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Traffic pollution has been recognized as directly worsening respiratory symptoms of allergic subjects, although whether urban air pollutants can also directly increase the allergenic potential of pollen has not yet been definitely proven. Therefore, the hypothesis that intra-urban air NO2 variation influences allergens expression in Cupressus sempervirens (Cs) L. pollen was tested.Mature microsporophylls were cut from Cs trees of similar age and height (14-17 m) present in three different sites of Florence (Italy) and processed in the laboratory. Cs pollen allergens amount was determined by a semi-quantitative analysis of electrophoretically separated pollen extracts fractions. NO2 air concentrations were recorded by air monitoring stations located at a distance not exceeding 50 m from each pollen collection site, and the relative annual mean values were acquired by a publicly available database (Tuscan Regional Agency for Environment Protection).Expression of three major Cs pollen allergens was non-linearly correlated with mean annual NO2 concentrations. Expression peak of all major allergens considered was reached at NO2 air concentration (67μg/m3), far below the value at risk for direct effect on the respiratory health (European Union Directive 2008/50/EC).The findings suggest that intra-urban NO2 variations do affect the expression of Cs pollen major allergens, and an apparent low risk NO2 concentration should be regarded as indirectly harmful for increasing the allergenic potential of pollen.

Objective To recapitulate the more recent epidemiologic studies on the association of air pollution with respiratory allergic diseases prevalence and to discuss the main limitations of current approaches used to establish a link between pollinosis and pollution. Data Sources Through the use of PubMed, we conducted a broad literature review in the following areas: epidemiology of respiratory allergic diseases, effect of pollution and climate changes on pollen grains, and immunomodulatory properties of pollen substances. Study Selections Studies on short- and long-term exposure to air pollutants, such as gaseous and particulate materials, on allergic sensitization, and on exacerbation of asthma symptoms were considered. Results Trend in respiratory allergic disease prevalence has increased worldwide during the last 3 decades. Although recent epidemiologic studies on a possible association of this phenomenon with increasing pollution are controversial, botanic studies suggest a clear effect of several pollutants combined to climatic changes on the increased expression of allergenic proteins in several pollen grains. The current literature suggests the need for considering both pollen allergen and pollutant contents for epidemiologic evaluation of environmental determinants in respiratory allergies. We propose that a measure of allergenic potential of pollens, indicative of the increase in allergenicity of a polluted pollen, may be considered as a new risk indicator for respiratory health in urban areas. Conclusion Because public greens are located in strict proximity to the anthropogenic sources of pollution, the identification of novel more reliable parameters for risk assessment in respiratory allergic diseases is an essential need for public health management and primary prevention area.

Eosinophils are major effectors of Th2-related pathologies, frequently found infiltrating several human cancers. We recently showed that eosinophils play an essential role in anti-tumor responses mediated by immunotherapy with the &lsquo, alarmin&rsquo, intereukin-33 (IL-33) in melanoma mouse models. Here, we analyzed the mechanisms by which IL-33 mediates tumor infiltration and antitumor activities of eosinophils. We show that IL-33 recruits eosinophils indirectly, via stimulation of tumor cell-derived chemokines, while it activates eosinophils directly, up-regulating CD69, the adhesion molecules ICAM-1 and CD11b/CD18, and the degranulation marker CD63. In co-culture experiments with four different tumor cell lines, IL-33-activated eosinophils established large numbers of stable cell conjugates with target tumor cells, with the polarization of eosinophil effector proteins (ECP, EPX, and granzyme-B) and CD11b/CD18 to immune synapses, resulting in efficient contact-dependent degranulation and tumor cell killing. In tumor-bearing mice, IL-33 induced substantial accumulation of degranulating eosinophils within tumor necrotic areas, indicating cytotoxic activity in vivo. Blocking of CD11b/CD18 signaling significantly reduced IL-33-activated eosinophils&rsquo, binding and subsequent killing of tumor cells, indicating a crucial role for this integrin in triggering degranulation. Our findings provide novel mechanistic insights for eosinophil-mediated anti-tumoral function driven by IL-33. Treatments enabling tumor infiltration and proper activation of eosinophils may improve therapeutic response in cancer patients.

Appropriate murine models of shrimp tropomyosin (ST) allergy would be useful in investigating the mechanisms underlying food allergy in human subjects, as well as for the pre-clinical evaluation of efficacy and safety of novel therapeutic approaches. These models should mimic immune and clinical features of human disease, including anaphylactic response. We sensitized C3H/HeJ mice by the oral route with purified ST using cholera toxin (CT) as adjuvant. ST-specific IgE, IgG1, IgG2a and IgA responses were evaluated by ELISA. Spleen cell proliferation and cytokine production by allergen-specific activation were assessed. Jejunum and colon fragments were collected to evaluate the local expression of cytokine genes by PCR. Local and systemic anaphylactic reactions induced by oral ST challenge were scored according to symptoms observed. Faecal samples were collected to assess local IgA production and histamine levels. Oral sensitization with ST plus CT induced in mice significant levels of serum IgE and IgG1 and faecal IgA. ST-specific cell proliferation and IL-4, IL-13 and IFN-gamma cytokine production were induced in the spleen. After oral challenge, 100% of mice had anaphylactic symptoms while no symptoms were observed in challenged naive mice. Faecal histamine content after ST challenge appeared significantly increased in sensitized mice when compared with that observed in pre-immune mice. Jejunum mRNA expression of T(h)2 cytokines was up-regulated by ST sensitization. These results support the importance of the oral way of sensitization and of the in-depth characterization of the anaphylactic response for the development of a suitable in vivo model of food allergy.

