Injury to the cavernous nerves during a radical prostatectomy (RP) procedure can cause post-RP erectile dysfunction. We previously demonstrated that TNF-α was increased in the major pelvic ganglion (MPG) of the rat following bilateral cavernous nerve injury (BCNI). TNF-α is known to recruit macrophages. This study utilized real-time qPCR and Western blot to evaluate changes in gene and protein expression of general macrophage markers and markers of macrophage subtypes (neurotoxic M1 and neuroprotective M2) and investigated whether an increase in TNF-α concentration led to enhanced recruitment of M1 macrophages to the MPG following BCNI. We demonstrated that BCNI increased gene expression of both M1 and M2 macrophage markers; however, the protein expression of an M1 macrophage marker was increased following BCNI while that of an M2 macrophage marker was not. Immunofluorescence (IF) imaging of the MPG following BCNI indicated co-localization of TNF-α and an M1 macrophage marker, suggesting recruitment of M1 macrophages by TNF-α. These results indicate that commercially available TNF-α antagonists may prevent post-RP erectile dysfunction.

TNF-α is increased following bilateral cavernous nerve injury, leading to enhanced recruitment of neurotoxic M1 macrophages

251st National Meeting (2016)

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