PubMed · 13057382
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1953. RAGWEED dermatitis.. https://pubmed.ncbi.nlm.nih.gov/13057382/
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Ambrosia artemisiifolia L. (common ragweed), an annual invasive plant, was introduced more than 100 years ago from North America to Europe. Like the majority of other invasive plants in Europe, it develops in open, disturbed areas such as fields, wastelands, roadsides, and riverbanks. Recently, arbuscular mycorrhizal fungi (AMF) have been suspected to play a role in some plant invasion processes. As the common ragweed is known to be colonized by AMF in its native range, the intensity of mycorrhizal root colonization was studied in 35 natural populations in eastern France. About 94% of the A. artemisiifolia populations sampled were mycorrhizal. Root colonization levels varied from 1 to 40% depending on the ecological sites, with lower levels for agricultural habitats and higher levels in disturbed sites, such as wastelands or roadsides. A subsequent greenhouse experiment showed positive impacts of AMF on the growth and development of A. artemisiifolia. It is proposed that the spread of this invasive plant species could be facilitated by AMF, underlining the need to integrate symbiotic interactions in future work on invasive plant processes.
We have previously demonstrated that protection from allergic inflammation by Ascaris suum infection was characterized by a global increase in interleukin-10 (IL-10) and the development of protective CD4(+)/CD25(+) T cells (L. Schopf, S. Luccioli, V. Bundoc, P. Justice, C. C. Chan, B. J. Wetzel, H. H. Norris, J. F. Urban, Jr., and A. Keane-Myers, Investig. Ophthalmol. Vis. Sci. 46:2772-2780, 2005). Here, we used A. suum pseudocoelomic fluid (PCF) in lieu of infection to define molecular mechanisms of allergic protection in a mouse model of allergic inflammation. Mice were sensitized with ragweed (RW) and PCF (RW/PCF), PCF alone, or RW alone and then challenged intratracheally, intranasally, and supraocularly with RW. Histological examination of the eyes and lungs, analysis of the bronchoalveolar lavage fluid (BALF), and characterization of ex vivo cytokine responses were performed to determine allergic inflammatory responses. RW/PCF-treated mice had suppressed allergic immune responses compared to mice given RW alone. To investigate whether IL-10 was involved in PCF-mediated allergic protection, similar experiments were performed using mice genetically deficient for IL-10. Persistent protection from allergic disease was observed in the absence of IL-10, indicating the primary mechanism of PCF protection is IL-10 independent. Ex vivo and in vitro analysis of PCF-treated dendritic cells (DC) demonstrated reduced activation receptor expression and cytokine production in response to either RW or lipopolysaccharide stimulation. These findings extend previous studies that showed infection with A. suum alters expression of allergic disease and suggest that PCF can contribute to this effect by interference with DC function.
BACKGROUND/AIM: Involvement of programmed death-1 (PD-1) and its ligands has been demonstrated in experimental allergic airway disease. Here, the authors aimed to examine whether PD-1 and its ligands are involved in the development of experimental allergic conjunctivitis (EC) in mice. METHODS: EC was induced in Balb/c mice by active immunisation with short ragweed pollen (RW) in alum. 10 days later (day 10), the mice were challenged with eye drops containing RW. 24 hours after the challenge, conjunctivas, spleens, and sera were harvested for histological analysis, cytokine assays, and measurement of RW specific Ig levels. The actively immunised mice were treated with anti-PD-1, anti-PD-L1, anti-PD-L2 antibodies (Abs), or normal rat immunoglobulin G (nrIgG) during either the induction (day 0, 2, 4, 6, and 8) or the effector (2 hours before RW challenge on day 10) phase. RESULTS: Ab treatment during the induction phase did not affect eosinophil infiltration although immune responses were modulated. In contrast, treatment with anti-PD-L2 Ab, but not anti-PD-1 or anti-PD-L1 Ab, during the effector phase significantly increased eosinophil infiltration into the conjunctiva without affecting systemic immune responses. CONCLUSIONS: Similar to allergic airway inflammation, PD-L2 is involved in the development of EC during the effector phase but not the induction phase.