Objective: TLR insufficiency increases newborn's susceptibility to infectious disease. Methods: The peripheral blood of four premature births has been collected weekly from the 28th gestational week (GW) until maturity at 36th 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 36th, TLR 3 decreased at the 33rd and TLR7 increased at the 34th GW significantly, whereas NFkB and its activator TBK1 were highest transcribed in the 28th and 32nd GW. Low TLR4 transcription in addition to late MD-2 maturation (33rd 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 (35th week) as well as beta 2 microglobulin (35th 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 28th and 36th 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 35th GW.
[1]Fudan Univ, Childrens Hosp, Div Neonatol, Shanghai 201102, Peoples R China.
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