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Differential Response of Respiratory Dendritic Cell Subsets to Influenza Virus Infection
- J. Virol. 2008
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This article cites 40 articles, 23 of which can be accessed free
Ultrafine Carbon Black Particles Cause Early Airway Inflammation and Have Adjuvant Activity in a Mouse Allergic Airway Disease
, 2005
"... To gain more insight into the mechanisms of particulate matter (PM)-induced adjuvant activity, we studied the kinetics of airway toxicity/inflammation and allergic sensitization to ovalbumin (OVA) in response to ultrafine carbon black particles (CBP). Mice were exposed intranasally to OVA alone or i ..."
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To gain more insight into the mechanisms of particulate matter (PM)-induced adjuvant activity, we studied the kinetics of airway toxicity/inflammation and allergic sensitization to ovalbumin (OVA) in response to ultrafine carbon black particles (CBP). Mice were exposed intranasally to OVA alone or in combination with different concentrations of CBP. Airway toxicity and inflamma-tion were assessed at days 4 and 8. Immune adjuvant effects were studied in the lung draining peribronchial lymph nodes (PBLN) at day 8. Antigen-specific IgE was measured at days 21 and 28, whereas allergic airway inflammation was studied after OVA challenges (day 28). Results show that a total dose of 200 mg CBP per mouse, but not 20 mg or 2 mg, induced immediate airway inflammation. This 200 mg CBP was the only dose that had immune adjuvant activity, by inducing enlargement of the PBLN and increasing OVA-specific production of Th2 cytokines (IL-4, IL-5, and IL-10). The immune adjuvant activity of 200 mg CBP dosing was further examined. Whereas increased OVA-specific IgE levels in serum on day 21 confirms systemic sensitization, this was further supported by allergic airway inflammation after challenges with OVA. Our data show a link between early airway toxicity and adjuvant effects of CBP. In addition, results indicate that local cytokine production early after exposure to CBP is predictive of allergic airway inflammation. In addition this model appears suitable for studying the role of airway toxicity, in-flammation and other mechanisms of particle adjuvant activity, and predicting the adjuvant potential of different particles. Key Words: ultrafine particles; adjuvant; allergy; intranasal; inflammation.
Two distinct activation states of plasmacytoid dendritic cells
"... induced by influenza virus and CpG 1826 oligonucleotide ..."
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induced by influenza virus and CpG 1826 oligonucleotide
Role for dendritic cells in immunoregulation during experimental vaginal candidiasis. Infect. Immun
, 2006
"... This article cites 38 articles, 28 of which can be accessed free ..."
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Cited by 2 (0 self)
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This article cites 38 articles, 28 of which can be accessed free
Forecast Alert
- IT Spending, Worldwide, 2008-2015, 4Q11 Update. 2012 http://www.gartner.com: http://www.gartner.com/it/content/1870000/1870018/january_10_it_spending_forecast_4q11_update_rgordon.p df?userId=57517080
, 2011
"... This article cites 42 articles, 15 of which can be accessed free ..."
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This article cites 42 articles, 15 of which can be accessed free
Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection �
, 2007
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Neutrophils regulate airway responses in a model of fungal allergic airways disease
- J
, 2006
"... Neutrophils infiltrate airway walls in patients with allergic airway diseases and in animal models of these illnesses, but their contribution to the pathogenesis of airway allergy is not established. We hypothesized that, in a mouse model of airway allergy to the ubiquitous environmental mold, Asper ..."
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Neutrophils infiltrate airway walls in patients with allergic airway diseases and in animal models of these illnesses, but their contribution to the pathogenesis of airway allergy is not established. We hypothesized that, in a mouse model of airway allergy to the ubiquitous environmental mold, Aspergillus fumigatus, airway neutrophils contribute to disease severity. Ab-mediated neutrophil depletion resulted in reduced airway hyperresponsiveness and remodeling, whereas conditional transgenic overex-pression of the neutrophil chemotactic molecule, CXCL1, in airway walls resulted in worsened allergic responses. This worsened phenotype was associated with a marked increase in the number of airway neutrophils but not other lung leukocytes, including eosinophils and lymphocyte subsets, and depletion of neutrophils in sensitized mice with transgenic overexpression of CXCL1 resulted in attenuated airway responses. The number of lung neutrophils correlated with lung matrix metalloproteinase 9 (MMP-9) activity both in the context of neutrophil depletion and with augmented neutrophil recruitment to the airways. Although wild-type and MMP-9-deficient neutrophils homed to the inflamed airways to a similar extent, transfer of wild-type, but not MMP-9-deficient, neutrophils to MMP-9-deficient animals resulted in augmented allergic airway responses. Taken together, these data implicate neutrophils in the pathogenesis of fungal allergic airway disease. The Journal of Immunology, 2006, 176: 2538– 2545. A llergic airway diseases are among the most common ail-ments in industrialized societies, affecting some 10 % ofthe population (1) and occur in response to a myriad of inhaled Ags. The pathogenesis of these illnesses centers on pro-
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"... Facilitated antigen uptake and timed exposure to TLR ligands dictate the antigen-presenting potential of plasmacytoid DCs ..."
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Facilitated antigen uptake and timed exposure to TLR ligands dictate the antigen-presenting potential of plasmacytoid DCs
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"... Facilitated antigen uptake and timed exposure to TLR ligands dictate the antigen-presenting potential of plasmacytoid DCs ..."
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Facilitated antigen uptake and timed exposure to TLR ligands dictate the antigen-presenting potential of plasmacytoid DCs
