Objective: TLR insufficiency increases newborn's susceptibility to infectious disease.
Methods: The peripheral blood of four premature births has been collected weekly from the 28(th) gestational week (GW) until maturity at 36(th) GW. Microarray assays were used to derive dynamic follow-up data of TLR1-10 and other TLR signaling pathway associated factor changes.
Results: The follow-up results showed that the transcription level of TLR1 increased at the 36(th), TLR 3 decreased at the 33(rd) and TLR7 increased at the 34(th) GW significantly, whereas NFkB and its activator TBK1 were highest transcribed in the 28(th) and 32(nd) GW. Low TLR4 transcription in addition to late MD-2 maturation (33(rd) GW) indicated a lack of defense mechanisms against bacterial infections in preterm births particular in the first weeks after birth. Late transcriptional enhancements of TLR1 and MYD88 (35(th) week) as well as β 2 microglobulin (35(th) GW) also indicated a weak immune system in the early maturation stages.
Conclusion: The transcription levels of TLR1, 3, 7 and the signaling pathway associated cofactors were different transcribed during the 28(th) and 36(th) GWs of the premature newborns. In the early stage after preterm birth, beside peak transcriptions of NFkB and TBK1, the immune system is not fully developed and maturation takes place mainly between the 33th and 35(th) GW.
Keywords: NFkB; TLR; TLR4; immune system; preterm birth.