@Article{ecn.2007.0091,
AUTHOR = {Denis Arsenijevic, Noemi Hernadfalvi, Claudia von Meyenburg, Brigitte Onteniente, Denis Richard, Wolfgang Langhans},
TITLE = {Role for nerve growth factor in the in vivo regulation of glutathione in response to LPS in mice},
JOURNAL = {European Cytokine Network},
VOLUME = {18},
YEAR = {2007},
NUMBER = {2},
PAGES = {47--55},
URL = {http://www.techscience.com/ECN/v18n2/65993},
ISSN = {1952-4005},
ABSTRACT = {Since the redox state regulator glutathione (GSH) influences lipopolysaccharide (LPS) anorexia, we
studied the roles of tumour necrosis factor-alpha (TNFα) and nerve growth factor (NGF) in the GSH response to
intraperitoneal (ip) LPS injection in mice. Basal NGF and GSH levels were up-regulated in brain and liver of
TNFα-knock-out (KO) mice, and this was associated with attenuated LPS anorexia. The increases in NGF and
GSH presumably contributed to the attenuated anorexia in response to LPS because transgenic mice over-expressing
NGF (NGF-tg) also had increased GSH levels and displayed attenuated anorexia compared to the
corresponding wild type (WT) mice. Attenuated LPS anorexia in NGF-tg mice was accompanied by reduced
serum TNFα and IFNγ levels compared to WT mice. In response to a second injection of LPS, NGF and GSH
levels, but not TNFα levels changed. This suggests that in vivo tissue GSH changes following LPS in LPS-naïve or
LPS-pretreated mice are regulated by NGF rather than TNFα. The finding that genetic TNFα deficiency did not
inhibit the acute GSH response to LPS supports this interpretation. In sum, the results indicate i) that a decrease
or increase in NGF is accompanied by a decrease or increase in GSH levels and ii) that elevated NGF and/or GSH
levels attenuate some of the responses to LPS such as anorexia and cytokine production.},
DOI = {10.1684/ecn.2007.0091}
}