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JCI early table of contents for Jan. 2, 2013
Date:1/2/2013

Bacterial imbalance contributes to intestinal inflammation and carcinogenesis

Instability in the composition of gut bacterial communities (dysbiosis) has been linked to common human intestinal disorders, including inflammatory bowel disease and colorectal cancer; however, it is unclear if dysbiosis can instigate disease or if it is a consequence of the underlying disorder. In this issue of the Journal of Clinical Investigation, researchers led by Mathias Chamaillard at the University Lille Nord de France in Lille, France, examined intestinal inflammation and tumorigenesis in a mouse model of dysbiosis. Dysbiosis enhanced intestinal inflammation and increased the risk for inflammation-associated colon cancer. Treatment with antibiotics or transplantation of fecal material from normal mice reduced disease risk and instigated long-term, beneficial alterations in intestinal bacteria. Conversely, transplantation of normal mice with dysbiotic fecal material increased intestinal inflammation and enhanced the risk of inflammation-associated colon cancer. These results demonstrate that gut bacterial communities play an integral role in protecting against intestinal inflammation and associated tumorigenesis.

TITLE:
NOD2-mediated dysbiosis predisposes mice to transmissible colitis and colorectal cancer

AUTHOR CONTACT:
Mathias Chamaillard
Inserm, Lille, , FRA
Phone: +33359317427; Fax: +33359317480; E-mail: mathias.chamaillard@inserm.fr

View this article at: http://www.jci.org/articles/view/62236?key=555e9b1899800b97fd0b


AUTOIMMUNITY

Identifying the molecular causes of vision loss in demyelinating disease

Demyelinating diseases, such as multiple sclerosis (MS), are frequently associated with the progressive loss of vision. The retinal nerve damage is thought to be caused by immune system-mediated inflammation; however, other demyelinating disorders, such as Pelizaeus-Merzbacher disease, do not involve the immune system, suggesting that there are other causes of retinal nerve damage. Deimination is a protein modification that is altered in patients with MS and PMD. In this issue of the Journal of Clinical Investigation, researchers led by Sanjoy Bhattacharya at the University of Miami investigated the role of deimination in retinal nerve damage in a mouse model of demyelinating disease (ND4 mice). They found that deimination was reduced in patients with demyelinating diseases and in ND4 mice that exhibited vision loss. Decreases in deamination could be detected in the mice prior to the onset of other symptoms. Bhattacharya and colleagues found that they could improve visual function in ND4 mice by restoring deimination. These results demonstrate that loss of deimination underlies nerve damage in demyelinating diseases and may be a suitable target for therapeutic intervention.

TITLE:
Deimination restores inner retinal visual function in murine demyelinating disease

AUTHOR CONTACT:
Sanjoy Bhattacharya
University of Miami Miller School of Medicine, Miami, FL, USA
Phone: 3054824103; Fax: 3053266547; E-mail: sbhattacharya@med.miami.edu

View this article at: http://www.jci.org/articles/view/64811?key=1cb7e7315edf5b9d1258


ALSO IN THIS ISSUE

TITLE:
Acylated and unacylated ghrelin impair skeletal muscle atrophy in mice

AUTHOR CONTACT:
Nicoletta Filigheddu
University of Piemonte Orientale "A. vogadro", Novara, ITA
Phone: +390321660529; E-mail: nicoletta.filigheddu@med.unipmn.it

View this article at: http://www.jci.org/articles/view/39920?key=7f092a50dd972f0c715c

TITLE:
An obligate cell-intrinsic function for CD28 in regulatory T cells

AUTHOR CONTACT:
Laurence A. Turka
Beth-Israel-Deaconess Medical Center, Boston, MA, USA
Phone: 617.735.2919; Fax: 617.735.2902; E-mail: lturka@bidmc.harvard.edu

View this article at: http://www.jci.org/articles/view/65013?key=630d9a4611663eb4a7da

TITLE:
CXCR5+ T helper cells mediate protective immunity against tuberculosis

AUTHOR CONTACT:
Shabaana Khader
Children's Hopsital Of Pittsburgh, Pittsburgh, USA
Phone: 412-692-7767; Fax: ; E-mail: Shabaana.Khader@chp.edu

View this article at: http://www.jci.org/articles/view/65728?key=60dce6e4ce9ae64833e6

TITLE:
Oligodendrocyte precursors induce early blood-brain-barrier opening after white matter injury

AUTHOR CONTACT:
Ken Arai
MGH, Charlestown, MA, USA
Phone: 617-724-9503; E-mail: karai@partners.org

View this article at: http://www.jci.org/articles/view/65863?key=9c438cec347734578a1a

TITLE:
Superior T memory stem cell persistence supports long-lived T cell memory

AUTHOR CONTACT:
Mario Roederer
Vaccine Research Center, NIAID, NIH, Bethesda, MD, USA
Phone: 301 594-8491; Fax: 301 480-2788; E-mail: roederer@nih.gov

View this article at: http://www.jci.org/articles/view/66327?key=3ec7275bf89c124b5d89

TITLE:
EWS/ATF1 expression induces sarcomas from neural crest-derived cells in mice

AUTHOR CONTACT:
Yasuhiro Yamada
Center for iPS Cell Research and Application, Kyoto University, Kyoto, JPN
Phone: 0753667034; E-mail: y-yamada@cira.kyoto-u.ac.jp

View this article at: http://www.jci.org/articles/view/63572?key=17816fd8927b745083a6


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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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