Expression of E-selectin, P-selectin, and intercellular adhesion molecule-1 during experimental murine listeriosis

Santiago López, Neus Prats, Alberto Jesús Marco

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    Abstract

    The expression of adhesion molecules E-selectin, P-selectin, and intercellular adhesion molecule-1 (ICAM-1) was immunohistochemically investigated during the course of experimental murine listeriosis. Infection was monitored by microbiological count of blood, liver, and spleen. After an early generalized expression of P-selectin and ICAM-1, a later regulation occurred specifically to areas of inflammation. Expression of E-selectin was faint and inconstantly detected in all of the studied organs. In the liver, typical lesions of murine listeriosis were related to the expression of ICAM- 1 on sinusoidal endothelial cells and the biliary system and to the de novo expression of P-selectin in hepatic portal vessels. Inflammation in the spleen was related to the expression of ICAM-1 on red pulp sinusoidal cells, especially in the marginal sinus. High endothelial venules of inflamed lymph nodes also expressed P-selectin and ICAM-1. Lesions in the Central nervous system appeared on day 3 after infection as a pyogranulomatous lepto- meningitis associated with an intense expression of P-selectin and ICAM-1 in meningeal vessels, especially those in the hippocampal sulcus, suggesting a way through which inflammation initially reach the central nervous system during experimental murine listeriosis; Leptomeningitis was followed by the presence of ventriculitis, which was related to the upregulation of ICAM-1 on choroid plexus epithelial cells, periventricular vessels and ependymal cells. Up-regulation of P-selectin and ICAM-1 during experimental murine listeriosis could play an important role in the recruitment of leukocytes, especially to the liver, lymphoid organs, and central nervous system.
    Original languageEnglish
    Pages (from-to)1391-1397
    JournalAmerican Journal of Pathology
    Volume155
    DOIs
    Publication statusPublished - 1 Jan 1999

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