scholarly journals Manipulating the microbiome alters regenerative outcomes in Xenopus laevis tadpoles vis lipopolysaccharide signalling

2021 ◽  
Author(s):  
Phoebe A Chapman ◽  
Campbell B Gilbert ◽  
Thomas J Devine ◽  
Daniel T Hudson ◽  
Joanna Ward ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Skin Microbiome ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tail Regeneration ◽  
Rrna Sequencing ◽  
Bacterial Lipopolysaccharides ◽  
Tadpole Skin ◽  
Editing Level

Xenopus laevis tadpoles can regenerate functional tails, containing spinal cord, notochord, muscle, fin, blood vessels and nerves, except for a brief refractory period at around one week of age. At this stage, amputation of the tadpole's tail may either result in scarless wound healing, or the activation of a regeneration programme, which replaces the lost tissues. We recently demonstrated a link between bacterial lipopolysaccharides and successful tail regeneration in refractory stage tadpoles, and proposed that this could result from lipopolysaccharides binding to Toll-like receptor 4 (TLR4). Here, we have used 16S rRNA sequencing to show that the tadpole skin microbiome is highly variable between sibships and that the community can be altered by raising embryos in the antibiotic gentamicin. Six gram-negative genera, including Delftia and Chryseobacterium, were over-represented in tadpoles that underwent tail regeneration. Lipopolysaccharides purified from a commensal Chryseobacterium spp. XDS4, an exogenous Delftia spp. or Escherichia coli could significantly increase the number of antibiotic-raised tadpoles that attempted regeneration. Conversely, the quality of regeneration was impaired in native-raised tadpoles exposed to the antagonistic lipopolysaccharide of Rhodobacter sphaeroides. Knocking down TLR4 using CRISPR/Cas9 also reduced regeneration quality, but not quantity, at the level of the cohort. However, we found that the editing level of individual tadpoles was a poor predictor of regenerative outcome. In conclusion, our results suggest that variable regeneration in refractory stage tadpoles depends at least in part on the skin microbiome and lipopolysaccharide signalling, but that signalling via TLR4 cannot account for all of this effect.

scholarly journals Cationic Lipid and Bacterial Lipopolysaccharides Both Activate Toll-Like Receptor 4 Pathways via Different Binding Regions

2014 ◽  
Vol 106 (2) ◽  
pp. 308a
Author(s):  
Caroline Lonez ◽  
Kate Irvine ◽  
Monique Gangloff ◽  
Malvina Pizzuto ◽  
Boris Schmidt ◽  
...  
Keyword(s):  
Cationic Lipid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Binding Regions ◽  
Bacterial Lipopolysaccharides

scholarly journals Exploring the cytotoxic mechanisms of Pediocin PA-1 towards HeLa and HT29 cells by comparison to known bacteriocins: Microcin E492, enterocin heterodimer and Divercin V41

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0251951
Author(s):  
George P. Buss ◽  
Cornelia M. Wilson
Keyword(s):  
Bioinformatic Analysis ◽  
3D Modelling ◽  
Future Research ◽  
Toll Like Receptor ◽  
Sequence Alignments ◽  
Toll Like Receptor 4 ◽  
Dual Effect ◽  
Ht29 Cells ◽  
The Difference

The purpose of this study was to explore potential mechanisms of cytotoxicity towards HeLa and HT29 cells displayed by Pediocin PA-1. We did this by carrying out sequence alignments and 3D modelling of related bacteriocins which have been studied in greater detail: Microcin E492, Enterocin AB heterodimer and Divercin V41. Microcin E492 interacts with Toll-Like Receptor 4 in order to activate an apoptosis reaction, sequence alignment showed a high homology between Pediocin PA-1 and Microcin E492 whereas 3D modelling showed Pediocin PA-1 interacting with TLR-4 in a way reminiscent of Microcin E492. Furthermore, Pediocin PA-1 had the highest homology with the Enterocin heterodimer, particularly chain A; Enterocin has also shown to cause an apoptotic response in cancer cells. Based on this we are led to strongly believe Pediocin PA-1 interacts with TLRs in order to cause cell death. If this is the case, it would explain the difference in cytotoxicity towards HeLa over HT29 cells, due to difference in expression of particular TLRs. Overall, we believe Pediocin PA-1 exhibits a dual effect which is dose dependant, like that of Microcin. Unfortunately, due to the COVID-19 pandemic, we were unable to carry out experiments in the lab, and the unavailability of important data meant we were unable to provide and validate out solid conclusions, but rather suggestions. However, bioinformatic analysis is still able to provide information regarding structure and sequence analysis to draw plausible and evidence based conclusions. We have been able to highlight interesting findings and how these could be translated into future research and therapeutics in order to improve the quality of treatment and life of cancer patients.

scholarly journals Exploring the cytotoxic mechanisms of Pediocin PA-1 towards HeLa and HT29 cells by comparison to known bacteriocins: Microcin E492, Enterocin Heterodimer and Divercin V41.

