| First Author | Bonneh-Barkay D | Year | 2012 |
| Journal | J Neuropathol Exp Neurol | Volume | 71 |
| Issue | 11 | Pages | 948-58 |
| PubMed ID | 23041842 | Mgi Jnum | J:323185 |
| Mgi Id | MGI:6852213 | Doi | 10.1097/NEN.0b013e31826eaee7 |
| Citation | Bonneh-Barkay D, et al. (2012) Exacerbation of experimental autoimmune encephalomyelitis in the absence of breast regression protein 39/chitinase 3-like 1. J Neuropathol Exp Neurol 71(11):948-58 |
| abstractText | We previously reported that YKL-40, the human analog of mouse breast regression protein 39 ([BRP-39] chitinase 3like 1), is elevated in the cerebrospinal fluid of patients with a variety of neuroinflammatory conditions, such as multiple sclerosis and traumatic brain injury. Expression of YKL-40 in the CNS was predominantly associated with reactive astrocytes in the vicinity of inflammatory lesions. Because previous studies have shown that reactive astrocytes play a critical role in limiting immune infiltration in the mouse model of experimental autoimmune encephalomyelitis, we explored the role of BRP-39 in regulatingneuroinflammation in experimental autoimmune encephalomyelitis. Using BRP-39--deficient (BRP-39(-/-)) mice, we demonstrate the importance of BRP-39 in modulating the severity of clinical experimentalautoimmune encephalomyelitis and CNS neuroinflammation. At disease onset, absence of BRP-39 had little effect on clinical disease orlymphocytic infiltrate, but by 14 days after immunization, differences in clinical scores were evident. By 28 days after immunization, BRP-39(-/-) mice showed more severe and persistent clinical disease than BRP-39(+/+) controls. Histopathological evaluation showed that BRP-39(-/-) mice had more marked lymphocytic and macrophage infiltrates and gliosis versus BRP-39(+/+) mice. These findings support the role of BRP-39 expression in limiting immune cell infiltration into the CNS and offer a new target to modulate neuroinflammation. |
