Campbell, S.J., Perry, V.H., Pitossi, F., Butchart, A.G., Chertoff, M., Waters, S. and Anthony, D.C.
Hepatic CC chemokines control the magnitude of the inflammatory response within the injured rodent brain.
Journal of Neuroimmunology, 154, (1-2), . (doi:10.1016/j.jneuroim.2004.06.010).
Full text not available from this repository.
Hepatic CXC chemokines, behaving as acute phase proteins, regulate
neutrophil mobilisation and recruitment following focal IL-1h-mediated
inflammation to the rat brain. To determine whether this response was
specific to CXC chemokines or whether it represented a more
generalised response to acute brain inflammation, we examined brain
and liver production of MCP-1, a CC chemokine, when rats were
microinjected with TNF-a into the brain. As early as 2h after the TNF-a
challenge, MCP-1 mRNA and protein were observed in the liver by
Taqman RT-PCR and ELISA. The serum MCP-1 level was also elevated
between 2 and 4 h, which was consistent with maximal mobilisation of
leukocytes into the blood. Monocyte recruitment was most marked in the
liver after 6 h, but was delayed in the brain until 24 h. Elevated hepatic
and serum chemokines are implicated in the control of leukocytosis and
leukocyte recruitment to the brain and liver, since dexamethasone pretreatment
attenuated the hepatic MCP-1 response, modulated leukocyte
mobilisation and reduced monocyte entry not only to the brain but also
to the liver. Thus hepatic chemokine production controls and amplifies
the CNS response to inflammation by controlling the rate, timing,
magnitude and composition of leukocyte recruitment to the damaged
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