Intercellular Adhesion Molecule-1 Expression on Glia Following Brain Injury: Participation of Interleukin-1β

Abstract

Interleukin-1 (IL-1), one of the most important inflammatory cytokines, promotes glia to express intercellular adhesion molecule-1 (ICAM-1) in vitro. IL-1 is known to be produced in situ immediately after brain insults and recently we have found that glia, including astrocytes, express ICAM-1 in vivo following cortical stab wounds. To evaluate the participation of IL-1 beta in posttraumatic ICAM-1 expression on glia in vivo, we performed the following experiments. A cortical stab wound was made in the brain of a mouse. ICAM-1-immunopositive glia began to emerge around the wound from 6 h postlesioning. The number of cells reached a maximum at 48 h and persisted until 7 days postlesioning. Next, a neutralizing monoclonal antibody against IL-1 beta was infused into the wound immediately following the injury. This treatment resulted in a significant reduction of ICAM-1-positive glia at 24 and 48 h postlesioning. We conclude, therefore, that IL-1 beta affects ICAM-1 expression on glia in vivo after experimental brain injury and presumably plays an important role in brain wound repair.

Novel Pharmacologic Strategies in the Treatment of Experimental Traumatic Brain Injury: 1998

“…The adhesion of these leukocytes to the endothelium requires upregulation of the intracellular adhesion molecule (ICAM-1), a member of the immunoglobulin supergene family. An upregulation of ICAM-1 has been described following spinal cord trauma (Hamada et al, 1996), cerebral ischemia (Wang and Feuerstein, 1995), cortical stab injury (Shibayama et al, 1996), and cortical weight-drop trauma in the rat (Carlos et al, 1995;Isaksson et al, 1997). Interestingly, the posttraumatic upregulation of ICAM-1 expression observed in astroglia following cortical stab wound injury has been causally linked to IL-Iß (Shibayama et al, 1996).…”

“…An upregulation of ICAM-1 has been described following spinal cord trauma (Hamada et al, 1996), cerebral ischemia (Wang and Feuerstein, 1995), cortical stab injury (Shibayama et al, 1996), and cortical weight-drop trauma in the rat (Carlos et al, 1995;Isaksson et al, 1997). Interestingly, the posttraumatic upregulation of ICAM-1 expression observed in astroglia following cortical stab wound injury has been causally linked to IL-Iß (Shibayama et al, 1996). Moreover, there is increasing evidence that the complement system plays an important role in tissue damage associated with brain trauma (Mollnes and Fosse, 1994), and complement mRNA has been shown to increase in the ipsilateral hippocampus and cortex following perforant path transection (Johnson et al, 1992).…”

Soluble ICAM-1 in CSF Coincides with the Extent of Cerebral Damage in Patients with Severe Traumatic Brain Injury

“…Apart from enzymatic cleavage, the soluble form of ICAM-1 is also believed to be produced anew, since two distinct mRNAs, one for membrane-bound ICAM-1 and one for soluble ICAM-1, have been demonstrated (Simmons et al, 1988;Staunton et al, 1989;Wakatsuki et al, 1995). sICAM-1 in CSF may originate from cerebral endothelial cells and astrocytes, since these cell-types were shown to express (ICAM-1 in vitro (Frohman et al, 1989;Satoh et al, 1991a;Rieckmann et al, 1995a) and in vivo (Cannella et al, 1995;Sharief et al, 1993;Sobel et al, 1990;Shibayama et al, 1996;Isaksson et al, 1997).…”

Spinal Cord Injury in ICAM-1–Deficient Mice: Assessment of Functional and Histopathological Outcome

“…However, as measured by image analysis there were no significant differences between groups. Microglial as well as astroglial cells have been reported to express ICAM-1 (Shrikant et al, 1995;Shibayama et al, 1996). Our findings indicate that ICAM-1 is not a crucially important molecule for the postinjury activation of these cell-types.…”