Article

Differential affection of intestinal immune cell populations after cerebral ischemia in mice.

Department of Psychiatry, Charité-Universitätsmedizin Berlin, Berlin, Germany.
NeuroImmunoModulation (Impact Factor: 1.78). 03/2009; 16(3):213-8. DOI: 10.1159/000205514
Source: PubMed

ABSTRACT Infections cause a major clinical problem within the first days after cerebral stroke. In a mouse model we have recently demonstrated that stroke leads to immunodepression facilitating spontaneous bacterial pneumonia and bacteremia. So far, it has been unknown whether poststroke immunomodulation impairs local intestinal immune populations which may promote gut barrier dysfunction leading to translocation of intestinal microorganisms and microbial products. In this study, we investigated changes in intestinal intraepithelial, lamina propria and Peyer's patch immune cell populations after experimental stroke.
129SV mice were subjected to experimental stroke by filament occlusion of the middle cerebral artery or sham operation. After 24 h, animals were sacrificed, and intraepithelial lymphocytes, lamina propria lymphocytes and Peyer's patches were isolated and leukocyte subpopulations analyzed by flow cytometry.
Peyer's patches revealed a significant reduction of T and B cell counts after cerebral ischemia, while no differences in natural killer cells and macrophages were observed. In contrast, no significant changes in intraepithelial and lamina propria lymphocyte subsets were observed in middle cerebral artery animals compared to controls.
Cerebral ischemia has differential effects on cellularity of gut-associated lymphoid tissue. Further studies on the mechanisms involved in quantitative changes of gut immune cells as well as on the function of these cells are needed to better understand the consequences of stroke-induced alterations of the local intestinal immune compartment for the enhanced susceptibility to infections after stroke.

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    • "The height and depth of the intestinal villi, a critical factor critical for mucosal integrity, were shown to be damaged by permanent MCAO, potentially allowing indigenous gut bacteria to migrate into otherwise sterile body cavities (Tascilar et al., 2010). This work has been corroborated in animal models (Maes et al., 2008; Schulte-Herbruggen et al., 2009), where it has been suggested that stress, and therefore possibly the HPA axis, is a significant contributing factor to bacterial translocation (Tascilar et al., 2010). Studies specifically investigating the intestinal immune system have shown decreased levels of lymphocytes in Peyer's patches following cerebral ischemia (Schulte-Herbruggen et al., 2009). "
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