Differential Activation of Cytokine Secretion in Primary Human Colonic Fibroblast/Myofibroblast Cultures

Rogler, Gerhard; Gelbmann, Cornelia M.; Vogl, Daniela; Brunner, Matthias; Schölmerich, J; Falk, Werner; Andus, Tilo; Brand, Korbinian

doi:10.1080/003655201300051216

Cited by 62 publications

(51 citation statements)

References 44 publications

(52 reference statements)

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“…Indications for the additional requirement of cognate interactions between macrophages and intestinal epithelial cells for the complete differentiation into resident intestinal tissue macrophages was indeed obtained in cocultures of monocytes with multicellular spheroids of intestinal epithelial cells. In these in vitro cocultures, the monocytes acquired an intestinal macrophage-like phenotype, characterized by reduced CD14, CD16, CD11b, and CD11c expression and reduced LPS-stimulated IL-1β mRNA expression [64]. This effect, however, was not seen in transwell coculture of monocytes with the same epithelial cells or epithelial cell-conditioned medium and, hence, is likely to require direct cell-cell contacts between macrophages and intestinal epithelial cells [64].…”

Section: Regulation Of Phenotype and Functions Of Intestinal Macrophagesmentioning

confidence: 87%

Intestinal macrophages: differentiation and involvement in intestinal immunopathologies

2009

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Intestinal macrophages, preferentially located in the subepithelial lamina propria, represent the largest pool of tissue macrophages in humans. As an adaptation to the local antigen-and bacteria-rich environment, intestinal macrophages exhibit several distinct phenotypic and functional characteristics. Notably, microbe-associated molecular pattern receptors, including the lipopolysaccharide (LPS) receptors CD14 and TLR4, and also the Fc receptors for IgA and IgG are absent on most intestinal macrophages under homeostatic conditions. Moreover, while macrophages in the intestinal mucosa are refractory to the induction of proinflammatory cytokine secretion, they still display potent phagocytic activity. These adaptations allow intestinal macrophages to comply with their main task, i.e., the efficient removal of microbes while maintaining local tissue homeostasis. In this paper, we review recent findings on the functional differentiation of monocyte subsets into distinct macrophage populations and on the phenotypic and functional adaptations that have evolved in intestinal macrophages in response to their antigen-rich environment. Furthermore, the involvement of intestinal macrophages in the pathogenesis of celiac disease and inflammatory bowel diseases is discussed.

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Section: Regulation Of Phenotype and Functions Of Intestinal Macrophagesmentioning

confidence: 87%

Intestinal macrophages: differentiation and involvement in intestinal immunopathologies

2009

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“…Recent studies suggest that stromal cells, in particularly fibroblast and myofibroblasts, represent potential mediators of Ag presentation and T cell attraction to the inflammatory site (52,53). Fibroblast and myofibroblasts have been shown to produce a number of important mediators during inflammatory responses, including IL-6, IL-8, M-CSF, and GM-CSF (54,55).…”

Section: Discussionmentioning

confidence: 99%

Monocyte Chemoattractant Protein-1 Production by Intestinal Myofibroblasts in Response to Staphylococcal Enterotoxin A: Relevance to Staphylococcal Enterotoxigenic Disease

Pinchuk¹,

Beswick²,

Saada³

et al. 2007

The Journal of Immunology

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Food poisoning due to staphylococcal enterotoxins A and B (SEA and SEB) affects hundreds of thousands of people annually. SEA and SEB induce massive intestinal cytokine production, which is believed to be the key factor in staphylococcal enterotoxin enteropathy. MHC class II molecules are the major receptors for staphylococcal enterotoxins. We recently demonstrated that normal human subepithelial intestinal myofibroblasts (IMFs) express MHC class II molecules. We hypothesized that IMFs are among the first cells to respond to staphylococcal enterotoxins and contribute to the cytokine production associated with staphylococcal enterotoxin pathogenesis. We demonstrated here that primary cultured IMFs bind staphylococcal enterotoxins in a MHC class II-dependent fashion in vitro. We also demonstrated that staphylococcal enterotoxins can cross a CaCo-2 epithelial monolayer in coculture with IMFs and bind to the MHC class II on IMFs. IMFs responded to SEA, but not SEB, exposure with 3- to 20-fold increases in the production of proinflammatory chemokines (MCP-1, IL-8), cytokines (IL-6), and growth factors (GM-CSF and G-CSF). The SEA induction of the proinflammatory mediators by IMFs resulted from the efficient cross-linking of MHC class II molecules because cross-linking of class II MHC by biotinylated anti-HLA-DR Abs induced similar cytokine patterns. The studies presented here show that MCP-1 is central to the production of other cytokines elicited by SEA in IMFs because its neutralization with specific Abs prevented the expression of IL-6 and IL-8 by IMFs. Thus, MCP-1 may play a leading role in initiation of inflammatory injury associated with staphylococcal enterotoxigenic disease.

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“…In this scenario, the inducer cells would be hyperactivated lymphocytes that induce and subsequently continuously trigger myofibroblasts. In fact, rheumatoid fibroblast-like synoviocytes have been shown to overexpress the chemokine CXCL12, mediating the migration and accumulation of CXCR4-expressing T cells (49,50,55,56). Moreover, the production of homeostatic chemokines has been reported in several autoimmune disorders (57)(58)(59)(60)(61)(62)(63)(64).…”

Section: Stromal Compartments In Inflammatory Lesionsmentioning

confidence: 99%

“…Moreover, the production of homeostatic chemokines has been reported in several autoimmune disorders (57)(58)(59)(60)(61)(62)(63)(64). Also during inflammatory bowel disease, a central role for intestinal fibroblasts in attracting and retaining immune cells during inflammation was postulated (49,50,56).…”

Section: Stromal Compartments In Inflammatory Lesionsmentioning

confidence: 99%

Cellular Interactions in Lymph Node Development

Cupedo

Mebius

2005

The Journal of Immunology

111

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The organized accumulation of lymphocytes is a biological phenomenon used to optimize both homeostatic immune surveillance, as well as chronic responses to pathogenic stimuli. During embryonic development, circulating hemopoietic cells gather at predestined sites throughout the body, where they are subsequently arranged in T and B cell-specific areas characteristic of secondary lymphoid organs. In contrast, the body seems to harbor a limited second set of selected sites that support formation of organized lymphoid aggregates. However, these are only revealed at times of local, chronic inflammation, when so-called tertiary lymphoid structures appear. Once thought of as two distinct phenomena, recent insights suggest that highly similar networks of paracrine interactions regulate the formation of both secondary and tertiary lymphoid structures. This review will focus on these cellular interactions between organizing and inducing cell populations leading to the formation of lymph nodes or organized inflammatory infiltrates.

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Differential Activation of Cytokine Secretion in Primary Human Colonic Fibroblast/Myofibroblast Cultures

Cited by 62 publications

References 44 publications

Intestinal macrophages: differentiation and involvement in intestinal immunopathologies

Intestinal macrophages: differentiation and involvement in intestinal immunopathologies

Monocyte Chemoattractant Protein-1 Production by Intestinal Myofibroblasts in Response to Staphylococcal Enterotoxin A: Relevance to Staphylococcal Enterotoxigenic Disease

Cellular Interactions in Lymph Node Development

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