Corticosteroids as Adjunctive Therapy in the Treatment of Influenza: An Updated Cochrane Systematic Review and Meta-analysis DOI
Louise Lansbury,

Chamira Rodrigo,

Jo Leonardi‐Bee

и другие.

Critical Care Medicine, Год журнала: 2019, Номер 48(2), С. e98 - e106

Опубликована: Ноя. 17, 2019

Corticosteroids may be beneficial in sepsis, but uncertainty remains over their effects severe influenza. This systematic review updates the current evidence regarding corticosteroids treatment of influenza and examines effect dose on outcome.

Язык: Английский

Proteomic and Metabolomic Characterization of COVID-19 Patient Sera DOI Creative Commons
Bo Shen, Xiao Yi, Yaoting Sun

и другие.

Cell, Год журнала: 2020, Номер 182(1), С. 59 - 72.e15

Опубликована: Май 28, 2020

Язык: Английский

Процитировано

1418

Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters DOI
Marco Del Giudice, Steven W. Gangestad

Brain Behavior and Immunity, Год журнала: 2018, Номер 70, С. 61 - 75

Опубликована: Март 1, 2018

Язык: Английский

Процитировано

612

Systemic lupus erythematosus: Diagnosis and clinical management DOI
Andrea Fava, Michelle Petri

Journal of Autoimmunity, Год журнала: 2018, Номер 96, С. 1 - 13

Опубликована: Ноя. 16, 2018

Язык: Английский

Процитировано

589

Therapeutic Mechanisms of Glucocorticoids DOI
Jolien Vandewalle,

Astrid Luypaert,

Karolien De Bosscher

и другие.

Trends in Endocrinology and Metabolism, Год журнала: 2017, Номер 29(1), С. 42 - 54

Опубликована: Ноя. 20, 2017

Язык: Английский

Процитировано

454

Therapeutic strategies for COVID-19: progress and lessons learned DOI Open Access
Guangdi Li, Rolf Hilgenfeld, Richard J. Whitley

и другие.

Nature Reviews Drug Discovery, Год журнала: 2023, Номер 22(6), С. 449 - 475

Опубликована: Апрель 19, 2023

Язык: Английский

Процитировано

430

Inflammation in psychiatric disorders: what comes first? DOI
Moisés Evandro Bauer, Antônio Lúcio Teixeira

Annals of the New York Academy of Sciences, Год журнала: 2018, Номер 1437(1), С. 57 - 67

Опубликована: Май 11, 2018

Abstract Neuropsychiatric disorders (i.e., mood and schizophrenia) inflammation are closely intertwined, possibly powering each other in a bidirectional loop. Depression facilitates inflammatory reactions promotes depression neuropsychiatric disorders. Patients with exhibit all cardinal features of inflammation, including increased circulating levels inducers, activated sensors, mediators targeting tissues. Inflammation may contribute to the pathophysiology clinical progression these Of note, proinflammatory cytokines modulate behavior cognition by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), impairing plasticity. What sources this chronic inflammation? Increasing evidence indicates that changes regulation, metabolism, diet/microbiota, negative health behaviors important triggers inflammation. Finally, recent data indicate early‐life stress is associated overt prior development

Язык: Английский

Процитировано

418

Tuberculosis: progress and advances in development of new drugs, treatment regimens, and host-directed therapies DOI
Simon Tiberi, Nelita du Plessis, Gerhard Walzl

и другие.

The Lancet Infectious Diseases, Год журнала: 2018, Номер 18(7), С. e183 - e198

Опубликована: Март 23, 2018

Язык: Английский

Процитировано

333

Discriminating mild from critical COVID-19 by innate and adaptive immune single-cell profiling of bronchoalveolar lavages DOI Creative Commons
Els Wauters, Pierre Van Mol, Abhishek D. Garg

и другие.

Cell Research, Год журнала: 2021, Номер 31(3), С. 272 - 290

Опубликована: Янв. 21, 2021

Abstract How the innate and adaptive host immune system miscommunicate to worsen COVID-19 immunopathology has not been fully elucidated. Here, we perform single-cell deep-immune profiling of bronchoalveolar lavage (BAL) samples from 5 patients with mild 26 critical in comparison BALs non-COVID-19 pneumonia normal lung. We use pseudotime inference build T-cell monocyte-to-macrophage trajectories model gene expression changes along them. In COVID-19, CD8 + resident-memory (T RM ) CD4 T-helper-17 H17 cells undergo active (presumably antigen-driven) expansion towards end trajectory, are characterized by good effector functions, while they remain more naïve. Vice versa, T-cells T-helper-1 characteristics H1 -like) expressing exhaustion markers EX enriched halfway their where also exhibit show evidence inflammation-associated stress at trajectories. Monocyte-to-macrophage that chronic hyperinflammatory monocytes alveolar macrophages, otherwise anti-inflammatory antigen-presenting characteristics, depleted. contribute an ATP-purinergic signaling-inflammasome footprint could enable associated fibrosis disease-severity. Finally, viral RNA-tracking reveals infected lung epithelial cells, a significant proportion neutrophils macrophages involved clearance.

Язык: Английский

Процитировано

330

Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation DOI Creative Commons
Agorastos Agorastos, Panagiota Pervanidou, George P. Chrousos

и другие.

Frontiers in Psychiatry, Год журнала: 2019, Номер 10

Опубликована: Март 11, 2019

Early life stressors display a high universal prevalence and constitute major public health problem. Prolonged psychoneurobiological alterations as sequelae of early stress (ELS) could represent developmental risk factor mediate for disease, leading to higher physical mental morbidity rates in later life. ELS exert programming effect on sensitive neuronal brain networks related the response during critical periods development thus lead enduring hyper- or hypo-activation system altered glucocorticoid signaling. In addition, emotional autonomic reactivity, circadian rhythm disruption, functional structural changes brain, well immune metabolic dysregulation have been lately identified important factors chronically impaired homeostatic balance after ELS. Furthermore, human genetic background epigenetic modifications through stress-related gene expression interact with these explain inter-individual variation vulnerability resilience stress. This narrative review presents relevant evidence from mainly research ten most acknowledged neurobiological allostatic pathways exerting adverse effects even decades (hypothalamic-pituitary-adrenal axis, nervous system, inflammation, oxidative stress, cardiovascular gut microbiome, sleep genetics, epigenetics, structural, correlates). Although findings back causal relation between psychobiological maladjustment life, precise trajectories their temporal coincidence has not elucidated yet. Future studies should prospectively investigate putative mediators sequence, while considering potentially delayed time-frame phenotypical expression. Better screening strategies are needed better individual prevention treatment.

Язык: Английский

Процитировано

316

Tumors induce de novo steroid biosynthesis in T cells to evade immunity DOI Creative Commons
Bidesh Mahata,

Jhuma Pramanik,

Louise van der Weyden

и другие.

Nature Communications, Год журнала: 2020, Номер 11(1)

Опубликована: Июль 17, 2020

Abstract Tumors subvert immune cell function to evade responses, yet the complex mechanisms driving evasion remain poorly understood. Here we show that tumors induce de novo steroidogenesis in T lymphocytes anti-tumor immunity. Using a transgenic steroidogenesis-reporter mouse line identify and characterize steroidogenic cells, defining global gene expression identity of these steroid-producing cells regulatory networks by using single-cell transcriptomics. Genetic ablation restricts primary tumor growth metastatic dissemination models. Steroidogenic dysregulate immunity, inhibition pathway is sufficient restore This study demonstrates as mechanism immunosuppression potential druggable target.

Язык: Английский

Процитировано

310