title: IgE cross-reactivity between Ascaris and domestic mite allergens: the role of tropomyosin and the nematode polyprotein ABA-1.
abstract: BACKGROUND
  Analysis of cross-reactivity between the nematode Ascaris ssp. and dust mites, two important allergen sources in the tropics, will contribute in understanding their influence on asthma and atopy. The objective of this study was to investigate immunoglobulin E (IgE) cross-reactivity between Ascaris and two domestic mites in the tropics.
  
  
  METHODS
  Sera from 24 asthmatic patients were used in ELISA and immunoblotting IgE-binding inhibition assays using Ascaris, Blomia tropicalis and Dermatophagoides pteronyssinus extracts and the recombinants Blo t 10, ABA-1 and Blo t 13 as competitors. Identification of Ascaris allergens was confirmed by mass spectrometry (LC-MS/MS).
  
  
  RESULTS
  We detected at least 12 human IgE-binding components in Ascaris extract. Blomia tropicalis and D. pteronyssinus inhibited 83.3% and 79% of IgE-binding to Ascaris, while Ascaris inhibited 58.3% and 79.3% to B. tropicalis and D. pteronyssinus respectively. Mite tropomyosin inhibited 85% of IgE-binding to Ascaris. Affinity-purified human IgE to rBlo t 10 identified an allergen of 40 kDa in Ascaris extract, further confirmed as tropomyosin by LC-MS/MS. We found no evidence of IgE cross-reactivity between rABA-1 and any allergen component in mite extracts, including rBlo t 13.
  
  
  CONCLUSIONS
  There is cross-reactivity between Ascaris and mites, determined by several allergens including tropomyosin and glutathione-S-transferase. In addition to its potential impact on asthma pathogenesis, Ascaris infection and mite allergy diagnosis relying on the determination of specific IgE could be affected by this cross-reactivity. ABA-1 has no cross-reactive counterpart in mite extracts, suggesting its usefulness as a more specific marker of Ascaris infection.
authors.affiliation: Institute for Immunological Research, University of Cartagena, Cartagena, Colombia.
authors.forename: N
authors.initials: N
authors.lastname: Acevedo
authors.forename: J
authors.initials: J
authors.lastname: Sánchez
authors.forename: A
authors.initials: A
authors.lastname: Erler
authors.forename: D
authors.initials: D
authors.lastname: Mercado
authors.forename: P
authors.initials: P
authors.lastname: Briza
authors.forename: M
authors.initials: M
authors.lastname: Kennedy
authors.forename: A
authors.initials: A
authors.lastname: Fernandez
authors.forename: M
authors.initials: M
authors.lastname: Gutierrez
authors.forename: K Y
authors.initials: KY
authors.lastname: Chua
authors.forename: N
authors.initials: N
authors.lastname: Cheong
authors.forename: S
authors.initials: S
authors.lastname: Jiménez
authors.forename: L
authors.initials: L
authors.lastname: Puerta
authors.forename: L
authors.initials: L
authors.lastname: Caraballo
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000276:immunology*; D000818:Animals; D039741:Antigens, Dermatophagoides / Q000276:immunology*; D052179:Antigens, Plant; D001200:Ascaris / Q000276:immunology*; D001249:Asthma / Q000276:immunology / Q000503:physiopathology; D002648:Child; D003429:Cross Reactions; D005260:Female; D005982:Glutathione Transferase / Q000276:immunology; D015801:Helminth Proteins / Q000276:immunology; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000503:physiopathology; D007073:Immunoglobulin E / Q000276:immunology; D008297:Male; D008875:Middle Aged; D008925:Mites / Q000276:immunology*; D014335:Tropomyosin / Q000276:immunology*; D055815:Young Adult
chemical_list: C093689:ABA-1 protein, Ascaris suum; D000485:Allergens; D039741:Antigens, Dermatophagoides; D052179:Antigens, Plant; D015801:Helminth Proteins; D014335:Tropomyosin; D007073:Immunoglobulin E; D005982:Glutathione Transferase