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Using a mouse model of allergic lung inflammation, we found that mice deficient of Fgr, a Src family tyrosine kinase highly expressed in myelomonocytic cells, fail to develop lung eosinophilia in response to repeated challenge with aerosolized OVA. Both tissue and airway eosinophilia were markedly reduced in fgr(-/-) mice, whereas mice with the sole deficiency of Hck, another Src family member, responded normally. Release of allergic mediators, such as histamine, IL-4, RANTES/CCL5, and eotaxin/CCL11, in the airways of OVA-treated animals was equal in wild-type and fgr(-/-) mice. However, lung eosinophilia in Fgr-deficient mice correlated with a defective accumulation of GM-CSF and IL-5 in the airways, whereas secretion of these cytokines by spleen cells in response to OVA was normal. Examination of mRNA expression in whole lung tissue allowed us to detect comparable expression of transcripts for eotaxin/CCL11, macrophage-inflammatory protein-1 alpha/CCL3, macrophage-inflammatory protein-1 beta/CCL4, monocyte chemoattractant protein-1/CCL2, TCA-3/CCL1, IL-4, IL-10, IL-2, IL-3, IL-9, IL-15, and IFN-gamma in OVA-sensitized wild-type and fgr(-/-) mice. In contrast, the increase in IL-5 and IL-13 mRNA expression was lower in fgr(-/-) compared with wild-type mice. These findings suggest that deficiency of Fgr results in a marked reduction of lung eosinophilia and the establishment of a positive feedback loop based on autocrine secretion of eosinophil-active cytokines. These results identify Fgr as a novel pharmacological target to control allergic inflammation.

The level of exhaled nitric oxide (FENO) is increased in house dust mite (HDM)-sensitized asthmatic children after exposure to HDM antigen, and inhaled steroids can prevent this increase. The aim of this study was to evaluate whether montelukast could prevent an increase in FENO levels in allergic asthmatic children after a brief period of exposure to relevant allergens. Sixteen children were evaluated at the residential house 'Istituto Pio XII' (Misurina, Bellunio, Italy) in the Italian Alps, a dust mite-free environment. FENO levels were evaluated before (t0) and immediately after (t1) the children were exposed to HDM allergens for 2 weeks in their homes at sea level. No significant difference in FENO was observed in the fluticasone-treated group of children after 2 weeks at sea level. In the group treated with montelukast, an increase in FENO was observed between t0 and t1, which failed to reach statistical significance. These preliminary data suggest that oral montelukast could be effective in preventing the relapse in airway inflammation in allergic asthmatic children who are occasionally exposed to relevant allergens for a short period of time.

The purpose of this study was to assess the frequency of reported food-induced symptoms, and of food allergy or intolerance in 169 allergic patients monosensitized to grass pollen and in a control group of 50 patients who were monosensitized to Dermatophagoides. This study clearly demonstrates that patients with grass pollen-allergic respiratory disease report adverse food reactions more frequently than patients allergic to Dermatophagoides. This increased incidence is due to a high percentage of adverse reactions to some vegetable foods, especially peanut, garlic, tomato, onion; and fruits, such as peach; and animal foods, such as egg (white) and pork. By separating the food-allergic patients from the food-intolerant patients, the number of subjects with food intolerance was higher than that of the patients with food allergy. Crossreactivity between pollen allergens and fruits and vegetable allergens may explain the association between pollen allergy and food allergy, but not the higher incidence of food intolerance. An increased intestinal permeability to macromolecules may be hypothesized as part of a primary defect in permeability in "atopic (pollen allergic?) constitution."

The aim of this study was to compare a recent multiple allergosorbent chemiluminescent assay (MAST-CLA) with the RAST for the diagnosis of inhalant allergic disease in 232 patients with rhinitis and/or bronchial asthma. As judged by concordance of clinical history, skin prick tests to a range of six allergens common to our geographic area, and by nasal provocation tests, 70 patients were non-allergic and 162 allergic: 70 to grasses, 46 to mites, four to mugwort, eight to pellitory, and 34 were sensitive to several allergens. In our patient sample that, among other things, comprises subjects with fairly rare monoallergies, MAST-CLA testing gave results which closely corresponded to positive RAST for the allergens studied, and demonstrated a close correlation with the diagnosis of inhalant-specific allergy. Our results showed that, for overall allergens, MAST-CLA was lightly less sensitive and more specific than RAST (the two in vitro tests gave an identical overall efficiency).

Sera obtained from 212 patients with rhinopathy and/or asthma of allergic origin (pollens and/or mites) and from 87 apparently healthy controls were studied for the presence of organ and non organ specific autoantibodies. These were determined by indirect immunofluorescence techniques (5) using test tissue from monkeys (thyroid) and rats (stomach, liver and kidney). Two groups were matched for age and sex and the tests were performed using the double-blind method. The incidence observed was not dissimilar to that detected in healthy subjects, with the exclusion of smooth-muscle antibodies. These were present to a lesser extent in patients with respiratory allergies (0.94%) in contrast with the incidence of 5.73% in normal subjects (P less than 0.01). On the basis of our findings, it seems possible to hypothesize that allergic patients have a lesser tendency to autoimmune diseases because the immune system is committed to the IgE-mediated immunoreactions. In conclusion, autoantibodies do not seem to play a role in the pathogenesis of respiratory allergies to inhaled allergens.

Immunoconglutinins (Ic) are a group of predominantly IgM antibodies formed towards antigenic determinants exposed in fixed complement components (C3b and C4). Ic production is stimulated by bacterial and viral infections; elevated titers were also found in a number of other diseases involving completement-fixing reactions in vivo. High titers have been associated with the infectious morbidity within a particular population. The object of this investigation was to determine the correlations of autostimulated Ic titre with several parameters in 100 atopic nondesensitized subjects with respiratory allergies and in 140 non atopic, healthy, individuals. Eighty of them had rhinitis and/or conjunctivitis, 9 asthma and 11 rhinitis and asthma. All the atopics were studied also after at least 6 months of specific immunotherapy. None of the subjects received any other therapy at the time of study. Atopic subjects with high titers of Ic are significantly more numerous than controls, without significant correlation with the kind and beginning of atopic syndrome, and with immunotherapy. These results might be attributed to a higher incidence of infections in the atopic population. The Ic might play an important role in the immunoregulation involving complement system.

The purpose of this study was to compare the new multiple allergosorbent chemiluminescent assay (MAST CLA) system with the RAST and skin prick tests as an adjunct to the diagnosis of inhalant allergies. In this report, MAST CLA and RAST have given similar results, but no technique is as sensitive as skin tests for allergen-specific diagnosis of inhalant allergic disease.