Project description:Staphylococcus aureus lipoteichoic acid (aLTA) and Lactobacillus plantarum LTA (pLTA) engage the same Toll-like receptor 2 (TLR2) signaling pathway, but exert different effects on the innate immune/inflammatory responses. aLTA is the leading cause of gram-positive bacterial sepsis induced by S. aureus, whereas pLTA is considered as a promising therapeutic agent for pathogen-induced septic shock. The mechanisms underlying the different functions of aLTA and pLTA remain unclear. We used human oligo microarrays to investigate the transcriptomes of human THP-1 monocytes upon exposure to aLTA and pLTA. Differential gene expression profiles were observed between the aLTA- and pLTA-treated cells. The expression levels of 1301 genes in aLTA-treated cells were changed more than 2 fold. These genes are critically involved in immune/inflammatory responses, cell adhesion, cell signal transduction, transcription factors, anion transport, proteolysis and oxidative processes. Especially, a variety of genes that encode cytokines/chemokines and other related molecules such as those belonging to the IRAK, TRAF, NF-κB, and STAT families were remarkably up-regulated by aLTA stimulation. In contrast, the expression levels of only 93 genes were altered by more than 1.5 fold in pLTA-treated cells, and these genes are almost not correlative with immune/inflammatory responses and other related processes compared with those of aLTA-treated cells. The different functions of aLTA and pLTA were further compared with the differential expressions of a selected group of genes, i.e., IRAKs, TRAFs and some cytokines/chemokines through RT-PCR and ELISA assays. The gene expression of IRAK2 could be markedly induced by aLTA, but significantly inhibited by pLTA treatment. These results suggest that the different functions of aLTA and pLTA on innate immunity and inflammation might be due to their different effects on the expression of some genes related with the innate immune/inflammatory responses, such as IRAK2 etc.

Project description:Staphylococcus aureus lipoteichoic acid (aLTA) and Lactobacillus plantarum LTA (pLTA) engage the same Toll-like receptor 2 (TLR2) signaling pathway, but exert different effects on the innate immune/inflammatory responses. aLTA is the leading cause of gram-positive bacterial sepsis induced by S. aureus, whereas pLTA is considered as a promising therapeutic agent for pathogen-induced septic shock. The mechanisms underlying the different functions of aLTA and pLTA remain unclear. We used human oligo microarrays to investigate the transcriptomes of human THP-1 monocytes upon exposure to aLTA and pLTA. Differential gene expression profiles were observed between the aLTA- and pLTA-treated cells. The expression levels of 1301 genes in aLTA-treated cells were changed more than 2 fold. These genes are critically involved in immune/inflammatory responses, cell adhesion, cell signal transduction, transcription factors, anion transport, proteolysis and oxidative processes. Especially, a variety of genes that encode cytokines/chemokines and other related molecules such as those belonging to the IRAK, TRAF, NF-κB, and STAT families were remarkably up-regulated by aLTA stimulation. In contrast, the expression levels of only 93 genes were altered by more than 1.5 fold in pLTA-treated cells, and these genes are almost not correlative with immune/inflammatory responses and other related processes compared with those of aLTA-treated cells. The different functions of aLTA and pLTA were further compared with the differential expressions of a selected group of genes, i.e., IRAKs, TRAFs and some cytokines/chemokines through RT-PCR and ELISA assays. The gene expression of IRAK2 could be markedly induced by aLTA, but significantly inhibited by pLTA treatment. These results suggest that the different functions of aLTA and pLTA on innate immunity and inflammation might be due to their different effects on the expression of some genes related with the innate immune/inflammatory responses, such as IRAK2 etc. We analyzed gene expression change by aLTA and pLTA in THP1 cell to find the active pathway and related biology function.

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Pintalia alta

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