Epididymitis is a commonly diagnosed disease associated with
male infertility. However, little is known about the molecules that are involved in its development. This study was to identify critical genes associated with
lipopolysaccharide-induced
epididymitis and analyze the molecular mechanism of
epididymitis through
RNA sequencing. Experimental
epididymitis models were generated by administering male Sprague-Dawley rats'
lipopolysaccharide. A total of 1378 differentially expressed genes, including 531 upregulated and 847 downregulated genes, were identified in the
epididymitis model rats compared with those in
sham-operated rats by
RNA sequencing. Functional enrichment analyses suggested that the upregulated genes were markedly enriched in
inflammation-related biological processes, as well as in the
tumor necrosis factor (TNF) signaling pathway,
cytokine-
cytokine receptor interactions,
complement and coagulation cascades, and in the
chemokine signaling pathway. Four downregulated genes (
collagen type XXVIII alpha 1 chain [Col28α1],
cyclin-dependent kinase-like 1 [Cdkl1],
phosphoserine phosphatase [Psph], and
fatty acid desaturase 2 [Fads2]) and ten upregulated genes (
CCAAT/enhancer-binding protein beta [Cebpβ], C-X-C motif
chemokine receptor 2 [Cxcr2],
interleukin 11 [
Il11], C-C motif
chemokine ligand 20 [Ccl20],
nuclear factor-kappa-B inhibitor alpha [Nfkbiα],
claudin 4 [Cldn4], matrix
metallopeptidase 9 [Mmp9],
heat shock 70 kDa protein 8 [Hspa8], intercellular
cell adhesion molecule-1 [Icam1], and Jun) were successfully confirmed by real-time polymerase chain reaction. Western blot demonstrated that CDKL1 was decreased, while MMP9 and NFKBIA were increased in the experimental model group compared with those in the
sham-operated group. Our study sheds new light on the understanding of the early response of the epididymis during bacterial
epididymitis.