INVESTIGADORES
PITOSSI Fernando Juan
artículos
Título:
Central Nervous System Injury Triggers Hepatic CC and CXC Chemokine Expression that Is Associated with Leukocyte Mobilization and Recruitment to Both
Autor/es:
SANDRA J. CAMPBELL; V. HUGH PERRY; FERNANDO PITOSSI; ANGUS G. BUTCHART; MARIELA CHERTOFF; SARA WATERS; ROBERT DEMPSTER; DANIEL C. ANTHONY
Revista:
AMERICAN JOURNAL OF PATHOLOGY
Editorial:
AMER SOC INVESTIGATIVE PATHOLOGY, INC
Referencias:
Año: 2005 vol. 165 p. 1487 - 1497
ISSN:
0002-9440
Resumen:
The administration of interleukin-1_ to the brain induces
hepatic CXC chemokine synthesis, which increases
neutrophil levels in the blood, liver, and
brain. We now show that such hepatic response is not
restricted to the CXC chemokines. CCL-2, a CC chemokine,
was released by the liver in response to a
tumor necrosis factor (TNF)-_ challenge to the brain
and boosted monocyte levels. Furthermore, a clinically
relevant compression injury to the spinal cord
triggered hepatic chemokine expression of both
types. After a spinal cord injury, elevated CCL-2 and
CXCL-1 mRNA and protein were observed in the liver
by TaqMan reverse transcriptase-polymerase chain
reaction and enzyme-linked immunosorbent assay as
early as 2 to 4 hours. Simultaneously, we observed
elevated levels of these chemokines and circulating
leukocyte populations in the blood. Leukocytes were
recruited to the liver at this early stage, whereas at the
site of challenge in the central nervous system, few
were observed until 24 hours. Artificial elevation of
blood CCL-2 triggered dose-dependent monocyte
mobilization in the blood and enhanced monocyte
recruitment to the brain after TNF-_challenge. Attenuation
of hepatic CCL-2 production with corticosteroids
resulted in reduced monocyte levels after the
TNF-_ challenge. Thus, combined production of CC
and CXC hepatic chemokines appears to amplify the
central nervous system response to injury.