scholarly journals Erratum to: Early Life Hypoxic or Hypoxic/Hypercapnic Stress Alters Acute Ventilatory Sensitivity in Adult Mice

Author(s):  
Kui Xu ◽  
Solomon Raju Bhupanapadu Sunkesula ◽  
Pengjing Huang ◽  
Constantinos P. Tsipis ◽  
Thomas Radford ◽  
...  
Keyword(s):  
Author(s):  
Dan-Dan Wang ◽  
Fang Wu ◽  
Ling-Yu Zhang ◽  
Ying-Cai Zhao ◽  
Cheng-Cheng Wang ◽  
...  

2015 ◽  
Vol 55 ◽  
pp. 128-143 ◽  
Author(s):  
Christine Kohl ◽  
Xiao-Dong Wang ◽  
Jocelyn Grosse ◽  
Céline Fournier ◽  
Daniela Harbich ◽  
...  

Chemosphere ◽  
2021 ◽  
pp. 133135
Author(s):  
Yixi Li ◽  
Zhenzi Zuo ◽  
Bing Zhang ◽  
Huan Luo ◽  
Bo Song ◽  
...  

2020 ◽  
Vol 319 (3) ◽  
pp. G361-G374 ◽  
Author(s):  
Eloisa Salvo ◽  
Patricia Stokes ◽  
Ciara E. Keogh ◽  
Ingrid Brust-Mascher ◽  
Carly Hennessey ◽  
...  

Here we describe long-lasting impacts on the microbiota-gut-brain (MGB) axis following administration of low-dose dextran sodium sulfate (DSS) to weaning mice (P21), including gut dysbiosis, colonic inflammation, and brain/behavioral deficits in adulthood (P56). Early-life DSS leads to acute colonic inflammation, similar to adult mice; however, it results in long-lasting deficits in the MGB axis in adulthood (P56), in contrast to the transient deficits seen in adult DSS. This model highlights the unique features of pediatric inflammatory bowel disease.


2019 ◽  
Vol 11 (498) ◽  
pp. eaav5519 ◽  
Author(s):  
Karin Steinbach ◽  
Ilena Vincenti ◽  
Kristof Egervari ◽  
Mario Kreutzfeldt ◽  
Franziska van der Meer ◽  
...  

Epidemiological studies associate viral infections during childhood with the risk of developing autoimmune disease during adulthood. However, the mechanistic link between these events remains elusive. We report that transient viral infection of the brain in early life, but not at a later age, precipitates brain autoimmune disease elicited by adoptive transfer of myelin-specific CD4+ T cells at sites of previous infection in adult mice. Early-life infection of mouse brains imprinted a chronic inflammatory signature that consisted of brain-resident memory T cells expressing the chemokine (C-C motif) ligand 5 (CCL5). Blockade of CCL5 signaling via C-C chemokine receptor type 5 prevented the formation of brain lesions in a mouse model of autoimmune disease. In mouse and human brain, CCL5+ TRM were located predominantly to sites of microglial activation. This study uncovers how transient brain viral infections in a critical window in life might leave persisting chemotactic cues and create a long-lived permissive environment for autoimmunity.


2010 ◽  
Vol 17 (4) ◽  
pp. 229-239 ◽  
Author(s):  
Rattanjeet Vig ◽  
John R. Gordon ◽  
Bernard Thébaud ◽  
A. Dean Befus ◽  
Harissios Vliagoftis

2008 ◽  
Vol 211 (2) ◽  
pp. 503-510 ◽  
Author(s):  
Rieko Muramatsu ◽  
Yuji Ikegaya ◽  
Norio Matsuki ◽  
Ryuta Koyama

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