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TiHo Bibliothek elib - Tierärztliche Hochschule Hannover

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Untersuchung des Chemokins MIP-3 β/CCL19<br />

chemotactic activity for mononuclear cells in the migration assay, proving that the<br />

measured CSF protein is available in the active form.<br />

Conclusions: The hypothesis was confirmed that MIP-3β/CCL19 is involved in the<br />

pathogenesis of SRMA/MUO, possibly perpetuating an autoimmune reaction.<br />

The marked chemotactic activity for mononuclear cells leads to the assumption that<br />

this chemokine could be associated with the migration of mononuclear cells into the<br />

subarachnoid space of dogs. The elevation of CSF MIP-3β/CCL19 in IVDD suggests<br />

that it also plays a role in the secondary wave in spinal cord injuries (SCI). CSF MIP-<br />

3β/CCL19 concentration may serve as a prognostic indicator in SCI, be a precious<br />

biomarker for developing new treatment schemes and for verifying the success of<br />

treatment.<br />

1. Introduction<br />

In several neurologic diseases a pleocytosis is often detected in the cerebrospinal<br />

fluid (CSF). Lymphocytes and plasma cells have been shown to prevail in the cell<br />

count in viral infections (Wamsley and Alleman 2004), chronic steroid responsive<br />

meningitis-arteritis (SRMA) (Tipold and Jaggy 1994), granulomatous<br />

meningoencephalomyelitis (GME) and in necrotizing encephalitides (NE) (Wamsley<br />

and Alleman 2004; Talarico and Schatzberg 2010). A neutrophilic pleocytosis is<br />

characteristic for bacterial infections and the acute stage of SRMA (Tipold and Jaggy<br />

1994). A mixed cell population can be seen in protozoal diseases, chronic bacterial<br />

infections, necrotic lesions, and in GME (Wamsley and Alleman 2004). In addition to<br />

inflammatory lesions, mild mixed cell pleocytosis can also be seen with situations<br />

such as acute intervertebral disc herniation that results in central nervous system<br />

(CNS) myelomalacia or infarction (Chrisman 1992).<br />

Chemokines are important factors in the mechanism of cell migration and thus play a<br />

relevant role in the pathogenesis of inflammation in the CNS (Dogan and Karpus<br />

2004). They upregulate surface molecules on circulating inflammatory cells in the<br />

periphery which enable them to more efficiently adhere to the endothelial cells of the<br />

blood-brain barrier (BBB) and react to the CNS chemokine gradients (Constantin<br />

33

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