Endotoxins released by Gram-negative bacteria are potent stimulators of tumor
necrosis factor α (TNF-α) production. The objectives of this study were to evaluate
plasma levels of TNF-α, TNF-α secretion, and mRNA levels of TNF and
TNF-α receptor type 1 (TNFR1) following exposure to
lipopolysaccharide (LPS). For this, we used cultured endometrial cells or organ
cultures, throughout the estrous cycle, after hormone treatment with
medroxyprogesterone acetate (MPA), and during pyometra. Plasma TNF-α concentrations
were increased in animals at estrus (P < 0.05) compared to other groups. In the
LPS-challenged endometrium, secretion of TNF-α by tissues collected during estrus
increased (P < 0.001) compared to that of other groups. LPS, alone or combined
with TNF-α, upregulated TNF gene expression in the feline
endometrium at diestrus (P < 0.001 for both treatments), in queens treated
short-term with MPA (P < 0.01 and P < 0.05, respectively) and in queens treated
long-term with MPA (P < 0.01 and P < 0.001, respectively). During pyometra,
TNF and TNFR1 mRNA were increased only after
tissues were challenged with TNF-α and LPS (P < 0.001 and P < 0.01,
respectively). When cultured endometrial cells were challenged with LPS, the
concentration of TNF-α increased only in epithelial cells after 4 h and 12 h (P <
0.05 and P < 0.01, respectively). Since LPS did not affect stromal cells, but
TNF-α increased its own transcript after 2 h (P < 0.01), 4 h (P < 0.05) and 12
h (P < 0.001), we assume that stromal cells are not directly involved in pathogen
recognition, as was the case for epithelial cells.