title: Reduced efficacy of treatment of strongyloidiasis in HTLV-I carriers related to enhanced expression of IFN-gamma and TGF-beta1.
abstract: Strongyloidiasis, a human intestinal infection caused by Strongyloides stercoralis (S. stercoralis), is difficult to cure with drugs. In particular, a decrease of the efficacy of treatment has been reported in patients dually infected with S. stercoralis and human T-cell leukaemia virus type I (HTLV-I), both of which are endemic in Okinawa, Japan. However, the factors influencing this resistance remain unclear. In the present study, patients infected with S. stercoralis, with or without HTLV-I infection, were treated with albendazole, followed up for one year and separated into two groups, cured and non-cured. The cure rate of S. stercoralis was lower in HTLV-I carriers (P < 0.05). Serum levels of S. stercoralis-specific IgA, IgE, IgG, IgG1 and IgG4 antibodies were estimated, and a decrease of IgE (P < 0.05) and an increase of IgG4 (P < 0.05) were observed in the non-cured group, especially in HTLV-I carriers. RT-PCR of cytokines using peripheral blood mononuclear cells revealed that S. stercoralis patients with HTLV-I showed a high frequency of expression of IFN-gamma and TGF-beta1, whereas those without HTLV-I showed no expression of these cytokines. IFN-gamma- and TGF-beta1-positive HTLV-I carriers showed a decrease of IgE (P < 0.05), an increase of IgG4 (P < 0.01) and a lower cure rate (P < 0.01) compared with those who were negative for both cytokines. These results suggest that persistent infection with HTLV-I affected S. stercoralis-specific immunity and reduced therapeutic efficacy.
authors.affiliation: Department of Medical Zoology, Saitama Medical School, Moroyama, Saitama, Japan. satoma@saitama-med.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Satoh
authors.forename: H
authors.initials: H
authors.lastname: Toma
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Takara
authors.forename: Y
authors.initials: Y
authors.lastname: Shiroma
authors.forename: S
authors.initials: S
authors.lastname: Kiyuna
authors.forename: K
authors.initials: K
authors.lastname: Hirayama
mesh_terms: D000368:Aged; D015766:Albendazole / Q000627:therapeutic use; D000818:Animals; D000871:Anthelmintics / Q000627:therapeutic use; D000909:Antibodies, Helminth / Q000097:blood / Q000276:immunology; D005243:Feces / Q000469:parasitology; D005260:Female; D005786:Gene Expression Regulation; D015490:HTLV-I Infections / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D006801:Humans; D016867:Immunocompromised Host; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000235:genetics; D007411:Intestinal Diseases, Parasitic / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000469:parasitology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017171:Strongyloides stercoralis / Q000276:immunology / Q000302:isolation & purification; D013322:Strongyloidiasis / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000096:biosynthesis* / Q000235:genetics; D017211:Treatment Failure
chemical_list: D000871:Anthelmintics; D000909:Antibodies, Helminth; D007074:Immunoglobulin G; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D007073:Immunoglobulin E; D007371:Interferon-gamma; D015766:Albendazole