Taenia crassiceps carbohydrates stimulate IL-6 expression in naïve murine macrophages via Toll-like receptors (TLRs)

Dissanayake, Senarath; Amith, Ray; Shahin, Allen

doi:10.1016/j.molimm.2004.03.020

Cited by 30 publications

(22 citation statements)

References 44 publications

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“…LNFPIII was one of the first purely carbohydrate moieties shown to signal through a TLR as well as one of the most finely characterized, because the nonfucosylated homologue of LNFPIII, lacto-N-neotetraoase (LNnT), does not signal through TLR4, establishing the necessity of the fucose residue for activity. LNFPIII contains the asialo and asulfo Lewis X trisaccharide, and Dissanayake et al (7) recently reported that Lewis X activates APCs via TLR4, corroborating our findings. Interestingly, although not yet shown to be a TLR4-dependent pathway, Helicobacter pylori, which express Lewis X on their LPS, induce Th2 responses, whereas those bacteria that are Lewis negative drive proinflammatory responses (8).…”

supporting

confidence: 92%

A Helminth Glycan Induces APC Maturation via Alternative NF-κB Activation Independent of IκBα Degradation

Thomas

Carter

Da’dara

et al. 2005

The Journal of Immunology

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Activation of APCs via TLRs leads to activation of NF-κB, a key transcription factor in cells of the immune system most often associated with induction of Th1-type and proinflammatory responses. The neoglycoconjugate lacto-N-fucopentaose III (12-25 molecules)-dextran (LNFPIII-Dex) activates dendritic cells (DCs) via TLR4, as does LPS. However, unlike LPS, LNFPIII-Dex-activated cells induce Th2-type CD4+ T cell responses. This observation led us to ask whether LNFPIII-activated APCs were differentially activating NF-κB, and if so, could this partly account for how DCs mature in response to these two different pathogen-associated molecular patterns (PAMPs). In this study, we show that LNFPIII-Dex stimulation of APCs induces rapid, but transient NF-κB translocation and activity in the nucleus, in comparison with the persistent activation induced by LPS. We then demonstrate that transient vs persistent NF-κB activation has important implications in the development of the APC phenotype, showing that the second wave of NF-κB translocation in response to LPS is required for production of the proinflammatory mediator NO. In contrast to LPS, LNFPIII-stimulated APCs that only transiently activate NF-κB do not induce degradation of the known IκB family members or production of NO. However, cells stimulated with LNFPIII rapidly accumulate p50, suggesting that an alternative p105 degradation-dependent mechanism is primarily responsible for NF-κB activation downstream of LNFPIII. Finally, we show that while NF-κB translocation in LNFPIII-stimulated APCs is transient, it is required for the development of the DC 2 phenotype, confirming a crucial and multifaceted role for NF-κB in innate immune responses.

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supporting

confidence: 92%

A Helminth Glycan Induces APC Maturation via Alternative NF-κB Activation Independent of IκBα Degradation

Thomas

Carter

Da’dara

et al. 2005

The Journal of Immunology

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“…One of the putative receptors most studied has been TLR4 (Thomas et al 2003;Dissanayake et al 2004;Taylor et al 2005c); however, TLR4 is mainly known to induce strong pro-inflammatory cytokines after triggerring it with different bacterial and/or intracellular parasites (Schnare et al 2001). To explore the possibility that mTSA may act via TLR4-signaling in the Th2 biasing, we used C3H/HeJ mice that had defective activity of TLR4.…”

Section: Resultsmentioning

confidence: 99%

Carbohydrate components of Taenia crassiceps metacestodes display Th2-adjuvant and anti-inflammatory properties when co-injected with bystander antigen

et al. 2006

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Common helminth infections promote Th2-skewed immune responses in their hosts. We have studied the role of intact carbohydrate structures on Taenia crassiceps compounds in the induction of biased type 2 and anti-inflammatory immune responses on peptidestimulated T cells by using DO11.10 transgenic (OVA Tg) mice. While OVA Tg mice co-injected with OVA peptide [323][324][325][326][327][328][329][330][331][332][333][334][335][336][337][338][339]

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“…Also the egg stage contains dsRNA that activate TLR3 in myeloid dendritic cells (Aksoy et al, 2005). In addition, phosphorylcholine containing secretory components of filarial nematode activates TLR4 (Goodridge et al, 2005) and carbohydrates of Taenia crassiceps carbohydrates has been postulated to stimulate IL6 expression through TLRs (Dissanayake et al, 2004). M. corti being a multicellular helminth parasite with a diversity of antigens likely contains unique motifs that recognize TLR receptors and directly elicits inflammatory responses in the brain.…”

Section: Discussionmentioning

confidence: 99%

Expression and distribution of Toll‐like receptors in the brain during murine neurocysticercosis

Mishra

Teale

2006

Journal of Neuroimmunology

148

153

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In a mouse model of neurocysticercosis, the expression and distribution of Toll like receptors (TLRs) was investigated by using both gene array analyses and in situ immunofluoresence microscopy (IF). In the normal uninfected brain, mRNA of all the TLRs are constitutively expressed albeit TLR5, TLR7, TLR8 and TLR9 to a lesser extent. In these animals, however, expression of TLR1, TLR3, TLR4 and TLR9 proteins was not detected. In contrast, parasite infection increased both gene and protein level expression of all the TLRs several fold except TLR5 where only the mRNA was upregulated. Importantly, TLRs were differentially distributed among various central nervous system (CNS) cell types and infiltrating leukocytes. TLR2 was almost exclusively localized to nervous tissue cells, particularly astrocytes, while TLR1 and TLR9 proteins were essentially limited to infiltrating leukocytes. All other TLRs tested were detected in both CNS and immune cell types. Interestingly, ependymal cells and neurofilaments of the cerebellar white matter of infected mice exhibited a substantial upregulation of TLR7 and TLR8 protein respectively. These data provide a comprehensive analysis of TLR expression in the normal and parasite infected brain and suggest a role for TLRs in the interplay of immune cells and CNS cells during infection.

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Taenia crassiceps carbohydrates stimulate IL-6 expression in naïve murine macrophages via Toll-like receptors (TLRs)

Cited by 30 publications

References 44 publications

A Helminth Glycan Induces APC Maturation via Alternative NF-κB Activation Independent of IκBα Degradation

A Helminth Glycan Induces APC Maturation via Alternative NF-κB Activation Independent of IκBα Degradation

Carbohydrate components of Taenia crassiceps metacestodes display Th2-adjuvant and anti-inflammatory properties when co-injected with bystander antigen

Expression and distribution of Toll‐like receptors in the brain during murine neurocysticercosis

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