The Journal of Experimental Medicine
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Published online October 29, 2007
doi:10.1084/jem.20071032
The Journal of Experimental Medicine, Vol. 204, No. 12, 2837-2852
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Chassin et al.
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ARTICLE

 Hormonal control of the renal immune response and antibacterial host defense by arginine vasopressin

Cécilia Chassin1,2, Mathias W. Hornef3, Marcelle Bens1,2, Michael Lotz3, Jean-Michel Goujon4, Sophie Vimont5,7, Guillaume Arlet5,7, Alexandre Hertig6,7, Eric Rondeau6,7, and Alain Vandewalle1,2

1 Institut National de la Santé et de la Recherche Médicale (INSERM), U773, Centre de Recherche Biomédicale Bichat-Beaujon (CRB3), BP 416, 75018 Paris, France
2 Université Paris 7–Denis Diderot, site Bichat, Paris, 75870 Paris, France
3 Institute for Medical Microbiology and Hygiene, University of Freiburg, 79104 Freiburg, Germany
4 Service d'Anatomie et Cytologie Pathologiques, Centre Hospitalier Universitaire de Poitiers, Université de Poitiers, 86021 Poitiers, France
5 Service de Bactériologie and 6 INSERM, U702, Hôpital Tenon, 75970 Paris, France
7 Université Paris 6–Pierre et Marie Curie, site St. Antoine, Paris, 75571 Paris, France

CORRESPONDENCE Alain Vandewalle: vandewal{at}bichat.inserm.fr

Ascending urinary tract infection (UTI) and pyelonephritis caused by uropathogenic Escherichia coli (UPEC) are very common infections that can cause severe kidney damage. Collecting duct cells, the site of hormonally regulated ion transport and water absorption controlled by vasopressin, are the preferential intrarenal site of bacterial adhesion and initiation of inflammatory response. We investigated the effect of the potent V2 receptor (V2R) agonist deamino-8-D-arginine vasopressin (dDAVP) on the activation of the innate immune response using established and primary cultured collecting duct cells and an experimental model of ascending UTI. dDAVP inhibited Toll-like receptor 4–mediated nuclear factor {kappa}B activation and chemokine secretion in a V2R-specific manner. The dDAVP-mediated suppression involved activation of protein phosphatase 2A and required an intact cystic fibrosis transmembrane conductance regulator Cl– channel. In vivo infusion of dDAVP induced a marked fall in proinflammatory mediators and neutrophil recruitment, and a dramatic rise in the renal bacterial burden in mice inoculated with UPECs. Conversely, administration of the V2R antagonist SR121463B to UPEC-infected mice stimulated both the local innate response and the antibacterial host defense. These findings evidenced a novel hormonal regulation of innate immune cellular activation and demonstrate that dDAVP is a potent modulator of microbial-induced inflammation in the kidney.

Abbreviations used: AVP, arginine vasopressin; cAMP, cyclic AMP; CCD, cortical collecting duct; CFTR, cystic fibrosis transmembrane conductance regulator; dDAVP, deamino-8-D-AVP; ENaC, epithelial sodium channel; Gly, glybenclamide; ICAM, intracellular adhesion molecule; MIP-2, macrophage inflammatory protein 2; MPO, myeloperoxydase; MyD88. myeloid differentiation factor 88; NPPB, 5-nitro-2(3phenylpropyl-amino)benzoate; PKA, protein kinase A; PP1 and PP2A, protein phosphatase 1 and 2A, respectively; RANTES, regulated on activation, normal T cell expressed and secreted; Ser/Thr, serine/threonine; siRNA, small-interfering RNA; TLR, Toll-like receptor; UPEC, uropathogenic Escherichia coli; UTI, urinary tract infection; V2R, V2 receptor.


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