Dataset Information

Targeting Campylobacter signalling to modulate biofilm dynamics (J4-3088)

ABSTRACT: Campylobacter spp. cause food-borne illnesses worldwide due to contaminated food and cross-contamination. This is at least partly the result of Campylobacter resistance in the food production chain, as modern food production facilitates the emergence and spread of resistance through intensive use of antimicrobials and international trade in raw materials and food products. The biofilm 'lifestyle' of Campylobacter contributes to this spread as it enables them to withstand stress in the environment both outside and inside the host. Campylobacter adhesion and biofilm formation has major implications for the food industry, where biofilms can be persistent sources of contamination. Lavender essential oil, ethanol extracts, and its main compounds (linalool, linalyl acetate) reduce the AI-2 biosensor response in Vibrio harveyi without lowering AI-2 levels or affecting the luxS gene in Campylobacter jejuni. This suggests lavender compounds may block AI-2 detection—likely by interfering with its receptor—offering a natural strategy to disrupt bacterial communication, biofilm formation, and virulence.

INSTRUMENT(S):

ORGANISM(S): Campylobacter Jejuni Subsp. Jejuni Nctc 11168 = Atcc 700819

SUBMITTER: Blaž Jug

LAB HEAD: Dr Anja Klančnik

PROVIDER: PXD067187 | Pride | 2026-02-27

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	File_names_directory.txt	Txt
	QEX02_MF_210427_CAM1_373.msf	Msf
	QEX02_MF_210427_CAM1_373.raw	Raw
	QEX02_MF_210427_CAM2_375.msf	Msf
	QEX02_MF_210427_CAM2_375.raw	Raw

Items per page:

1 - 5 of 25

Similar Datasets

Project description:In a transcriptome based trail, we figured out that the deletion of luxS has a massive influence to cell growth and metabolism of Streptococcus sanguinis SK36. The biofilm defective luxS deletion mutant was comlemented by transgenic sahH from Pseudomonas aeruginosa. Thus 209 of 216 influenced genes of the luxS mutant compared to the isogenic wildype were restored in their expression (fold change of n ≥ 3; p ≤ 0.05), including genes involved in cell division processes, stress response and catabolite control. Phenotypically, the reduced biofilm depth of S. sanguinis SR DELTAluxS was elevated to wild type level by the complementation with sahH. Neither the addition of physiological concentrated artificial autoinducer 2 (AI-2) to the culture of S. sanguinis SR DELTAluxS nor the presence of the wild type strain in a trans-well assay had a cumulative effect on biofilm thickness of the luxS mutant. Furthermore, we identified 9 genes in the sahH complemented luxS mutant, which were regulated directly by AI-2 (fold change ≥ 3; p ≤ 0.05), amongst them genes involved in competence development. So we concluded that AI-2 has no influence on biofilm growth, but regulative functions in competence development in S. sanguinis. Further, we figured out the suitability of transgenic sahH for the complementation of the interrupted Pfs/LuxS pathway without restoration of AI-2 release acquiring an essential tool for further investigations on AI-2. Aim: Is the presence of AI-2 necessary for the biofilm formation of S. sanguinis SK36? What is the impact of a deletion of luxS, is a disrupted activated methionine cycle the reason for the hampered biofilm depth causes by its inactivation? Materials and Methods: S. sanguinis SK36, S. sanguinis SR ΔluxS, and S. sanguinis SR ΔluxS/sahH were grown in CDM/sucrose for 24 h anaerobically; biofilm depth was measured by safranine and crystal violet stain. Biofilm morphology was investigated by scanning electron microscopy. The AI-2 release was monitored hourly to identify the time period of its release. For transcriptome analysis total RNA was isolated after 8 hours of growth and used for microarray analysis.

Project description:We have shown the quorum-sensing signals acylhomoserine lactones (AHLs), autoinducer-2 (AI-2), and indole influence the biofilm formation of Escherichia coli. Here, we investigate how the environment, i.e., temperature, affects indole and AI-2 signaling in E. coli. We show in biofilms that indole addition leads to more extensive differential gene expression at 30ï°C (186 genes) than at 37ï°C (59 genes), that indole reduces biofilm formation (without affecting growth) more significantly at 25ï°C and 30ï°C than at 37ï°C, and that the effect is associated with the quorum-sensing protein SdiA. The addition of indole at 30ï°C compared to 37ï°C most significantly repressed genes involved in uridine monophosphate (UMP) biosynthesis (carAB, pyrLBI, pyrC, pyrD, pyrF, and upp) and uracil transport (uraA). These uracil-related genes are also repressed at 30ï°C by SdiA, which confirms SdiA is involved in indole signaling. Also, compared to 37ï°C, indole more significantly decreased flagella-related qseB, flhD, and fliA promoter activity, enhanced antibiotic resistance, and inhibited cell division at 30ï°C. In contrast to indole and SdiA, the addition of (S)-4,5-dihydroxy-2,3-pentanedione (the AI-2 precursor) leads to more extensive differential gene expression at 37ï°C (63 genes) than at 30ï°C (11 genes), and, rather than repressing UMP synthesis genes, AI-2 induces them at 37ï°C (but not at 30ï°C). Also, the addition of AI-2 induces the transcription of virulence genes in enterohemorrhagic E. coli O157:H7 at 37oC but not at 30oC. Hence, cell signals cause diverse responses at different temperatures, and indole- and AI-2-based signaling are intertwined. Experiment Overall Design: We performed seven sets of microarray experiments in LB medium (Table 2): (i) biofilm cells of the BW25113 wild-type strain grown for 7 h at 30Â°C vs. 37Â°C to determine the effect of temperature on E. coli biofilm formation (initial absorbance of 0.05), (ii) biofilm cells of the tnaA mutant grown for 7 h with 1 mM indole vs. no indole at 30Â°C to determine the effect of temperature on indole signaling in E. coli (initial absorbance of 0.05), (iii) biofilm cells of the tnaA mutant grown for 7 h with 1 mM indole vs. no indole at 37Â°C to determine the effect of temperature on indole signaling in E. coli, (iv) suspension cells of the wild-type strain vs. the sdiA mutant at an absorbance of 4.0 at 600 nm at 30Â°C (since production of indole takes place primarily in the stationary phase) to discern the genes that SdiA controls (initial absorbance of 0.05), (v) biofilm cells of the sdiA mutant grown for 7 h with 1 mM indole vs. no indole at 30Â°C to determine gene expression in response to indole in the absence of SdiA, (vi) suspension cells of the luxS mutant with 100 micro M AI-2 vs. no AI-2 at 30Â°C for 3 h to determine the effect of temperature on AI-2 signaling in E. coli (initial absorbance of 0.5), and (vii) suspension cells of the luxS mutant with 100 micro M AI-2 vs. no AI-2 at 37Â°C for 3 h to determine the effect of temperature on AI-2 signaling in E. coli. Ten g of glass wool (Corning Glass Works, Corning, N.Y.) was used to form large amounts of biofilms (Ren et al., 2004a) in 250 mL LB in 1 L Erlenmeyer shake flasks. RNA was isolated from the suspension and biofilm cells as described previously (Ren et al., 2004b).

Dataset Information

Targeting Campylobacter signalling to modulate biofilm dynamics (J4-3088)

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets