Histamine signaling inhibition reduces inflammation in a mouse model of skin inflammation

DANIELA MONTAGNA; MÓNICA VERMEULEN; SOLEDAD GORI; ALEJANDRA DUARTE; JULIETA ALCAIN; ARIEL STRAZZA

Aachen

Simposio; 15th International Symposium on Dendritic Cells; 2018

EFIS

Histamine (HIS) plays a key role in inflammation and allergy, acting through four G-protein coupledreceptors (H1R-H4R). Previously, we proved that HIS acting on dendritic cells (DCs) enhances crosspresentationof the soluble antigen ovalbumin (OVA), and prevents apoptosis after damage signalssuch as heat-shock.In this work, we assessed whether HIS has a relevant role in the modulation of chronic inflammatorydiseases in vivo. For this, chronic contact dermatitis was induced by applying 20 µl ofdinitrofluorobencene (DNFB, 0.3% in acetone/water) for 5 consecutive days in BALB/c mice. We alsoapplied 20 µl of thioperamide (Thio, 10-7M), an H3/H4 receptor antagonist, at the same time to onegroup of mice (DNFB-Thio), while the other group received vehicle (DNFB-Ct).First, the Thio-treated group showed a minor degree of epithelial damage and inflammation, andreduced leukocyte infiltration. Also, seven days after the first administration of DNFB, when weanalyzed the draining lymph nodes, we noted an increase in the CD11b+ CD11cantigenpresentingcells that produce IL-10 (DNFB-Ct 1.55% ± 0.317%, DNFB-Thio 2.28% ± 0.433%, p