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Attenuation of Toll-Like Receptor Expression and Function in Latent Tuberculosis by Coexistent Filarial Infection with Restoration Following Antifilarial Chemotherapy

  1. Author:
    Babu, S.
    Bhat, S. Q.
    Kumar, N. P.
    Anuradha, R.
    Kumaran, P.
    Gopi, P. G.
    Kolappan, C.
    Kumaraswami, V.
    Nutman, T. B.

  2. Author Address

    Babu, Subash, Bhat, Sajid Q.; Kumar, N. Pavan, Anuradha, R.] NIH, Int Ctr Excellence Res, Madras, Tamil Nadu, India. [Babu, Subash] NCI, Sci Applicat Int Corp, Frederick, MD 21701 USA. [Kumaran, Paul, Gopi, P. G.; Kolappan, C.; Kumaraswami, V.] TB Res Ctr, Madras, Tamil Nadu, India. [Nutman, Thomas B.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
    1. Year: 2009
  2. Journal: Plos Neglected Tropical Diseases
    1. 3
    2. 7
    3. Pages: 1, e489-7, e489
  4. Type of Article: Article
  1. Abstract:

    Mycobacterium tuberculosis (Mtb) and filarial coinfection is highly prevalent, and the presence of filarial infections may regulate the Toll-like receptor (TLR)-dependent immune response needed to control Mtb infection. By analyzing the baseline and mycobacterial antigen-stimulated expression of TLR1, 2, 4, and 9 (in individuals with latent tuberculosis [TB] with or without filarial infection), we were able to demonstrate that filarial infection, coincident with Mtb, significantly diminishes both baseline and Mtb antigen-specific TLR2 and TLR9 expression. In addition, pro-inflammatory cytokine responses to TLR2 and 9 ligands are significantly diminished in filaria/TB-coinfected individuals. Definitive treatment of lymphatic filariasis significantly restores the pro-inflammatory cytokine responses in individuals with latent TB. Coincident filarial infection exerted a profound inhibitory effect on protective mycobacteria-specific TLR-mediated immune responses in latent tuberculosis and suggests a novel mechanism by which concomitant filarial infections predispose to the development of active tuberculosis in humans.

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  2. DOI: 10.1371/journal.pntd.0000489
  3. PMID: 19636364

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