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IL-16 is critical for Tropheryma whipplei replication in Whipple's disease.

Benoit Desnues 1 Didier Raoult 2 Jean-Louis Mege 2
1 URMITE - Unité de Recherche sur les Maladies Infectieuses Tropicales Emergentes
URMITE - Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes
2 URMITE - Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes
Abstract : Whipple's disease (WD) is a rare systemic disease caused by Tropheryma whipplei. We showed that T. whipplei was eliminated by human monocytes but replicated in monocyte-derived macrophages (Mphi) by inducing an original activation program. Two different host molecules were found to be key elements for this specific pattern. Thioredoxin, through its overexpression in infected monocytes, was involved in bacterial killing because adding thioredoxin to infected Mphi inhibited bacterial replication. IL-16, which was up-regulated in Mphi, enabled T. whipplei to replicate in monocytes and increased bacterial replication in Mphi. In addition, anti-IL-16 Abs abolished T. whipplei replication in Mphi. IL-16 down-modulated the expression of thioredoxin and up-regulated that of IL-16 and proapoptotic genes. In patients with WD, T. whipplei replication was higher than in healthy subjects and was related to high levels of circulating IL-16. Both events were corrected in patients who successfully responded to antibiotics treatment. This role of IL-16 was not reported previously and gives an insight into the understanding of WD pathophysiology.
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https://hal-amu.archives-ouvertes.fr/hal-02025871
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Submitted on : Tuesday, February 19, 2019 - 9:54:21 PM
Last modification on : Thursday, March 4, 2021 - 3:08:45 AM

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  • HAL Id : hal-02025871, version 1
  • PUBMED : 16177102

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UNIV-AMU | CNRS

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Benoit Desnues, Didier Raoult, Jean-Louis Mege. IL-16 is critical for Tropheryma whipplei replication in Whipple's disease.. Journal of Immunology, Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists, 2005, 175 (7), pp.4575-82. ⟨hal-02025871⟩

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