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. 2023 Mar 20;11(3):793. doi: 10.3390/microorganisms11030793

Table 1.

Probiotics involved in the inhibition of QS mechanisms of foodborne pathogenic bacteria.

Microorganism QSI Target Type of Study Mechanism Reference
Lb. reuteri LR 21 Reuterin C. perfringens 13124 In vitro Repression of toxins-producing genes (cpa and pfo) and agrB and luxS. [17]
Lb. acidophilus GP1B CE/CFS C. difficile
(ribotype 027)
In vitro Inhibition of AI-2 production and downregulation of luxS and tcdA, tcdB, and txeR (virulence genes).
Growth inhibition of C. difficile in the colon.
[18]
Lb. fermentum Lim2 Inactivated CE C. difficile 027 In vitro Anti AI-2 activity due to repression of lux gene. Expression of virulence genes also reduced. QSIs are not measured. [19]
Lb. reuteri RC-14 CFS Staph. aureus MN8 In vitro Cyclo-dipeptides inhibited the expression of agr and tst genes as well as disrupting saeRS system. [20]
B. subtilis Fengycin Staph. aureus Cross-sectional analysis
(Thai population)
Fengycin competes with AIP for binding to agrC. [21]
Lb. helveticus Biosurfactant Staph. aureus In vitro Inhibition of biofilm formation by interfering with AI-2 signaling and biofilm-related genes expression (dltB, sarA, agrA, and icdA). [22]
In vivo Prevention of hemolytic activity through biofilm formation inhibition.
Lb. plantarum KCTC10887BP LPA Staph. aureus In vitro Biofilm formation was inhibited. LPA induced AI-2 release in Staph. Aureus, which repressed biofilm-related genes. [23]
Lb. acidophillus 30SC N/A E. coli O157:H7 43894 In vivo Inhibition of AI-2 synthesis and modulation of microbial gut community. [24]
Lb. rhamnosus GG microcapsules N/A E. coli In vitro Repression of lsrK and luxS genes (disruption in AI-2/luxS-typeQS network). [13]
Lb. acidophilus A4 EPS E. coli O157:H7 In vitro Repression levels of curli genes (crl, csgA, and csgB) and chemotaxis (cheY) related to biofilm formation. [25]
Bifidobacterium longum ATCC15707 CE E. coli O157:H7 In vitro Inhibition of AI-2 activity and virulence gene expression (NifU, DsbA, and FlgI). [26]
Lb. acidophilus A4 N/A E. coli (EHEC) In vitro Downregulation of biofilm-related genes (crl, csgA, and csgB) and chemotaxis (cheY). [27]
Lb. brevis 3M004 N/A P. aeruginosa PA002 biofilm formation In vitro Degradation of AIs and repression of biofilm formation, pyocyanin, and polysaccharide synthesis-related genes (lasA, lasB, and PhzAB). [28]
Lb. casei CRL 431
Lb. acidophilus CRL 730
DKPs P. aeruginosa In vitro DKPs compete with AI for binding QS receptors. [29]
Lb. rhamnosus GG CFS P. aeruginosa In vitro Inhibition of AHL synthesis. [30]
Lb. casei PTCC 1608 Lyophilized postbiotics P. aeruginosa In vitro Repression of QS genes controlling biofilm formation and virulence (rhlI, rhlR, and pelf), potentially due to organic acid content. [31]
B. subtilis BR4 Stigmatellin Y P. aeruginosa (ATCC 27853) In vitro Stigmatellin Y competes with PQS signal for binding with PqsR gene, and thus, PqsR-PQS QS pathway is disrupted. [32]
B. paralicheniformis ZP1 Lactonase P. aeruginosa In vitro Inhibition of biofilm formation due to AHL hydrolysis by lactonase. [33]
