MHTP [2-methoxy-4-(7-methoxy-1,2,3,4-tetrahydroisoquinolin-1-yl)
phenol], a synthetic isoquinolinic
alkaloid, presented anti-inflammatory activity in several experimental models of acute
inflammation as
lipopolysaccharide (LPS)-induced
acute lung injury and phlogistic agent-induced
edema and presented low preclinical toxicity. The aim of this study was to determine the
MHTP effect on
ovalbumin (OVA)-induced pulmonary allergic
inflammation. In other to realize this study, female BALFB/c mice were sensitized and challenged with OVA (OVA group) and treated with
MHTP (
MHTP group) by nasal instillation. Inflammatory, allergic, and immunomodulatory parameters such as migration of inflammatory cells to the lung tissue, pulmonary histological analysis, serum level of
IgE-
allergen specific,
cytokine secretion, and lung T cell population characterization were analyzed and the data were considered statistically significant with p < 0.05. OVA-sensitized and OVA-challenged and
MHTP (5.0 mg/kg)-treated mice presented reduction on total leukocyte migration into the bronchoalveolar lavage (BALF) dependent of lymphocyte and eosinophil migration (p < 0.001 and p < 0.01) as compared with the OVA group. Flow cytometric analysis showed that
MHTP treatment decreased the percentage of granulocytes (p < 0.001) into the BALF and lung tissue histological analyzes demonstrated that the
MHTP treatment decreased leukocyte migration and mucus production. In addition, treatment with
MHTP decreased the number of CD3+CD4+ T cells independently of CD8+ T cell reduction into the BALF. The treatment also reduced significantly (p < 0.05) the serum level of
IgE-OVA specific followed by reduction of
IL-4,
IL-13, and
IL-17 production. Surprisingly, the
MHTP treatment increased significantly (p < 0.05) the IFN-γ production in the BALF of these animals. Therefore, the results presented here showed that
MHTP treatment, by nasal instillation, in a mouse model of OVA-induced pulmonary
allergy has
anti-allergic and immunomodulatory effects dependent on a Th1-skewed
cytokine production that ameliorate the pulmonary allergic
inflammation.