B. Cárdaba

Molecular cloning of major allergen from Cupressus arizonica pollen: Cup a 1

The family Cupressaceae is a relevant source of allergens that causes winter respiratory allergies. Cloning and sequencing the major antigen of Cupressus arizonica is important for a better diagnosis and treatment of sensitized patients.

Analysis of polymorphisms in olive pollen allergy: IL13, IL4RA, IL5 and ADRB2 genes.

Background: Previous results demonstrated that sensitization to specific olive pollen allergens could be related with a different clinical pattern (asthma and/or rhinitis), and that specific patterns of sensitization are regulated by different HLA class II antigens. The authors analyze the possible implication of 7 genetic polymorphisms described as asthma susceptibility genes: IL13 (C–1112T and R130Q), IL4RA (I50V, Q551R), IL5 (C–746T) and ADRB2 (Q27E and R16G) in specific olive pollen allergic sensitization. Methods: The authors genotyped seven polymorphisms of the IL13, IL4RA, IL5 and ADRB2 genes in 146 patients allergic to olive pollen with seasonal rhinitis/asthma and 50 controls using the polymerase chain reaction-restriction fragment length polymorphism and real-time polymerase chain reaction techniques. Results: Two polymorphisms of IL13 were associated with allergy to olive pollen: the TT genotype of IL13 C–1112T was decreased (odds ratio, OR = 0.35, p = 0.006) whereas the RQ heterozygous genotype of IL13 R130Q increased in patients allergic to olive pollen (OR = 3.12, p = 0.009). The combined analysis of two IL4RA single nucleotide polymorphisms (SNPs) (I50V and Q551R) showed an association with asthma: IL4RA V50/Q551 was associated with risk (OR = 2.48, p = 0.007) whereas the IL4RA V50R551 haplotype was associated with protection (OR = 0.31, p = 0.003). Conclusions: The IL13 polymorphisms under study were associated with specific allergy to olive pollen: the IL13 C–1112T polymorphism as a protective factor and the IL13 R130Q polymorphism as a risk factor. Interestingly, although single polymorphisms of IL4RA are not associated with any phenotype analyzed, the interaction between IL4RA I50V/Q551R was strongly associated with the asthma phenotype. IL13 and IL4RA could be relevant markers for allergy to olive pollen and asthma development.

Allergy to olive pollen : T-cell response from olive allergic patients is restricted by DR7-DQ2 antigens

Backgound We have recently described the association between the IgE antibody response to Ole e I (the major antigen from olive tree pollen) and the DR7‐DQ2 haplotype in a Spanish population.

Update in the understanding of genetic predisposition to olive pollen sensitization

Olive tree pollen is one of the most important causes of allergy in the Mediterranean countries. Although the importance of this pollen provoking respiratory allergy is well established and documented, during the last decades, olive trees have been widely planted for ornamental purposes originating a new source of urban air pollution. This fact is one important reason why studies on olive pollen allergy are needed, in order to have more information about the prevention and possible modulation of this kind of sensitization. This article summarizes the advances in the study of genetic restrictions implicated in the susceptibility to the sensitization against the major allergen from this pollen: Ole e 1. Asthma and allergies are complex diseases involving genetic as well as environmental factors. The final clinical picture results from the interaction between genetic factors and environmental stimuli, and in addition, variables such as age, concurrent infections, and physiological factors, could promote differences in susceptibility. Despite this complexity, the allergic diseases are considered as an excellent model for the analysis of the genetic basis of the human immune response (1). The principal advantages are that they are common diseases with increasing prevalence and in addition, they have a well-defined clinical picture and the causative allergens may be identified and characterized so the immune response to them can be identified. The allergic reaction appears to require the interaction of environmental factors with a series of steps, which are genetically regulated. Genetic regulation of IgE responses to specific allergens may differ from that of the general atopic response. Probably, genetic associations are more readily detected with reactions to purified major allergens rather than complex allergen sources. The immunogenetic mechanisms underlying heightened IgE responsiveness seen in atopic diseases may be divided into two types: (a) antigen-specific and (b) nonantigen-specific (2–4).

Data set on a study of gene expression in peripheral samples to identify biomarkers of severity of allergic and nonallergic asthma

This article contains information related to the research article entitled “Biomarkers associated with disease severity in allergic and nonallergic asthma” (S. Baos, D. Calzada, L. Cremades, J. Sastre, J. Quiralte, F. Florido, C. Lahoz, B. Cárdaba, In press). Specifically, the clinical criteria stablished for selecting the study population (n=104 subjects) are described. Moreover, this article describes the criteria for selecting the 94 genes to be analyzed in PBMCs (peripheral blood mononuclear cells), it is provided a description of these genes and a Table with the genes most differentially expressed by clinical phenotypes and, finally it is detailed the experimental methodology followed for studying the protein expression of MSR1 (macrophage scavenger receptor 1), one of the genes evaluated in the research.

Immunological Mechanisms in Allergic Diseases and Allergen Tolerance: The Role of Treg Cells

The immune system regulates itself to establish an appropriate immune response to potentially harmful pathogens while tolerating harmless environmental antigens and self-antigens. A central role in this balance is played by regulatory T cells (Tregs) through various ways of actions. By means of molecule secretion and cell-cell contact mechanisms, Tregs may have the capacity to modulate effector T cells and suppress the action of proinflammatory cytokines across a broad range of cell types. As a result, abnormal regulatory T cell function has been pointed as a main cause in the development of allergic diseases, a major public health problem in industrialized countries, with a high socioeconomic impact. This prevalence and impact have created an international interest in improving the allergy diagnosis and therapy. Additionally, research has sought to gain a better understanding of the molecular mechanisms underlining this kind of disease, in order to a better management. At this respect, the role of Treg cells is one of the most promising areas of research, mainly because of their potential use as new immunotherapeutical approaches. Therefore, the aim of this review is to update the existing knowledge of the role of Tregs in this pathology deepening in their implication in allergen-specific therapy (AIT).

Eosinophils transcribe and translate messenger RNA for inducible nitric oxide

Because of the involvement of nitric oxide (NO) in inflammatory states such as parasitic and hypersensitivity disorders and the fact that eosinophils are one of the cell types implicated, we asked whether eosinophils were able to express mRNA specific to inducible NO synthase (iNOS) and iNOS protein and to secrete nitric oxide. iNOS protein was detected on eosinophil preparations by immunocytochemistry using iNOS mAb. Expression of iNOS protein was also detected by immunoblotting in human purified eosinophils and an eosinophilic leukemia cell line, Eol-3. Nitrite production was detected in the supernatant of human eosinophils and Eol-3 cells cultured for 24 h, and was completely inhibited in the presence of the NOS inhibitor N-methylester-L-arginine. iNOS cDNA was obtained by reverse transcription-PCR. After subcloning, sequencing of the 259-bp fragment from three different human eosinophils cDNAs revealed 97% identity with macrophage/monocyte iNOS. Our studies describe for the first time the presence of iNOS on eosinophil and a putative new role for this cell in inflammatory states such as asthma and parasitic disease.