Background: A rapid method for the purification of the major 43-kDa all_ergen of Cupressus arizonica pollen, Cup a 1, was developed. Methods: The salient feature was a wash of the pollen in acidic buffer, followed by an extraction of the proteins and their purification by chromatography. Immunoblotting, ELISA, and lectin binding were tested on both the crude extract and the purified Cup a 1. Biochemical analyses were performed to assess the Cup a 1 isoelectric point, its partial amino-acid sequence, and its glycan composition. Results: Immunochemical analysis of Cup a 1 confirmed that the all_ergenic reactivity is maintained after the purification process. Partial amino-acid sequencing indicated a high degree of homology between Cup a 1 and all_ergenic proteins from the Cupressaceae and Taxodiaceae families displaying a similar molecular mass. The purified protein shows one band with an isoelectric point of 5.2. Nineteen out of 33 sera (57%) from patients all_ergic to cypress demonstrated significant reactivity to purified Cup a 1. MALDI-TOF mass spectrometry indicated the presence of three N-linked oligosaccharide structures: GnGnXF3 (i.e., a horseradish peroxidase-type oligosaccharide substituted with two nonreducing N-acetylglucosamine residues), GGnXF3/GnGXF3 (i.e., GnGnXF with one nonreducing galactose residue), and (GF)GnXF3/Gn(GF)XF3 (with a Lewisa epitope on one arm) in the molar ratio 67:8:23. Conclusions: The rapid purification process of Cup a 1 all_owed some fine studies on its properties and structure, as well as the evaluation of its IgE reactivity in native conditions. The similarities of amino-acid sequences and some complex glycan stuctures could explain the high degree of cross-reactivity among the Cupressaceae and Taxodiaceae families.

Background Cypress pollen causes respiratory syndromes with different grades of severity, including asthma. IL-33, its receptor ST2, and dendritic cells (DCs) have been implicated in human respiratory allergy. Objective We sought to define a new mouse model of allergy to cypress pollen that recapitulates clinical parameters in allergic patients and to evaluate the implications of DCs and the IL-33/ST2 pathway in this pathology. Methods BALB/c mice, either wild-type or ST2 deficient (ST2 −/− ), were sensitized and challenged with the Cupressus arizonica major allergen nCup a 1. Local and systemic allergic responses were evaluated. Pulmonary cells were characterized by means of flow cytometry. DCs were stimulated with nCup a 1 and tested for their biological response to IL-33 in coculture assays. Results nCup a 1 causes a respiratory syndrome closely resembling human pollinosis in BALB/c mice. nCup a 1–treated mice exhibit the hallmarks of allergic pathology associated with pulmonary infiltration of eosinophils, T cells, and DCs and a dominant T H 2-type immune response. IL-33 levels were increased in lungs and sera of nCup a 1–treated mice and in subjects with cypress allergy. The allergen-specific reaction was markedly reduced in ST2 −/− mice, which showed fewer infiltrating eosinophils, T cells, and DCs in the lungs. Finally, stimulation of DCs with nCup a 1 resulted in ST2 upregulation that endowed DCs with increased ability to respond to IL-33–mediated differentiation of IL-5– and IL-13–producing CD4 T cells. Conclusions Our findings define a novel preclinical model of allergy to cypress pollen and provide the first evidence of a functionally relevant linkage between pollen allergens and T H 2-polarizing activity by DCs through IL-33/ST2.

A simple and sensitive immunoenzymatic assay for detection of specific IgE in hydatid disease is presented. Sera from 43 patients with hydatidosis, eight with schistosomiasis, two with taeniasis, two with cancer and 16 healthy blood donors were tested by both the immunoenzymatic technique and the classical radioallergosorbent test. Data were analysed in terms of different sensitivity and specificity of the two methods. The results indicate that the enzymatic method performed in microplates is as sensitive as the radioimmunological one (77% of positivity for both the tests), but the latter suffers from an higher rate of false positive reactions with sera from patients with other helminthic diseases (80% vs 20%). When the specific IgE evaluation is compared with other classical serological techniques, such as indirect haemagglutination and double diffusion in terms of different sensitivity in revealing an anti-Echinococcus immunological reactivity, the results suggest that specific IgE evaluation represents a useful addition to the classical serodiagnostic tests.