2021 ◽  
Author(s):  
George Paul Buss ◽  
Cornelia Wilson
Keyword(s):  
3D Modelling ◽  
Future Research ◽  
Toll Like Receptor ◽  
Reaction Sequence ◽  
Sequence Alignments ◽  
Toll Like Receptor 4 ◽  
Dual Effect ◽  
Ht29 Cells ◽  
The Difference

The purpose of this study was to explore potential mechanisms of cytotoxicity towards HeLa and HT29 cells displayed by Pediocin PA-1. We did this by carrying out sequence alignments and 3D modelling of related bacteriocins which have been studied in greater detail: Microcin E492, Eneterocin AB heterodimer and Divercin V41. Microcin E492 interacts with Toll-Like Receptor 4 in order to activate an apoptosis reaction, sequence alignment showed a high homology between Pediocin PA-1 and Microcin E492 and 3D modelling showed Pediocin PA-1 interacting with TLR-4 in a way reminiscent of Microcin E492. Furthermore, Pediocin PA-1 had the highest homology with the Enterocin heterodimer, particularly chain A; Enterocin has also shown to cause an apoptotic response in cancer cells. Based on this we are led to strongly believe Pediocin PA-1 interacts with TLRs in order to cause cell death. If this is the case it would explain the difference in cytotoxicity towards HeLa over HT29 cells, due to difference in expression of particular TLRs. Overall, we believe Pediocin PA-1 exhibits a dual effect which is dose dependant, like that of Microcin. Unfortunately, the COVID-19 pandemic meant that we were unable to carry out experiments in the lab, and the unavailability of important data meant we were unable to make solid conclusions but rather suggestions. However despite this we have still been able to highlight interesting findings and how these could be translated into future research and therapeutics in order to improve the quality of treatment and life of cancer patients.

scholarly journals Antifibrotics and Antioxidants of Chlorogenic Acid Inhibits Toll- Like Receptors-4 as Liver Fibrotic Marker

2021 ◽  
Vol 3 (2) ◽  
pp. 91-99
Author(s):  
Rosdiana Naibey ◽  
Widya Wasityastuti ◽  
Nungki Anggorowati ◽  
Nur Arfian
Keyword(s):  
Chlorogenic Acid ◽  
Control Group ◽  
Toll Like Receptor ◽  
Rt Pcr ◽  
Toll Like Receptor 4 ◽  
Control Group Design ◽  
Body Tissues ◽  
Post Test ◽  
Group 3

Introduction: Chlorogenic Acid (CGA) is an antifibrotic and antioxidant for fibrotic tissues. These double  roles be able to inhibit or fibrotic tissues chains because of internal and external issues.  For example, virus, bacteria or other pathogens and also by drugs, alcohol, cigarettes, etc. as external factor that affect quality of body tissues. Toll-Like Receptor-4 (TLR-4) as a marker fibrotic tissues.  It is a key for researcher could be find out by expression performance. The aim of this study is to reveal the CGA as a candidate of antifibrotic & antioxidant in liver fibrosis that induced by CCL4.    Methods: This is a pure experimental research with a simple experimental design or post-test only control group design. The total 29 mices of 2.5-month-old male Swiss mices with weigh 35-40 gram divided into 6 group: 3 groups of controls (injected by natrium chloride, CGA, and CCL4) and 3 groups of treated (injected by CGA doses 42 mg/kg, 63 mg/kg or 84 mg/kg).  Liver organ was used to examine the expression of TLR-4 by rt-PCR. This research revealed that expression of TLR-4 lower than the CCL4 control group (respectively, p=0.042; p=0.005; p=0.006; and p=0.001). Higher dose of CGA showed greater ability as anti-fibrotic through inhibit the expression of  TLR-4. Some research found the expression of TLR-4 has been decreased by treatment of Clorogenic Acid (CGA). Conclusion: To sum up, CGA has double roles to repair liver fibrotic tissues. The greater doses of CGA, the stronger inhibition of TLR-4 expression.

660 Deficiency of Toll-like receptor 4 leads to cardioprotection against doxorubicin-induced cardiomyopathy

2007 ◽  
Vol 6 (1) ◽  
pp. 142-143
Author(s):  
A RIAD ◽  
S BIEN ◽  
M GRATZ ◽  
S BERESWILL ◽  
H SCHULTHEISS ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 4

Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Tao Shang ◽  
Feng Ran ◽  
Qian Qiao ◽  
Zhao Liu ◽  
Chang-Jian Liu
Keyword(s):  
Nuclear Factor Κb ◽  
Tanshinone Iia ◽  
Myeloid Differentiation ◽  
Aortic Tissue ◽  
Toll Like Receptor ◽  
Sprague Dawley ◽  
Toll Like Receptor 4 ◽  
Tissue Samples ◽  
Myeloid Differentiation Factor ◽  
And Control

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12 / group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg / rat / d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphorylated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

Sign in / Sign up

Export Citation Format

Share Document