Early activation of mucosal dendritic cells and macrophages in acute <i>Campylobacter</i> colitis and cholera: An <i>in vivo</i> study

Pulimood, Anna; Ramakrishna, B. S.; Rita, Arockiasamy B; Srinivasan, Pattabiraman; Mohan, Vivek; Gupta, Sanjaykumar; Perakath, Benjamin; Kang, Gagandeep; Chandy, George; Balasubramanian, K.A.

doi:10.1111/j.1440-1746.2008.05325.x

Cited by 12 publications

(5 citation statements)

References 42 publications

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“…Upon treatment with T H 1 conditioned media these cells became more adherent, formed long dendrites, and tended to cluster (Figure 4B). These are features associated with DC maturation and heightened capacity to present antigen (42;43). These morphologic changes could be abrogated by treatment with 4-MU (Figure 4C).…”

Section: Resultsmentioning

confidence: 99%

Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse

Bollyky

Evanko

et al. 2010

Cell Mol Immunol

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Hyaluronan (HA) production by dendritic cells (DCs) is known to promote antigen presentation and to augment T-cell activation and proliferation. We hypothesized that pericellular HA can function as intercellular 'glue' directly mediating T cell-DC binding. Using primary human cells, we observed HA-dependent binding between T cells and DCs, which was abrogated upon pre-treatment of the DCs with 4-methylumbelliferone (4-MU), an agent which blocks HA synthesis. Furthermore, T cells regulate HA production by DCs via T cell-derived cytokines in a T helper (Th) subset-specific manner, as demonstrated by the observation that cell-culture supernatants from Th1 but not Th2 clones promote HA production. Similar effects were seen upon the addition of exogenous Th1 cytokines, IL-2, interferon c (IFN-c) and tumor necrosis factor a (TNF-a). The critical factors which determined the extent of DC-T cell binding in this system were the nature of the pre-treatment the DCs received and their capacity to synthesize HA, as T-cell clones which were pre-treated with monensin, added to block cytokine secretion, bound equivalently irrespective of their Th subset. These data support the existence of a feedforward loop wherein T-cell cytokines influence DC production of HA, which in turn affects the extent of DC-T cell binding.

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Section: Resultsmentioning

confidence: 99%

Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse

Bollyky

Evanko

et al. 2010

Cell Mol Immunol

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“…The data indicate that this mucosal immune activation is associated with Th1 polarization. While the significance of CD11c + cell redistribution towards the lumen is not clear, it is interesting to note that enrichment of dendritic cells at the superficial mucosa has been observed during the early stages of Campylobacter colitis in human patients38 and that dendritic cell redistribution has also been associated with NSAID-induced colitis in rats 39. One might also ask why CA-MLCK Tg mice are not ill.…”

Section: Discussionmentioning

confidence: 99%

Targeted Epithelial Tight Junction Dysfunction Causes Immune Activation and Contributes to Development of Experimental Colitis

et al. 2009

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Background & Aims-Inflammatory bowel disease (IBD) is a multifactorial disease thought to be caused by alterations in epithelial function, innate and adaptive immunity, and luminal microbiota. The specific role of epithelial barrier function remains undefined, although increased activity of intestinal epithelial myosin light chain kinase (MLCK), which is the primary mechanism of tumor necrosis factor (TNF)-induced barrier dysfunction, occurs in human IBD. We aimed to determine whether in an intact epithelium, primary dysregulation of the intestinal epithelial barrier by pathophysiologically relevant mechanisms can contribute to development of colitis.

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“…Instead, V. cholerae colonizes the small intestine and causes secretory diarrhea, mediated by the action of cholera toxin (CT) on intestinal epithelial cells (6). Still, cholera is associated with microscopic inflammatory changes of the human small intestine, which include the widening of intercellular spaces, apical junction abnormalities, vascular congestion, and an influx of neutrophils, mast cells, eosinophils, macrophages, and activated dendritic cells (7)(8)(9). In addition, a number of mucosal innate effector molecules, including bactericidal proteins, defensins, lactoferrin, myeloperoxidase, and BPIFB1 (LPLUNC1) are expressed in response to V. cholerae infection (10)(11)(12).…”

mentioning

confidence: 99%

Analysis of the Human Mucosal Response to Cholera Reveals Sustained Activation of Innate Immune Signaling Pathways

et al. 2018

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To better understand the innate immune response to infection, we tracked gene expression in the duodenal mucosa of 11 Bangladeshi adults with cholera, using biopsy specimens obtained immediately after rehydration and 30 and 180 days later. We identified differentially expressed genes and performed an analysis to predict differentially regulated pathways and upstream regulators. During acute cholera, there was a broad increase in the expression of genes associated with innate immunity, including activation of the NF-κB, mitogen-activated protein kinase (MAPK), and Toll-like receptor (TLR)-mediated signaling pathways, which, unexpectedly, persisted even 30 days after infection. Focusing on early differences in gene expression, we identified 37 genes that were differentially expressed on days 2 and 30 across the 11 participants. These genes included the endosomal Toll-like receptor gene, which was expressed in lamina propria cells. Underscoring a potential role for endosomal TLR-mediated signaling , our pathway analysis found that interferon regulatory factor 7 and beta 1 and alpha 2 interferons were among the top upstream regulators activated during cholera. Among the innate immune effectors, we found that the gene for DUOX2, an NADPH oxidase involved in the maintenance of intestinal homeostasis, was upregulated in intestinal epithelial cells during cholera. Notably, the observed increases in and expression were also modeled when Caco-2 or THP-1 cells, respectively, were stimulated with live but not with heat-killed organisms or cholera toxin alone. These previously unidentified features of the innate immune response to extend our understanding of the mucosal immune signaling pathways and effectors activated following cholera.

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Early activation of mucosal dendritic cells and macrophages in acute Campylobacter colitis and cholera: An in vivo study

Cited by 12 publications

References 42 publications

Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse

Th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse

Targeted Epithelial Tight Junction Dysfunction Causes Immune Activation and Contributes to Development of Experimental Colitis

Analysis of the Human Mucosal Response to Cholera Reveals Sustained Activation of Innate Immune Signaling Pathways

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