OBJECTIVE: The placenta constitutes a physical and immunological barrier against infectious agents. Toll-like receptors (TLRs) are essential components for the induction of innate immunity responses in different human tissues including the placenta. We investigated the expressions of TLR2 and TLR4 in the decidua and amniotic cells in non-inflamed placenta and placenta with infection. MATERIALS AND METHODS: There were a total 74 placentas (37 with infection and 37 without infection- 25 bacterial, 10 viral and 2 toxoplasma). TLR2 and TLR4 expressions were assessed using immunohistochemical technique. Positive cells were indicated by cytoplasmic staining and the percentage of positive in 100 cells was recorded and graded. The grades were 1+ (< 25%), 2+ (25-75%) and 3+ (> 75%). RESULTS: We found significantly higher expression of TLR2 in the amniotic cells and decidua cells in infected placentas as compared to non-inflamed placentas among the preterm placenta. A higher number of cases have TLR4 expression in the amnion of preterm infected placenta than in term placenta. This, however, is not statistically significant. CONCLUSION: Our findings suggest that TLR2 plays a role in the innate immunity in bacterial and viral infection in the placenta, however, their role in protection against toxoplasma may be limited. This study further supports the observations that TLR2 expression was higher in placenta with infection which strengthened the role of TLR2 in the protection of preterm placenta against infection.
OBJECTIVE: The placenta constitutes a physical and immunological barrier against infectious agents. Toll-like receptors (TLRs) are essential components for the induction of innate immunity responses in different human tissues including the placenta. We investigated the expressions of TLR2 and TLR4 in the decidua and amniotic cells in non-inflamed placenta and placenta with infection. MATERIALS AND METHODS: There were a total 74 placentas (37 with infection and 37 without infection- 25 bacterial, 10 viral and 2 toxoplasma). TLR2 and TLR4 expressions were assessed using immunohistochemical technique. Positive cells were indicated by cytoplasmic staining and the percentage of positive in 100 cells was recorded and graded. The grades were 1+ (< 25%), 2+ (25-75%) and 3+ (> 75%). RESULTS: We found significantly higher expression of TLR2 in the amniotic cells and decidua cells in infected placentas as compared to non-inflamed placentas among the preterm placenta. A higher number of cases have TLR4 expression in the amnion of preterm infected placenta than in term placenta. This, however, is not statistically significant. CONCLUSION: Our findings suggest that TLR2 plays a role in the innate immunity in bacterial and viral infection in the placenta, however, their role in protection against toxoplasma may be limited. This study further supports the observations that TLR2 expression was higher in placenta with infection which strengthened the role of TLR2 in the protection of preterm placenta against infection.
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