Host-plant sex and phenology of Buddleja cordata Kunth interact to influence arthropod communities.

Intraspecific variation in plants is expected to have profound impacts on the arthropod communities associated with them. Because sexual dimorphism in plants is expected to provide consistent variation among individuals of the same species, researchers have often studied the effect it has on associated arthropods. Nevertheless, most studies have focused on the effect of sexual dimorphism in a single or a few herbivores, thus overlooking the potential effects on the whole arthropod community. Our main objective was to evaluate effects of Buddleja cordata's plant-sex on its associated arthropod community. We surveyed 13 pairs of male and female plants every 2 months during a year (June 2010 to April 2011). Every sampling date, we measured plant traits (water content and leaf thickness), herbivory, and the arthropod community. We did not find differences in herbivory between plant sex or through time. However, we found differences in water content through time, with leaf water-content matching the environmental seasonality. For arthropod richness, we found 68 morphospecies associated with female and 72 with male plants, from which 53 were shared by both sexes. We did not observe differences in morphospecies richness; however, we found sex-associated differences in the diversity of all species and differences on the diversity of the most abundant species with an interesting temporal component. During peak flowering season, male plants showed higher values on both parameters, but during the peak fructification season female plants showed the higher values on both diversity parameters. Our research exemplifies the interaction between plant-phenology and plant-sex as drivers of arthropod communities' diversity, even when plant sexual-dimorphism is inconspicuous, and highlighting the importance of accounting for seasonal variation. We stress the need of conducting more studies that test this time-dependent framework in other dioecious systems, as it has the potential to reconcile previous contrasting observations reported in the literature.

A pathway-based association study reveals variants from Wnt signalling genes contributing to asthma susceptibility.

BACKGROUND: Genetic susceptibility to asthma is currently linked to a handful of genes which have a limited ability to predict the overall disease risk, suggesting the existence of many other genes involved in disease development. Accumulated evidence from association studies in genes related by biological pathways could reveal novel asthma genes. OBJECTIVE: To reveal novel asthma susceptibility genes by means of a pathway-based association study. METHODS: Based on summary data from a previous a genomewide association study (GWAS) of asthma, we first identified significant biological pathways using a gene-set enrichment analysis. We then mapped all tested single nucleotide polymorphisms (SNPs) on the genes contributing to significant pathways and prioritized those with a disproportionate number of nominal significant associations for further studies. For those prioritized genes, association studies were performed for selected SNPs in independent case-control samples (n = 1765) using logistic regression models, and results were meta-analysed with those from the GWAS. RESULTS: Two biological processes were significantly enriched: the cytokine-cytokine receptor interaction (P = 0.002) and the Wnt signalling (P = 0.012). From the 417 genes interacting in these two pathways, 10 showed an excess of nominal associations, including a known asthma susceptibility locus (encoding SMAD family member 3) and other novel candidate genes. From the latter, association studies of 14 selected SNPs evidenced replication in a locus near the frizzled class receptor 6 (FZD6) gene (P = 9.90 × 10-4 ), which had a consistent direction of effects with the GWAS findings (meta-analysed odds ratio = 1.49; P = 5.87 × 10-6 ) and was in high linkage disequilibrium with expression quantitative trait loci in lung tissues. CONCLUSIONS AND CLINICAL RELEVANCE: This study revealed the importance of two biological pathways in asthma pathogenesis and identified a novel susceptibility locus near Wnt signalling genes.

5-Lipoxygenase pathway gene polymorphisms: lack of association with asthma in a Spanish population.

BACKGROUND: Cysteinyl-leukotrienes are mediators of inflammatory responses in bronchial asthma. We studied the genes encoding the enzymes involved in their synthesis to identify risk factors for asthma. The promoter polymorphisms LTC4S -444 A/C, ALOX5 -176/-147, and ALOX5AP -169/-146 have been reported to be associated with bronchial asthma. METHODS: We analyzed the effects of LTC4S -444 A/C, ALOX5 -176/-147, and ALOX5AP -169/-146 on asthma susceptibility by means of a case-control study with 193 ethnically matched, unrelated individuals. Participants were classified as severe asthmatics, nonsevere asthmatics, and nonasthmatics, using a combination of 2 techniques: polymerase chain reaction-restricted fragment length polymorphism and multiplex capillary electrophoresis. RESULTS: No association was found between these polymorphisms and asthma, neither individually nor in combination. CONCLUSION: Although the studied polymorphisms have been previously reported to constitute risk factors for the disease, we found no association between LTC4S -444 A/C, ALOX5 -176/-147, and ALOX5AP -169/-146 polymorphisms and bronchial asthma.

Immunoglobulin E recognition patterns to purified Kiwifruit (Actinidinia deliciosa) allergens in patients sensitized to Kiwi with different clinical symptoms.

