title: Immunologic responses to Vibrio cholerae in patients co-infected with intestinal parasites in Bangladesh.
abstract: BACKGROUND
  Infection with intestinal helminths is common and may contribute to the decreased efficacy of Vibrio cholerae vaccines in endemic compared to non-endemic areas. However, the immunomodulatory effects of concomitant intestinal parasitic infection in cholera patients have not been systematically evaluated.
  
  
  METHODS
  We evaluated V. cholerae-specific immune responses in a cohort of patients with severe cholera. 361 patients completed 21 days of observation and 53 (15%) had evidence of a concomitant intestinal parasitic infection based on direct microscopy. Although there were no significant differences in the vibriocidal or lipopolysaccharide (LPS)-specific immune responses to V. cholerae, helminth-infected cholera patients had decreased fecal and serum IgA immune responses to the B subunit of cholera toxin (CTB) as well as a more modest decrease in serum IgG response to CTB. These findings remained significant for all classes of helminth infection and when controlling for potential confounding variables such as age and nutritional status. Although we hypothesized the differential effect on CTB and LPS immune responses was due to T-cell-dependent immunomodulatory effects of helminth infection, we did not find additional evidence to support a classic Th1 or Th2 polarization of the immune response to V. cholerae infection related to parasite infection.
  
  
  CONCLUSIONS
  The finding that helminth infection has a profound association with the mucosal humoral immune response to V. cholerae has implications for the development of protective immunity in cholera-endemic areas and provides an additional basis for deworming programs in cholera-endemic areas. Additional studies, including further characterization of the role of T cells in the immune response to human V. cholerae infection and the development of an animal model of co-infection, may provide additional insight into the mechanisms underlying these findings.
authors.affiliation: Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA. jbharris@partners.org
authors.forename: Jason B
authors.initials: JB
authors.lastname: Harris
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Podolsky
authors.forename: Taufiqur R
authors.initials: TR
authors.lastname: Bhuiyan
authors.forename: Fahima
authors.initials: F
authors.lastname: Chowdhury
authors.forename: Ashraful I
authors.initials: AI
authors.lastname: Khan
authors.forename: Regina C
authors.initials: RC
authors.lastname: Larocque
authors.forename: Tanya
authors.initials: T
authors.lastname: Logvinenko
authors.forename: Jennifer
authors.initials: J
authors.lastname: Kendall
authors.forename: Abu S G
authors.initials: AS
authors.lastname: Faruque
authors.forename: Cathryn R
authors.initials: CR
authors.lastname: Nagler
authors.forename: Edward T
authors.initials: ET
authors.lastname: Ryan
authors.forename: Firdausi
authors.initials: F
authors.lastname: Qadri
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Calderwood