefrótica/tratamento farmacológico , Pneumocystis carinii/genética , Pneumocystis carinii/isolamento & purificação , Pneumonia por Pneumocystis/diagnóstico , Pneumonia por Pneumocystis/fisiopatologia , Pneumonia por Pneumocystis/terapia
2.
Artigo em Inglês | MEDLINE | ID: mdl-34194525

RESUMO

Asthma has long been considered a disease of airway inflammation. The excessive or prolonged production of inflammatory mediators can result in airway remodeling and severe clinical syndromes such as dyspnea or even apnea. Therefore, pharmaceutical intervention is required to restrain the excessive release of such inflammatory mediators in control of asthma. Novel therapeutics and mechanistic insight are sought for the management of this chronic inflammatory disease. Andrographolide (AG) is a type of diterpenoid ester compound and is reported to demonstrate multiple properties such as antioxidation and anti-inflammation. However, the anti-inflammatory capacity of AG by regulating immunologic function in airway of asthma has not been fully studied to date. Therefore, this study investigates whether AG is capable of suppressing the inflammatory response of asthma in OVA-stimulated mice and the mechanism by which this is achieved. Animals were randomly divided into 4 groups: control group, OVA model group, OVA + AG (0.1 mg/ml) group, and OVA + dimethylsulfoxide (DMSO) group. The serum, BALF, and lung tissue of the mice were collected separately for the administration of ELISA, rt-PCR, western blot and pathological section and staining. We found that AG attenuated the OVA-induced production of IL-6, IL-17A, IL-17F, and RORγt; inhibited the OVA-mediated phosphorylation of JAK 1 and STAT3; and alleviated airway remodeling and the neutrophil infiltration of lung tissue. We conclude that AG inhibits the inflammatory response of asthma in OVA-stimulated mice by blocking the activation of Th17-regulated cytokines and the JAK1/STAT3 signaling pathway.

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