Abstrait
Malgré les progrès des techniques diagnostiques, de la chirurgie et de la prise en charge réanimatoire, et l’utilisation de traitements antibiotiques à large spectre, les taux de mortalité des péritonites sévères restent élevés, pouvant atteindre 60 % à 80 % (1, 2). Les travaux réalisés ces dernières années ont néanmoins permis de mieux comprendre les mécanismes de contrôle de la réponse immune et inflammatoire péritonéale; en particulier, de montrer les rôles respectifs des cellules résidentes de la cavité péritonéales — essentiellement cellules mésothéliales et macrophages — et des cellules recrutées — polynucléaires neutrophiles et cellules mononucléées — dans l’initiation et l’amplification de cette réponse immune et inflammatoire péritonéale. Dans ce chapitre, nous ne traiterons que des mécanismes de l’inflammation péritonéale des péritonites secondaires et non pas des péritonites primaires, des surinfections d’ascites, ni même des phénomènes inflammatoires chroniques engendrés par la dialyse péritonéale. Pour se faire, il sera tout particulièrement fait référence à des modèles murins de ligature cæcale et ponction (CLP). Ces modèles induisent une péritonite infectieuse polymicrobienne de sévérités différentes selon la taille des ponctions réalisées dans le cæcum.
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Moine, P. (2007). Le péritoine lors de l’inflammation. In: Mallédant, Y., Seguin, P. (eds) Les infections intra-abdominales aiguës. Le point sur …. Springer, Paris. https://doi.org/10.1007/978-2-287-69814-9_2
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DOI: https://doi.org/10.1007/978-2-287-69814-9_2
Publisher Name: Springer, Paris
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