Background: Early wheezing and asthma are relevant health problems in the tropics. Mite sensitization is an important risk factor, but the roles of others, inherent in poverty, are unknown. We designed a birth-cohort study in Cartagena (Colombia) to investigate genetic and environmental risk factors for asthma and atopy, considering as particular features perennial exposure to mites, parasite infections and poor living conditions. Methods: Pregnant women representative of the low-income suburbs of the city were randomly screened for eligibility at delivery; 326 mother-infant pairs were included at baseline and biological samples were collected from birth to 24 months for immunological testing, molecular genetics and gene expression analysis. Pre and post-natal information was collected using questionnaires.

In a socioeconomically deprived community from the tropics, sensitization to HDM allergens was very frequent at early life, especially to B. tropicalis. In contrast to expected according to the hygiene hypothesis, unhygienic/poverty conditions were risk factors for allergen sensitization. High CB total IgE levels were a risk factor for allergen sensitization but protected from recurrent wheezing.

Background In tropical zones, perennial exposure to house dust mite (HDM) allergens and helminth infections is present. Studying the impact of these conditions on the inception and evolution of allergic diseases is necessary to have an accurate view of their natural history. We aimed to evaluate the dynamics of genuine sensitization to Blomia tropicalis and Ascaris in children from the FRAAT birth cohort and the effects of helminth infection, environmental HDM allergen levels, and sociodemographic factors. Methods Children were followed up to 6 years old. Specific IgE to recombinant allergens from B. tropicalis (Blo t 5 and Blo t 12) and Ascaris spp (Asc l 3, Asc l 13 and Asc s 1) was measured by ELISA at different time points. Allergen levels were measured in dust when children were 6 months old. Results IgE sensitization increased over time up to 3 years old. Correlation among the specific IgE levels to B. tropicalis and Ascaris components is poor at year 1, but coefficients are high and significant (Spearman's rho coefficients >0.70) at year 6. Unhygienic conditions increased the odds of sensitization to B. tropicalis allergenic components. Blo t 5 levels were lower in the poorest. IgE response to Blo t 5 and Blo t 12 was less intense in children with high exposure to Blo t 5 (levels >80th percentile). Conclusion In this tropical community, the pattern of childhood IgE sensitization is different from that in developing countries and is influenced by the hygienic conditions.

BackgroundB-Cell Activating Factor (BAFF) is a cytokine regulating antibody production. Polymorphisms in the gene encoding BAFF were associated with the antibody response to Ascaris but not to mite allergens. In the present study we evaluated the relationship between BAFF and specific antibodies against Ascaris and mites in 448 controls and 448 asthmatics. Soluble BAFF was measured by ELISA and BAFF mRNA by qPCR. Surface expression of BAFF and its receptor (BAFF-R) was analyzed by flow cytometry.ResultsIndividuals with specific IgE levels to Ascaris >75th percentile had lower levels of soluble BAFF; those with specific IgG levels to Ascaris >75th percentile had reduced BAFF mRNA. Total IgE and specific IgE to mites were not related to BAFF levels. There were no differences in soluble BAFF or mRNA levels between asthmatics and controls. There was an inverse relationship between the cell-surface expression of BAFF-R on CD19+ B cells and BAFF levels at the transcriptional and protein level.ConclusionsThese findings suggest that differences in BAFF levels are related to the strength of the antibody response to Ascaris.

Helminth infections and allergic diseases are associated with IgE hyperresponsiveness but the genetics of this phenotype remain to be defined. Susceptibility to Ascaris lumbricoides infection and antibody levels to this helminth are associated with polymorphisms in locus 13q33-34. We aimed to explore this and other genomic regions to identify genetic variants associated with the IgE responsiveness in humans. Forty-eight subjects from Cartagena, Colombia, with extreme values of specific IgE to Ascaris and ABA-1, a resistance marker of this nematode, were selected for targeted resequencing. Burden analyses were done comparing extreme groups for IgE values. One-hundred one SNPs were genotyped in 1258 individuals of two well-characterized populations from Colombia and Sweden. Two low-frequency coding variants in the gene encoding the Acidic Mammalian Chitinase (CHIA rs79500525, rs139812869, tagged by rs10494133) were found enriched in high IgE responders to ABA-1 and confirmed by genetic association analyses. The SNP rs4950928 in the Chitinase 3 Like 1 gene (CHI3L1) was associated with high IgE to ABA-1 in Colombians and with high IgE to Bet v 1 in the Swedish population. CHIA rs10494133 and ABDH13 rs3783118 were associated with IgE responses to Ascaris. SNPs in the Tumor Necrosis Factor Superfamily Member 13b gene (TNFSF13B) encoding the cytokine B cell activating Factor were associated with high levels of total IgE in both populations. This is the first report on the association between low-frequency and common variants in the chitinases-related genes CHIA and CHI3L1 with the intensity of specific IgE to ABA-1 in a population naturally exposed to Ascaris and with Bet v 1 in a Swedish population. Our results add new information about the genetic influences of human IgE responsiveness; since the genes encode for enzymes involved in the immune response to parasitic infections, they could be helpful for understanding helminth immunity and allergic responses. We also confirmed that TNFSF13B has an important and conserved role in the regulation of total IgE levels, which supports potential evolutionary links between helminth immunity and allergic response.

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La duodenitis eosinofílica tiene una prevalencia entre 5,1 a 8,2 por 100000 personas. Se desconocen los mecanismos moleculares subyacentes de la enfermedad, pero la hipersensibilidad (alergias estacionales y alimentarias) juega un papel importante en su patogénesis, la predisposición alérgica se encuentra en el 25-35% de los casos. El diagnóstico incluye manifestaciones clínicas, hallazgos imagenológicos y evidencia histológica de infiltración eosinofílica >20 eosinófilos por campo de alto poder. Realizamos un informe de caso clínico y revisión de literatura. Hombre de 25 años con vitíligo que consulta a urgencias refiriendo síntomas de dispepsia, vómitos y dolor abdominal de máxima intensidad, en el examen médico se localiza dolor abdominal superior, con paraclínicos normales excepto un recuento de eosinófilos >2000 células/ul, la ecografía abdominal fue normal, la endoscopia superior reveló pangastritis eritematosa y duodenitis con pliegues rígidos y engrosados, la colonoscopia mostró hemorroides grado I. Coproscópico seriado negativo para parásitos, IgE total, IgA e IgG en rango normal, se reportó IgG positivo a Toxoplasma gondii, perfil de autoinmunidad negativo. En los siguientes 4 días aumenta el dolor abdominal y el recuento de eosinófilos, con endoscopia control y tomografía abdomino-pélvica contrastada que muestran duodeno edematizado con reflujo biliar severo, reporte histopatológico con duodenitis crónica atrófica y con pruebas para alergenos alimentarios positivo a cereales (centeno, soja, cebada), Manihot esculenta, plátano verde, tomate, leche de vaca, naranja y piña. Se indicó dieta restrictiva e inhibidor de la bomba de protones (pantoprazol), control ambulatorio a los 45 días de resolución de los síntomas con recuento de eosinófilos en sangre normal. Se presenta un caso de duodenitis eosinofílica relacionada con alergia alimentaria con mecanismos IgE independientes en un varón joven con vitíligo, que debutó con cuadro clí ral agudo y reflujo biliar, que se resolvió con dieta de eliminación y pantoprazol sin uso de corticoides.

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