Mucin depleted foci (
MDF) are precancerous lesions of the colon in
carcinogen-treated rodents and humans at high risk. Since
MDF show signs of
inflammation we hypothesized that the defective mucous production would expose them to the risk of being penetrated by intestinal bacteria, which can be sensed by
Toll-like receptors (Tlrs) and activate inflammatory pathways. To verify this hypothesis we tested the expression of 84 genes coding for Tlrs and associated pathways using RT-qPCR in
MDF (n = 7) from
1,2-dimethylhydrazine (
DMH)-treated rats. Among the 84 tested genes, 26 were differentially expressed in
MDF with 5 genes significantly up-regulated and 21 down-regulated when compared to the normal mucosa. Tlr2, as well as other downstream genes (Map4k4, Hspd1, Irak1, Ube2n), was significantly up-regulated. Among the genes regulating the NFkB pathway, only Map4k4 was significantly up-regulated, while 19 genes were not varied and 6 were down-regulated. Tlr2
protein was weakly expressed both in normal mucosa and
MDF. To determine whether
inflammation observed in
MDF could be caused by bacteria contacting or infiltrating crypts, we performed fluorescence in situ hybridization (FISH) experiments with a rRNA universal bacterial probe. None of the 21
MDF tested, showed bacteria inside the crypts, while among the colonic
tumors (n = 15), only one had very few bacteria on the surface and on the surrounding normal mucosa. In conclusion, the up-regulation of Tlr2 in
MDF, suggests a link between this receptor and
carcinogenesis, possibly related to a defective barrier function of these lesions. The data of FISH experiments do not support the hypothesis that
inflammation in
MDF and
tumors is stimulated by bacterial infiltration.