title: Serum mannose-binding lectin deficiency is associated with cryptosporidiosis in young Haitian children.
abstract: BACKGROUND
  Mannose-binding lectin (MBL) is a component of the innate immune response and binds microbial surfaces through carbohydrate recognition domains. MBL deficiency may contribute to susceptibility to a variety of infectious diseases, particularly in young children. MBL binds to the Cryptosporidium sporozoite and may be important in resistance to cryptosporidiosis.
  
  
  METHODS
  We studied the association of serum MBL levels and cryptosporidiosis in a case-control study of young Haitian children with cryptosporidiosis versus children who were control subjects.
  
  
  RESULTS
  Ninety-nine children were enrolled, as follows: 49 children with cryptosporidiosis, 41 healthy controls, and 9 children with diarrhea from other causes. Case children were more malnourished than controls, and 49% had persistent or chronic diarrhea. At enrollment, mean serum MBL levels were markedly lower in children with cryptosporidiosis (P = .002), as was the number of children with an MBL deficiency of < or = 70 ng/mL (P = .005). In multivariate analysis, the association of cryptosporidiosis and MBL deficiency persisted (P = .002; adjusted odds ratio, 22.4), as did the association of cryptosporidiosis with general malnutrition. The subset of children with cryptosporidiosis and MBL deficiency were more likely to be male (P = .025).
  
  
  CONCLUSIONS
  MBL may be an important component of innate immune protection against Cryptosporidium infection in young children. Additional studies are necessary to determine whether MBL intestinal losses, deficient epithelial expression, and/or genetic polymorphisms in the MBL gene contribute to MBL deficiency in cryptosporidiosis and other enteric infections in young children.
authors.affiliation: Department of Medicine Unit of Infectious Diseases, University of Vermont College of Medicine, Burlington, Vermont 05405, USA. beth.kirkpatrick@uvm.edu
authors.forename: B D
authors.initials: BD
authors.lastname: Kirkpatrick
authors.forename: C D
authors.initials: CD
authors.lastname: Huston
authors.forename: D
authors.initials: D
authors.lastname: Wagner
authors.forename: F
authors.initials: F
authors.lastname: Noel
authors.forename: P
authors.initials: P
authors.lastname: Rouzier
authors.forename: J W
authors.initials: JW
authors.lastname: Pape
authors.forename: G
authors.initials: G
authors.lastname: Bois
authors.forename: C J
authors.initials: CJ
authors.lastname: Larsson
authors.forename: W K
authors.initials: WK
authors.lastname: Alston
authors.forename: K
authors.initials: K
authors.lastname: Tenney
authors.forename: C
authors.initials: C
authors.lastname: Powden
authors.forename: J P
authors.initials: JP
authors.lastname: O'Neill
authors.forename: C L
authors.initials: CL
authors.lastname: Sears
mesh_terms: D016022:Case-Control Studies; D003457:Cryptosporidiosis / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D004198:Disease Susceptibility; D005260:Female; D006205:Haiti; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007223:Infant; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood / Q000172:deficiency* / Q000276:immunology
chemical_list: D037601:Mannose-Binding Lectin