The
cytokines IL-1alpha and IL-1beta are induced rapidly after insults to the CNS, and their subsequent signaling through the type 1
IL-1 receptor (IL-1R1) has been regarded as essential for a normal astroglial and microglial/macrophage response. To determine whether abrogating signaling through the IL-1R1 will alter the cardinal astrocytic responses to injury, we analyzed molecules characteristic of activated astrocytes in response to a penetrating
stab wound in wild type mice and mice with a targeted deletion of IL-1R1. Here we show that after a
stab wound injury,
glial fibrillary acidic protein (GFAP) induction on a per cell basis is delayed in the IL-1R1-null mice compared to wild type counterparts. However, the induction of
chondroitin sulfate proteoglycans,
tenascin, S-100B as well as
glutamate transporter proteins, GLAST and GLT-1, and
glutamine synthetase are independent of IL-1RI signaling. Cumulatively, our studies on
gliosis in the IL-1R1-null mice indicate that abrogating IL-1R1 signaling delays some responses of astroglial activation; however, many of the important neuroprotective adaptations of astrocytes to
brain trauma are preserved. These data recommend the continued development of
therapeutics to abrogate IL-1R1 signaling to treat
traumatic brain injuries. However, astroglial
scar related
proteins were induced irrespective of blocking IL-1R1 signaling and thus, other therapeutic strategies will be required to inhibit glial
scarring.