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10.4049/jimmunol.2101094 http://scihub22266oqcxt.onion/10.4049/jimmunol.2101094 35173037!8917060!35173037     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2022 ; 208 (6): 1467-1482 Nephropedia Template TP {{tp|p=35173037|t=2022. Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses |pdf=|usr=}}{{35173037}} gab.com Text Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35173037 #FOAvip Asthma is a chronic disease of childhood, but for unknown reasons, disease activity sometimes subsides as children mature. In this study, we present clinical and animal model evidence suggesting that the age dependency of childhood asthma stems from an evolving host response to respiratory viral infection. Using clinical data, we show that societal suppression of respiratory virus transmission during coronavirus disease 2019 lockdown disrupted the traditional age gradient in pediatric asthma exacerbations, connecting the phenomenon of asthma remission to virus exposure. In mice, we show that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-sensitive: robust in juvenile mice (4-6 wk old) but attenuated in mature mice (>3 mo old). Interestingly, allergen induction of the same asthmatic traits was less dependent on chronological age than viruses. Age-specific responses to SeV included a juvenile bias toward type 2 airway inflammation that emerged early in infection, whereas mature mice exhibited a more restricted bronchiolar distribution of infection that produced a distinct type 2 low inflammatory cytokine profile. In the basal state, aging produced changes to lung leukocyte burden, including the number and transcriptional landscape of alveolar macrophages (AMs). Importantly, depleting AMs in mature mice restored post-SeV pathology to juvenile levels. Thus, aging influences chronic outcomes of respiratory viral infection through regulation of the AM compartment and type 2 inflammatory responses to viruses. Our data provide insight into how asthma remission might develop in children. Twit Text FOAVip Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35173037 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35173037 #FOAvip English Wikipedia <ref>{{Cite pmid|35173037}}</ref> Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses #MMPMID35173037 Hazan G; Eubanks A; Gierasch C; Atkinson J; Fox C; Hernandez-Leyva A; Rosen AL; Kau AL; Agapov E; Alexander-Brett J; Steinberg D; Kelley D; White M; Byers D; Wu K; Keeler SP; Zhang Y; Koenitzer JR; Eiden E; Anderson N; Holtzman MJ; Haspel J J Immunol 2022[Mar]; 208 (6): 1467-1482 PMID35173037show ga Asthma is a chronic disease of childhood, but for unknown reasons, disease activity sometimes subsides as children mature. In this study, we present clinical and animal model evidence suggesting that the age dependency of childhood asthma stems from an evolving host response to respiratory viral infection. Using clinical data, we show that societal suppression of respiratory virus transmission during coronavirus disease 2019 lockdown disrupted the traditional age gradient in pediatric asthma exacerbations, connecting the phenomenon of asthma remission to virus exposure. In mice, we show that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-sensitive: robust in juvenile mice (4-6 wk old) but attenuated in mature mice (>3 mo old). Interestingly, allergen induction of the same asthmatic traits was less dependent on chronological age than viruses. Age-specific responses to SeV included a juvenile bias toward type 2 airway inflammation that emerged early in infection, whereas mature mice exhibited a more restricted bronchiolar distribution of infection that produced a distinct type 2 low inflammatory cytokine profile. In the basal state, aging produced changes to lung leukocyte burden, including the number and transcriptional landscape of alveolar macrophages (AMs). Importantly, depleting AMs in mature mice restored post-SeV pathology to juvenile levels. Thus, aging influences chronic outcomes of respiratory viral infection through regulation of the AM compartment and type 2 inflammatory responses to viruses. Our data provide insight into how asthma remission might develop in children. |*Age Factors[MESH] |Aging/*physiology[MESH] |Animals[MESH] |Asthma/epidemiology/*immunology[MESH] |COVID-19/epidemiology/*immunology[MESH] |Cytokines/metabolism[MESH] |Humans[MESH] |Influenza A virus/*physiology[MESH] |Influenza, Human/epidemiology/*immunology[MESH] |Lung/*immunology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Orthomyxoviridae Infections/*immunology[MESH] |Respirovirus Infections/*immunology[MESH] |SARS-CoV-2/*physiology[MESH] |Sendai virus/*physiology[MESH] |Th2 Cells/*immunology[MESH]Age-Dependent Reduction in Asthmatic Pathology through Reprogramming o(epmc).pdf DeepDyve Pubget Overpricing