BACKGROUND: Green kiwifruit allergy is on the rise. However, no surveys testing purified major kiwi allergens have been carried out in a large population, including both kiwi-sensitized [skin prick test (SPT)-positive] and truly kiwi-allergic patients. OBJECTIVE: To isolate major kiwifruit allergens, and to explore their relevance by in vitro and in vivo methods in a large kiwi-sensitized and -allergic population. METHODS: A large group (n=92) of kiwi-sensitized patients with different clinical symptoms were selected, and double-blind, placebo-controlled, food challenges to kiwi were performed in 52 of them. The three major IgE-binding proteins from kiwifruit extracts were isolated and characterized by N-terminal amino acid sequencing and molecular size and glycosylation analysis. The allergenic potency of the three kiwi allergens, and of avocado Pers a 1 as a model allergen associated with the latex-fruit syndrome, was tested by specific IgE quantitation, immunodetection assays and SPTs. RESULTS: The isolated kiwifruit allergens were identified as actinidin Act d 1, glycosylated thaumatin-like Act d 2 and a novel 40 kDa glycoprotein designated as Act d 3.02. Specific IgE to each of the three allergens was found in over 60% of sera from kiwi-sensitized patients, and Act d 1 and Act d 2 induced positive SPT responses in over 50% of the tested patients. A significant link between IgE levels to Act d 1 and Act d 3 and anaphylaxis was uncovered. Avocado Pers a 1 showed an in vitro sensitization prevalence of around 45%, but a low in vivo reactivity. CONCLUSION: Act d 1, Act d 2 and Act d 3 are major allergens in the population studied. Severe symptoms after kiwi ingestion are associated with high IgE levels to Act d 1 and Act d 3.

HER-2-neu: ¿posible diana del carcinoma vesical? / HER-2-neu: a possible target of bladder carcinoma?

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Contact urticaria caused by heat-sensitive raw fish allergens.

Patients allergic to fish usually present with skin reactions after handling raw fish. Less frequently, these reactions are seen without symptoms after oral intake, often in chefs and food handlers. We have attempted to explain the skin selectivity of such reactions in a 36-year-old woman with contact urticaria after handling raw fish. We obtained aqueous extracts of raw and cooked fish (sole and hake) for in vivo (prick test) and in vitro (SDS-PAGE, IgE Immunoblot) tests. Prick-by-prick test, 20-min closed patch test, rub test with fresh and cooked fish (sole, hake and cod) and specific IgE (CAP-system) to sole, cod and hake were performed. The strength of positive reaction to raw fish was greater than to cooked fish on both prick and prick-by-prick testing. Rub tests showed positive responses only to raw fish. Specific IgEs to sole (45 KU/l), hake (66.9 KU/l) and cod (18.7 KU/l) were obtained. IgE immunoblot recognized 3 antigens of 25, 48, 56 kDa in raw sole and 1 of 42 kDa in raw hake extracts. No IgE binding was observed with the cooked extracts or control sera. Our findings strongly suggest a Type-I hypersensitivity to fish. Immunoblot analyses demonstrated a loss of specific IgE binding to cooked extracts. We have reported a case of contact urticaria caused by heat-sensitive raw-fish allergens in a patient who probably became sensitized via the cutaneous route.

gp49B1-alpha(v)beta3 interaction inhibits antigen-induced mast cell activation.

We have identified the integrin alpha(v)beta3 as a ligand for mouse gp49B1, thus identifying a new class of ligand for a member of the family of inhibitory immunoreceptors that bear C2-type immunoglobulin-like domains. The specific interaction was shown by both cell-protein and cell-cell binding assays. In addition, we found that the interaction of alpha(v)beta3 with gp49B1 on bone marrow-derived mouse mast cells inhibited antigen-induced immunoglobulin E-mediated cell activation. Because neither gp49B1 nor alpha(v)beta3 exhibit substantive allelic variation, their newly appreciated interaction may reflect an innate pathway for down-regulating the activity of mast cells.

Anaphylaxis to calcitonin.

BACKGROUND: The calcitonin is an hormone produced by the thyroid gland C cells. The salmon calcitonin is used in some osteomuscular diseases. There are few references of allergic reaction to this hormone. We introduce a case of a sixty years old woman with several previous episodes of rhinitis, conjunctivitis and perspiration immediately after the administration of salmon calcitonin with nasal spray or intramuscular administration (Calsynar). There were some temporal periods of good tolerance between these episodes. METHODS: Skin prick test (SPT), nasal and intramuscular challenge test with commercial salmon calcitonin (Miacalcic) were performed. Leukocyte histamine release test with salmon calcitonin and serum tryptase levels at baseline and after intramuscular challenge test were performed. RESULTS: The patient skin prick test with commercial calcitonin (Miacalcic. 50 UI/ml) was positive and negative in controls. The nasal challenge test with a calcitonin nasal spray, up to 150 UI, was negative. The intramuscular challenge test with 25 UI of Miacalcic was positive with an immediate anaphylactic reaction. Whole blood histamine release studies were negative. Serum tryptase levels after intramuscular challenge did not increase significantly with regard to the basal levels. CONCLUSION: We have introduced a case of anaphylaxis by calcitonin that suggest an IgE mediated hypersensitivity reaction.