Anthelmintic Therapy Modifies the Systemic and Mycobacterial Antigen-Stimulated Cytokine Profile in Helminth-Latent Mycobacterium tuberculosis Coinfection.
Helminth infections are known to modulate cytokine responses in latent tuberculosis (LTB). However, very few studies have examined whether this modulation is reversible upon anthelmintic therapy. We measured the systemic and mycobacterial (TB) antigen-stimulated levels of type 1, type 2, type 17, and regulatory cytokines in individuals with LTB and with or without coexistentStrongyloides stercoralisinfection before and after anthelmintic therapy. Our data reveal that individuals with LTB and coexistentS. stercoralisinfection have significantly lower levels of systemic and TB antigen-stimulated type 1 (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], and interleukin-2 [IL-2]) and type 17 (IL-17A and/or IL-17F) cytokines and significantly higher levels of systemic but not TB antigen-stimulated type 2 (IL-4 and IL-5) and regulatory (transforming growth factor beta [TGF-β]) cytokines. Anthelmintic therapy resulted in significantly increased systemic levels of type 1 and/or type 17 cytokines and in significantly decreased systemic levels of type 2 and regulatory (IL-10 and TGF-β) cytokines. In addition, anthelmintic therapy resulted in significantly increased TB antigen-stimulated levels of type 1 cytokines only. Our data therefore confirm that the modulation of systemic and TB antigen-stimulated cytokine responses inS. stercoralis-LTB coinfection is reversible (for the most part) by anthelmintic treatment.
National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Rajamanickam
R
Anuradha
National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Saravanan
S
Munisankar
National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India.
Yukthi
Y
Bhootra
National Institute for Research in Tuberculosis, Chennai, India.
Chandrakumar
C
Dolla
National Institute for Research in Tuberculosis, Chennai, India.
Paul
P
Kumaran
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Thomas B
TB
Nutman
National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India sbabu@mail.nih.gov.|Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Subash
S
Babu
D000328:Adult; D000818:Animals; D000871:Anthelmintics / Q000494:pharmacology; D000942:Antigens, Bacterial / Q000276:immunology*; D060085:Coinfection; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006373:Helminthiasis / Q000276:immunology* / Q000378:metabolism* / Q000469:parasitology / Q000628:therapy; D006376:Helminths / Q000187:drug effects*; D006790:Host-Parasite Interactions / Q000187:drug effects / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000187:drug effects / Q000276:immunology; D006801:Humans; D055985:Latent Tuberculosis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis; D014376:Tuberculosis / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D055815:Young Adult
D000871:Anthelmintics; D000942:Antigens, Bacterial; D016207:Cytokines
Strongyloides; cytokines; helminths; immune responses; tuberculosis