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Another study, this one published in the American Journal of Epidemiology, found that male smokers in their 40s were more likely to experience erectile difficulties than older nonsmoking males. The risk of erectile dysfunction was nearly doubled for smoking men in their 40s compared to nonsmokers in their 50s.
Phosphodiesterase-5 (PDE5) inhibitors (sildenafil, tadalafil, and vardenafil) are agents currently in clinical use for nonmalignant conditions. We report the use of PDE5 inhibitors as modulators of the antitumor immune response. In several mouse tumor models, PDE5 inhibition reverses tumor-induced immunosuppressive mechanisms and enables a measurable antitumor immune response to be generated that substantially delays tumor progression. In particular, sildenafil, down-regulates arginase 1 and nitric oxide synthase–2 expression, thereby reducing the suppressive machinery of CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) recruited by growing tumors. By removing these tumor escape mechanisms, sildenafil enhances intratumoral T cell infiltration and activation, reduces tumor outgrowth, and improves the antitumor efficacy of adoptive T cell therapy. Sildenafil also restores in vitro T cell proliferation of peripheral blood mononuclear cells from multiple myeloma and head and neck cancer patients. In light of the recent data that enzymes mediating MDSC-dependent immunosuppression in mice are active also in humans, these findings demonstrate a potentially novel use of PDE5 inhibitors as adjuncts to tumor-specific immune therapy.
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Article, publication date, and citation information can be found at http://pharmrev.aspetjournals.org.
In vitro sildenafil down-regulates the myeloid suppressor cell suppressive marker IL-4R
By increasing the intracellular concentrations of cyclic guanosine monophosphate (cGMP), phosphodiesterase-5 (PDE5) inhibitors such as sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) have been used therapeutically to treat erectile dysfunction (12), pulmonary hypertension (13), and cardiac hypertrophy (14). More recently, they were shown to induce apoptosis in different human tumors such as colon carcinoma and chronic lymphocyte leukemia (15, 16). In our mouse models, we show that pharmacologic PDE5 blockade down-regulates MDSC suppressive pathways and restores antitumor immunity. Moreover, our in vitro experiments using PBMCs from multiple myeloma (MM) and head and neck cancer patients suggest that the same mechanisms found in mice are also present in humans and demonstrate a possible role for PDE5 inhibitors as an immune adjuvant in the clinical setting.
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