Limits...
Toll-like receptor-4 pathway is required for the pathogenesis of human chronic endometritis.

Ju J, Li L, Xie J, Wu Y, Wu X, Li W - Exp Ther Med (2014)

Bottom Line: Furthermore, the protein of the signaling adapter myeloid differentiation factor-88 and the accessory molecules (TNF receptor associated factor 6 and transforming growth factor-β-activated kinase 1) were also detected in all the assayed tissues.The altered TLR4 and its corresponding downstream signaling molecules in CE cells may be of relevance for the progression of the human CE.These findings indicate that the evaluation of expression patterns of TLR4 holds promise for the treatment of human CE.

View Article: PubMed Central - PubMed

Affiliation: Department of Gynecology, Nanjing Municipal Organ Hospital, Nanjing, Jiangsu 210018, P.R. China.

ABSTRACT
Toll-like receptor (TLR) signal transduction is a central component of the primary innate immune response to pathogenic challenge. TLR4, a member of the TLR family, is highly expressed in the endometrial cells of the uterus and could thus be a key link between human chronic endometritis (CE) and the immune system. However, the exact biological function of TLR4 in human CE remains largely unexplored. The present study aimed to examine the role of TLR4 in human CE. A comprehensive expression and activation analysis of TLR4 in the endometrial cells of the uterus from patients with human CE (n=25) and normal endometrial (NE) tissue (n=15) was performed. Western blot analyses demonstrated that compared with NE, the protein expression TLR4 markedly increased in human CE. Endometrial tissue scrapings were also used for total RNA extraction and were transcribed and amplified by reverse transcription quantitative polymerase chain reaction. The results showed that significant upregulation of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and downregulation of IL-10 mRNA was observed in CE compared with the NE group. Furthermore, the protein of the signaling adapter myeloid differentiation factor-88 and the accessory molecules (TNF receptor associated factor 6 and transforming growth factor-β-activated kinase 1) were also detected in all the assayed tissues. Of note, differential expression (CE versus NE) was observed by immunoblotting at each level of the nuclear factor-κB signaling cascade, including inhibitor κBα and P65 (all P<0.05). The altered TLR4 and its corresponding downstream signaling molecules in CE cells may be of relevance for the progression of the human CE. These findings indicate that the evaluation of expression patterns of TLR4 holds promise for the treatment of human CE.

No MeSH data available.


Related in: MedlinePlus

TLR4 expression is increased in human CE. Representative western blots from human CE and control NE tissues for the determination of the TLR4 protein levels expressed in the endometrial tissues (from three independent experiments). TLR4, Toll-like receptor-4; CE, chronic endometritis; NE, normal endometrial.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4217777&req=5

f1-etm-08-06-1896: TLR4 expression is increased in human CE. Representative western blots from human CE and control NE tissues for the determination of the TLR4 protein levels expressed in the endometrial tissues (from three independent experiments). TLR4, Toll-like receptor-4; CE, chronic endometritis; NE, normal endometrial.

Mentions: To investigate the potential role of TLR4 in the development of human CE, whether expression levels of TLR4 were altered in the pathological endometrium was first analyzed. The RT-qPCR and western blot analysis assays showed that the mRNA and protein expression levels of TLR4 were significantly increased in human CE (n=7) compared with NE (n=5) (Fig. 1). In addition, the upregulation of TLR4 in human CE was correlated with the induction of a series of inflammatory markers at the mRNA level, including interleukin (IL)-1β and TNF-α (Fig. 2A and B). However, the levels of IL-10 were markedly decreased in human CE compared with NE (Fig. 2C). Collectively, the altered pattern of TLR4 expression suggests that TLR4 may be involved in the development of the inflammatory response in human CE.


Toll-like receptor-4 pathway is required for the pathogenesis of human chronic endometritis.

Ju J, Li L, Xie J, Wu Y, Wu X, Li W - Exp Ther Med (2014)

TLR4 expression is increased in human CE. Representative western blots from human CE and control NE tissues for the determination of the TLR4 protein levels expressed in the endometrial tissues (from three independent experiments). TLR4, Toll-like receptor-4; CE, chronic endometritis; NE, normal endometrial.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4217777&req=5

f1-etm-08-06-1896: TLR4 expression is increased in human CE. Representative western blots from human CE and control NE tissues for the determination of the TLR4 protein levels expressed in the endometrial tissues (from three independent experiments). TLR4, Toll-like receptor-4; CE, chronic endometritis; NE, normal endometrial.
Mentions: To investigate the potential role of TLR4 in the development of human CE, whether expression levels of TLR4 were altered in the pathological endometrium was first analyzed. The RT-qPCR and western blot analysis assays showed that the mRNA and protein expression levels of TLR4 were significantly increased in human CE (n=7) compared with NE (n=5) (Fig. 1). In addition, the upregulation of TLR4 in human CE was correlated with the induction of a series of inflammatory markers at the mRNA level, including interleukin (IL)-1β and TNF-α (Fig. 2A and B). However, the levels of IL-10 were markedly decreased in human CE compared with NE (Fig. 2C). Collectively, the altered pattern of TLR4 expression suggests that TLR4 may be involved in the development of the inflammatory response in human CE.

Bottom Line: Furthermore, the protein of the signaling adapter myeloid differentiation factor-88 and the accessory molecules (TNF receptor associated factor 6 and transforming growth factor-β-activated kinase 1) were also detected in all the assayed tissues.The altered TLR4 and its corresponding downstream signaling molecules in CE cells may be of relevance for the progression of the human CE.These findings indicate that the evaluation of expression patterns of TLR4 holds promise for the treatment of human CE.

View Article: PubMed Central - PubMed

Affiliation: Department of Gynecology, Nanjing Municipal Organ Hospital, Nanjing, Jiangsu 210018, P.R. China.

ABSTRACT
Toll-like receptor (TLR) signal transduction is a central component of the primary innate immune response to pathogenic challenge. TLR4, a member of the TLR family, is highly expressed in the endometrial cells of the uterus and could thus be a key link between human chronic endometritis (CE) and the immune system. However, the exact biological function of TLR4 in human CE remains largely unexplored. The present study aimed to examine the role of TLR4 in human CE. A comprehensive expression and activation analysis of TLR4 in the endometrial cells of the uterus from patients with human CE (n=25) and normal endometrial (NE) tissue (n=15) was performed. Western blot analyses demonstrated that compared with NE, the protein expression TLR4 markedly increased in human CE. Endometrial tissue scrapings were also used for total RNA extraction and were transcribed and amplified by reverse transcription quantitative polymerase chain reaction. The results showed that significant upregulation of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and downregulation of IL-10 mRNA was observed in CE compared with the NE group. Furthermore, the protein of the signaling adapter myeloid differentiation factor-88 and the accessory molecules (TNF receptor associated factor 6 and transforming growth factor-β-activated kinase 1) were also detected in all the assayed tissues. Of note, differential expression (CE versus NE) was observed by immunoblotting at each level of the nuclear factor-κB signaling cascade, including inhibitor κBα and P65 (all P<0.05). The altered TLR4 and its corresponding downstream signaling molecules in CE cells may be of relevance for the progression of the human CE. These findings indicate that the evaluation of expression patterns of TLR4 holds promise for the treatment of human CE.

No MeSH data available.


Related in: MedlinePlus