Dynamic imaging of dendritic cell extension into the small bowel lumen in response to epithelial cell TLR engagement
By M. Chieppa, M. Rescigno, A. Huang, Ronald N. Germain. Journal of Experimental Medicine, 2006
737 citations recorded by the source corpus.
Cells lining the gastrointestinal tract serve as both a barrier to and a pathway for infectious agent entry. Dendritic cells (DCs) present in the lamina propria under the columnar villus epithelium of the small bowel extend processes across this epithelium and capture bacteria, but previous studies provided limited information on the nature of the stimuli, receptors, and signaling events involved in promoting this phenomenon. Here, we use immunohistochemical as well as dynamic explant and intravital two-photon imaging to investigate this issue. Analysis of CD11c–enhanced green fluorescent protein (EGFP) or major histocompatibility complex CII-EGFP mice revealed that the number of trans-epithelial DC extensions, many with an unusual “balloon” shape, varies along the length of the small bowel. High numbers of such extensions were found in the proximal jejunum, but only a few were present in the terminal ileum. The extensions in the terminal ileum markedly increased upon the introduction of invasive or noninvasive Salmonella organisms, and chimeric mouse studies revealed the key role of MyD88-dependent Toll-like receptor (TLR) signaling by nonhematopoietic (epithelial) elements in the DC extension response. Collectively, these findings support a model in which epithelial cell TLR signaling upon exposure to microbial stimuli induces active DC sampling of the gut lumen at sites distant from organized lymphoid tissues.
Subfields: Endocrinology, Immunology
View Paper: https://www.semanticscholar.org/paper/8c2f52a97c490c6c121b0d4f32f3025b9e38ec18
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Citations in the corpus
- Homeostatic immunity and the microbiota (2017, positive): “This process is believed to result, at least in part, from direct capture of microbes by DC (Chieppa et al., 2006; Niess et al., 2005; Rescigno et al., 2001) but could also result from capture of microbial outer membrane vesicles (OMVs) (Shen et al.”
- Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. (2007, positive): “The colonic luminal contents are abundant in microbiota (Hooper and Gordon, 2001) and intestinal DCs constantly sample these microbes (Chieppa et al., 2006; Niess et al 2006).”
- Role of the Microbiota in Immunity and inflammation (2014, background): “Commensals can also control oral antigen sampling by mucosal DCs and promote the induction of lamina propria resident macrophages associated with local expansion of Treg cells (Chieppa et al., 2006) (Niess and Adler, 2010).”
- Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk (2010, background): “DCs can penetrate epithelial monolayers in vitro and the intestinal epithelial barrier in vivo, and they take up bacteria directly (51, 221, 257).”
- Intestinal lamina propria dendritic cell subsets have different origin and functions. (2009, background): “…intestinal epithelium and send trans-epithelial dendrites (TEDs) toward the gut lumen to sense or sample luminal pathogens (Rescigno et al., 2001; Chieppa et al., 2006), and TEDs can be readily visualized in the lamina propria of Cx3cr1gfp/+ mice (Niess et al., 2005; Vallon- Eberhard et al.,…”
- Probiotics and immunity (2009, background): “This process can be induced by ligation of any of a variety of Toll-like receptors (TLRs) expressed on epithelial cells.(9) Whereas priming of T cells in Peyer’s patches or MLNs leads to effective local (mucosal) immune responses or tolerance depending on the encountered antigen, systemic immune res”
- Monocyte-mediated defense against microbial pathogens. (2008, background): “Intravital microscopy of small bowel explants (67) demonstrated that formation of DC extensions requires MyD88-mediated signals in nonhematopoietic cells, presumably intestinal epithelial cells.”