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. 2010 Oct 8;86(8):848–866. doi: 10.2183/pjab.86.848

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© 2010 The Japan Academy

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Mechanism of inflammatory fever. Peripheral stimuli such as endotoxins initiate macrophage to produce IL-1β, which somehow induces RANKL expression in septal/POA region. RANKL, by acting on RANK on the astrocytes, initiates COX-2 expression and PGE₂ production. PGE₂ modifies the GABA_A subunit composition via EP3-G_i/o pathway, and such a rapid modulation of GABA_A channel may inhibit the GABAergic activity of EP3-expressing neurons, allowing the excitation of raphe (rRPa) neurons, leading to sympathetic nerve-mediated thermogenesis.