INVESTIGADORES
PITOSSI Fernando Juan
artículos
Título:
Overexpression of IL-1â by adenoviral-mediated gene transfer in the rat brain causes a prolonged hepatic chemokine response, axonal injury and the suppression of spontaneous behaviour
Autor/es:
SANDRA CAMPBELL; ROB DEACON; YANYAN JIANG; CARINA FERRARI; FERNANDO J PITOSSI; DANIEL C ANTHONY
Revista:
NEUROBIOLOGY OF DISEASE
Editorial:
ACADEMIC PRESS INC ELSEVIER SCIENCE
Referencias:
Año: 2007 vol. 27 p. 151 - 163
ISSN:
0969-9961
Resumen:
Acute brain injury induces early and transient hepatic expression of
chemokines, which amplify the injury response and give rise to
movement of leukocytes into the blood and subsequently the brain
and liver. Here, we sought to determine whether an ongoing injury
stimulus within the brain would continue to drive the hepatic chemokine
response and how it impacts on behaviour and CNS integrity. We
generated chronic IL-1â expression in rat brain by adenoviralmediated
gene transfer, which resulted in chronic leukocyte recruitment,
axonal injury and prolonged depression of spontaneous
behaviour. IL-1â could not be detected in circulating blood, but a
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
gene transfer, which resulted in chronic leukocyte recruitment,
axonal injury and prolonged depression of spontaneous
behaviour. IL-1â could not be detected in circulating blood, but a
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
â expression in rat brain by adenoviralmediated
gene transfer, which resulted in chronic leukocyte recruitment,
axonal injury and prolonged depression of spontaneous
behaviour. IL-1â could not be detected in circulating blood, but a
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.
â could not be detected in circulating blood, but a
chronic systemic response was established, including extended production
of hepatic and circulating chemokines, leukocytosis, liver damage,
weight loss, decreased serum albumin and marked liver leukocyte
recruitment. Thus, hepatic chemokine synthesis is a feature of active
chronic CNS disease and provides an accessible target for the
suppression of CNS inflammation.