A model for G-CSF-induced fever and cooperative regulation of endosteal microenvironment by the SNS and neutrophils. As a classical function, G-CSF directly expands BM neutrophils from their progenitors, which constitutively express mPGES-1. In the meantime, G-CSF induces high sympathetic tone, which primes BM neutrophils to produce PGE₂, resulting in fever. In addition to the direct suppression of osteoblastic microenvironment, high sympathetic tone also initiates the indirect regulation of osteoblastic niche by the induction of OPN to anchor hematopoietic progenitors via PGE₂/EP4 signal. ADR, adrenergic receptors.