| 1. |
- Chu, Derek K, et al.
(författare)
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Indigenous enteric eosinophils control DCs to initiate a primary Th2 immune response in vivo.
- 2014
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 211:8, s. 1657-1672
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Tidskriftsartikel (refereegranskat)abstract
- Eosinophils natively inhabit the small intestine, but a functional role for them there has remained elusive. Here, we show that eosinophil-deficient mice were protected from induction of Th2-mediated peanut food allergy and anaphylaxis, and Th2 priming was restored by reconstitution with il4(+/+) or il4(-/-) eosinophils. Eosinophils controlled CD103(+) dendritic cell (DC) activation and migration from the intestine to draining lymph nodes, events necessary for Th2 priming. Eosinophil activation in vitro and in vivo led to degranulation of eosinophil peroxidase, a granule protein whose enzymatic activity promoted DC activation in mice and humans in vitro, and intestinal and extraintestinal mouse DC activation and mobilization to lymph nodes in vivo. Further, eosinophil peroxidase enhanced responses to ovalbumin seen after immunization. Thus, eosinophils can be critical contributors to the intestinal immune system, and granule-mediated shaping of DC responses can promote both intestinal and extraintestinal adaptive immunity.
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| 2. |
- Rydell-Törmänen, Kristina, et al.
(författare)
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Induction of Vascular Remodeling in the Lung by Chronic House Dust Mite Exposure.
- 2008
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Ingår i: American Journal of Respiratory Cell and Molecular Biology. - 1535-4989. ; 39, s. 61-67
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Tidskriftsartikel (refereegranskat)abstract
- Structural changes to the lung are known to be associated with chronic asthma. In addition to the well-described alterations to the airway wall, asthma is also associated with vascular modifications, although this aspect of remodeling is poorly understood. We therefore sought to evaluate the character and kinetics of vascular remodeling in response to chronic aeroallergen exposure. However, since many OVA-driven models used to investigate allergic airway disease do so in the absence of persistent airway inflammation, we chose instead to employ a protocol of chronic respiratory exposure to house dust mite extract (HDM), which has been shown to induce persistent airway inflammation consistent with that seen in human asthmatics. Mice were exposed to HDM intranasally for 7 or 20 consecutive weeks, and resolution of the inflammatory and remodeling response to allergen was investigated 4 weeks following the end of a 7-week exposure protocol. Measures of vascular remodeling, including total collagen deposition, procollagen I-production, endothelial and smooth muscle cell proliferation, smooth muscle area and presence of myofibroblasts were investigated histologically in lung vessels of different sizes and locations. We observed an increase in total collagen content which did not resolve upon cessation of allergen exposure. Other parameters were significantly increased following 7 and/or 20 weeks of allergen exposure, but returned to baseline following allergen withdrawal. We conclude that respiratory HDM exposure induces not only airway remodeling, but also pulmonary vascular remodeling, and in accordance with airway remodeling, some components of these structural changes may be irreversible.
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