Proinflammatory Cytokine Expression Contributes to Brain Injury Provoked By Chronic Monocyte Activation

Table 1 Quantitation of IL-1 β immunoreactivity in the cortex and hippocampus.

Number of IL-1β Immunoreactive Cells/1 mm²
Group	Cortex	Hippocampus	N	Cell Type Expressing IL-1β
Saline i.v. + saline i.c.v.	58 ± 23	36 ± 10	3	Neurons
Saline i.v. + LPS i.c.v.	107 ± 30	5 ± 1	3	Microglia, monocytes > neurons
BCG i.v. + LPS i.c.v.	124 ± 19^x	112 ± 28*^x	4	Microglia, monocytes > neurons
BCG i.v. + IL1ra + LPS i.c.v.	42 ± 39	32 ± 29	4	Microglia, monocytes > neurons
BCG i.v. +TNFbp + LPS i.c.v.	7 ± 5	2 ± 1	5	Microglia, monocytes > neurons

Asterisks denote statistical significance in glial IL-1β-expression between BCG + LPS and the saline + LPS group (*p < 0.05), crosses depict statistical significance between BCG + LPS- and TNF-bp-treated BCG + LPS group (^xp < 0.01). A single bolus of saline (10 µl) or LPS (100 µg/rat) was administered i.c.v. 2 weeks after the i.v. treatment with BCG or saline. The anticytokine treatments, both at a dose of 100 µg/10 µl, were administered i.c.v. 30 min before and 30 min after the injection of LPS (100 µg/rat, i.c.v.).

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