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© Christine Schmitt, Meriem El Ghachi, Jean-Marc Panaud
Bactérie Helicobacter pylori en microscopie électronique à balayage. Agent causal de pathologies de l'estomac : elle est responsable des gastrites chroniques, d'ulcères gastriques et duodénaux et elle joue un rôle important dans la genèse des cancers gastriques (adénocarcinomes et lymphomes).
Publication : American journal of respiratory and critical care medicine

CCL17 production by dendritic cells is required for NOD1-mediated exacerbation of allergic asthma

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in American journal of respiratory and critical care medicine - 15 Apr 2014

Ait Yahia S, Azzaoui I, Everaere L, Vorng H, Chenivesse C, Marquillies P, Duez C, Delacre M, Grandjean T, Balsamelli J, Fanton d'Andon M, Fan Y, Ple C, Werts C, Boneca IG, Wallaert B, Chamaillard M, Tsicopoulos A

Link to Pubmed [PMID] – 24661094

Am. J. Respir. Crit. Care Med. 2014 Apr;189(8):899-908

RATIONALE: Pattern recognition receptors are attractive targets for vaccine adjuvants, and polymorphisms of the innate receptor NOD1 have been associated with allergic asthma.

OBJECTIVES: To elucidate whether NOD1 agonist may favor allergic asthma in humans through activation of dendritic cells, and to evaluate the mechanisms involved using an in vivo model.

METHODS: NOD1-primed dendritic cells from allergic and nonallergic donors were characterized in vitro on their phenotype, cytokine secretion, and Th2 polarizing ability. The in vivo relevance was examined in experimental allergic asthma, and the mechanisms were assessed using transfer of NOD1-conditioned dendritic cells from wild-type or CCL17-deficient mice.

MEASUREMENTS AND MAIN RESULTS: NOD1 priming of human dendritic cells promoted a Th2 polarization profile that involved the production of CCL17 and CCL22 in nonallergic subjects but only CCL17 in allergic patients, without requiring allergen costimulation. Moreover, NOD1-primed dendritic cells from allergic donors exhibited enhanced maturation that led to abnormal CCL22 and IL-10 secretion compared with nonallergic donors. In mice, systemic NOD1 ligation exacerbated allergen-induced experimental asthma by amplifying CCL17-mediated Th2 responses in the lung. NOD1-mediated sensitization of purified murine dendritic cells enhanced production of CCL17 and CCL22, but not of thymic stromal lymphopoietin and IL-33, in vitro. Consistently, adoptive transfer of NOD1-conditioned dendritic cells exacerbated the Th2 pulmonary response in a CCL17-dependent manner in vivo.

CONCLUSIONS: Data from this study unveil a deleterious role of NOD1 in allergic asthma through direct induction of CCL17 by dendritic cells, arguing for a need to address vaccine formulation safety issues related to allergy.

http://www.ncbi.nlm.nih.gov/pubmed/24661094