title: Immunopathogenesis of human gastrointestinal infection by Anisakis simplex.
abstract: BACKGROUND
  Anisakis simplex is a parasite of fish, and in the case of human infestation, it should be considered as a possible cause of gastrointestinal disease, especially in countries where raw or undercooked fish is a frequent food. Clinical features of anisakiasis may simulate acute abdominal pain, such as that found in patients with gastric ulcers, appendicitis, and Crohn's disease. Furthermore, many cases of anisakiasis are diagnosed as eosinophilic gastroenteritis, which is a broad term for a specific disease.
  
  
  OBJECTIVE
  The purpose of this study was to investigate the immunopathogenesis of human gastrointestinal infestation by A simplex.
  
  
  METHODS
  Thirteen intestinal biopsy specimens from patients with anisakiasis were analyzed for the presence of messenger (m)RNA for different cytokines and inflammatory mediators by RT-PCR. Specific IgE, eosinophil cationic protein, eosinophil protein X, and tryptase levels were measured in each patient's serum. Also, cell cultures were set up with lymphocytes from some patients and stimulated in vitro with Anisakis and Ascaris antigens.
  
  
  RESULTS
  We performed immunologic phenotyping in 13 patients. All patients underwent biopsy after emergency surgery caused by episodes of acute abdominal pain. In all cases inflammatory infiltrate composed of eosinophils and lymphocytes was found in the intestinal wall. We demonstrated that after infestation, a T(H2)-type immune response occurred. Also, major basic protein, nitric oxide, and eotaxin were found in the tissue, and eosinophil cationic protein and eosinophil protein X levels were elevated in sera.
  
  
  CONCLUSIONS
  These data and in vitro lymphocyte cultures indicate that a T(H2) mechanism plays an important role in the inflammatory infiltrate produced by the anchorage of parasites in the gastrointestinal wall.
authors.affiliation: Immunology Department, Fundación Jiménez Díaz, Madrid, Spain.
authors.forename: V
authors.initials: V
authors.lastname: del Pozo
authors.forename: I
authors.initials: I
authors.lastname: Arrieta
authors.forename: T
authors.initials: T
authors.lastname: Tuñon
authors.forename: I
authors.initials: I
authors.lastname: Cortegano
authors.forename: B
authors.initials: B
authors.lastname: Gomez
authors.forename: B
authors.initials: B
authors.lastname: Cárdaba
authors.forename: S
authors.initials: S
authors.lastname: Gallardo
authors.forename: M
authors.initials: M
authors.lastname: Rojo
authors.forename: G
authors.initials: G
authors.lastname: Renedo
authors.forename: P
authors.initials: P
authors.lastname: Palomino
authors.forename: A I
authors.initials: AI
authors.lastname: Tabar
authors.forename: C
authors.initials: C
authors.lastname: Lahoz
mesh_terms: D015746:Abdominal Pain / Q000097:blood / Q000276:immunology / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D017129:Anisakiasis / Q000097:blood / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology; D017163:Anisakis / Q000276:immunology / Q000472:pathogenicity*; D001798:Blood Proteins / Q000032:analysis / Q000235:genetics; D002478:Cells, Cultured; D018925:Chemokines / Q000235:genetics; D016207:Cytokines / Q000235:genetics; D047091:Eosinophil Granule Proteins; D047208:Eosinophil-Derived Neurotoxin; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D012260:Ribonucleases; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D001798:Blood Proteins; D018925:Chemokines; D016207:Cytokines; D047091:Eosinophil Granule Proteins; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D047208:Eosinophil-Derived Neurotoxin; D012260:Ribonucleases