Does anybody know some papers about different concentrations of LPS stimulated macrophages that induce pro IL1 beta expression?
Please review the following:
Cytokine production by human fetal microglia and astrocytes. Differential induction by lipopolysaccharide and IL-1 beta.
S C Lee, et al. Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461.
Abstract
As part of a study on the role of cytokines in central nervous system development and dysfunction, we determined the pattern of cytokine production in highly purified cultures of microglia and astrocytes isolated from second-trimester human fetal brains. Levels of TNF-alpha, IL-1 beta, and IL-6 mRNA and protein were determined by Northern blot analysis and ELISA before and after stimulation with LPS, TNF-alpha, or IL-1 beta. In microglia, LPS induced mRNA for all three cytokines. High protein levels of IL-6 and TNF-alpha were also found in the medium, whereas IL-1 beta protein was mostly cell associated. IL-1 beta also induced message for all three cytokines, in the rank order of IL-1 beta > IL-6 > TNF-alpha. TNF-alpha induced mRNA and protein for IL-1 beta but not for TNF-alpha or IL-6. In contrast, LPS failed to stimulate either mRNA or protein expression for any of the three cytokines in astrocytes. On the other hand, IL-1 beta provided a strong stimulus for astrocytes. IL-1 beta induced mRNA and protein for both TNF-alpha and IL-6, but the kinetics of the response differed for the two cytokines. TNF-alpha mRNA and protein levels peaked early (at 4 h and 16 h, respectively) and were undetectable by 72 h, whereas IL-6 mRNA peaked later (at 16 h) and protein levels continued to accumulate in the medium through 72 h. IL-1 beta did not induce IL-1 beta mRNA or protein in astrocytes. TNF-alpha did not induce expression of any of the cytokines in astrocytes. In conclusion, our results demonstrate that cytokine production can be induced in human fetal microglia and astrocytes but that the stimuli for induction differed significantly for the two cell types. Whereas LPS was a potent stimulus for microglia, astrocytes primarily responded to IL-1 beta. The data further suggest that microglia may be key regulators of astrocyte response, working primarily through the expression of cell-associated IL-1 beta.
Differential involvement of IFN‐β in Toll‐like receptor‐stimulated dendritic cell activation. Katsuaki Hoshino, et al.
Abstract
Toll‐like receptor (TLR) can activate dendritic cells (DC) through common signaling pathways requiring a cytoplasmic adapter, MyD88. However, the signaling is differentially regulated among TLR family members. TLR4 can activate MyD88‐deficient bone marrow‐derived DC (BMDC), and lead to induction of IFN‐inducible genes and up‐regulation of co‐stimulatory molecules such as CD40, implying that the MyD88‐independent signaling pathway functions downstream of TLR4. Because these effects can also be induced by type I IFN, we have analyzed whether type I IFN is involved in TLR4‐induced responses. In response to lipopolysaccharide (LPS), IFN‐β gene expression was augmented in both wild‐type and MyD88‐deficient BMDC. Expression of all IFN‐inducible genes except immune‐responsive gene 1 (IRG1) was abolished and CD40 up‐regulation was decreased in LPS‐stimulated BMDC lacking either IFN‐α/β receptor (IFN‐α/βR) or signal transducer and activator of transcription 1 (STAT‐1). Similar to the LPS response, TLR9 signaling can also induce expression of IFN‐β and IFN‐inducible genes, and up‐regulation of CD40. However, all these effects were MyD88 dependent. Thus, in TLR4 signaling, IFN‐β expression can be induced either by the MyD88‐dependent or ‐independent pathway, whereas, in TLR9 signaling, it is dependent on MyD88. In CpG DNA‐stimulated DC, expression of IFN‐inducible genes except IRG1 was dependent on type I IFN signaling as in LPS‐stimulated DC. However, in contrast to TLR4 signaling, TLR9 signaling requires type I IFN signaling for CD40 up‐regulation. Taken together, this study demonstrates differential involvement of type I IFN in TLR4‐ and TLR9‐induced effects on DC.
Optimal Method to Stimulate Cytokine Production and Its Use
in Immunotoxicity Assessment
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