B. subtilis KATMIRA1933 Subtilisin L. monocytogenes biofilm formation
E. coli biofilm formation
In vitro Inhibition of proton motive forces and efflux pumps. [34]
Lb. plantarum C2 N/A E. coli DSM 30083
Enterobacter aerogenes DSM 30053
Yersinia enterolitica DSM 4780
Leuconostoc lactis 20202
Ent. durans DSM 20633
B. megaterium F6
In vitro Antibacterial activity by plantaricin produced through QS mechanism. (AI not measured). [11]
Lb. plantarum KU200656 CFS Staph. aureus
Listeria monocytogenes
E. coli
S. Typhimurium
In vitro Biofilm-related genes are downregulated by anti-biofilm activity. (Exact QSI mechanism is not measured). [35]
Lb. kefiri 8321 and 83113
Lb. plantarum 83114
CFS S. Enteritidis 115 In vitro Biofilm formation inhibition. (QSI mechanism not investigated). [36]
B. subtilis KATMIRA1933
B. amyloliquefaciens
B-1895
CE/CFS S. (Thompson, Enteritidis phage type 4, and Hadar) In vitro Biofilm inhibition due to the subtilosin effect. AI/luxS QS pathway is necessary for biofilm formation. [37]
W. viridescens WM33
W. confusa WM36 (LAB)
CFS S. Typhi and S. Typhimurium In vitro Inhibition of AI-2 activity and biofilm formation. [38]
Lb. reuteri PFS4
Ent. faecium PFS13 and
PFS14.
CFS S. Typhimurium and S. Enteritidis In vitro Inhibition of biofilm formation. (Mechanism not investigated). [39]
Lb. coryniformis NA-3 EPS B. cereus and
S. Typhimurium
In vitro Inhibition of biofilm formation. (Mechanism not investigated). [40]
B. subtilis ZK3814 Fengycin and surfactin Ent. faecalis OG1RF In vitro Inhibition of fsr system, which regulates expression of proteolytic activity related-genes (gelE/sprE). [41]
Pd. pentosaceus Crude biosurfactant B. subtilis andStaph. aureus
P. aeruginosa, Staph. aureus, and E. coli
In vitro Anti-QS and anti-biofilm activity. [42]
Lb. curvatus BSF206 and Pd. pentosaceus AC1-2 CFS Str. mutans In vitro Biofilm formation inhibition by downregulation of related genes (tfA, gtfB, ftf, and brpA). (Exact mechanism not known). [43]
Lb. paragasseri MJM60645 Crude extract Str. mutans In vitro Downregulation of biofilm-associated genes (gtfB, gtfC, gtfD,
gbpB, brpA, spaP, ftf, and smu0630) by iminosugar, a novel chemical compound produced.
[44]
Lb. rhamnosus GG Biosurfactant Str. mutans In vitro Anti-biofilm activity due to downregulation of biofilm-related genes (gtfB/C and ftf). [45]
Lb. plantarum K41 N/A Str. mutans In vitro and in vivo Inhibition of biofilm formation by inhibition of exopolysaccharide production. [46]
Lb. casei MCJΔ1 (expressed with AHL-lactonase AiiK gene) Lactonase Aeromonas hydrophila In vitro Enzymatic QQ activity of lactonase. [47]
Lb. curvatus B.67 and Lb. plantarum M.2 Postbiotics L. monocytogenes In vitro Repression of biofilm-related genes (flaA, fbp, agrA, prfA, and hlyA). [48]
Lb. curvatus CRL1579 Lactocin L. monocytogenes In vitro QSI mechanism not investigated. [49]
B. subtilis-9 N/A E. coli (ETEC), S. Typhimurium, Staph. aureus (MSRA) In vitro Biofilm inhibition in a cell-to-cell contact manner. Biofilm-related genes were repressed in ETEC (bssS, luxS, and ihfB). [50]
Lb. paracasei L10 CFS V. parahaemolyticus In vitro Biofilm formation significantly inhibited. (Mechanism not investigated). [51]
Lb. plantarum LRCC 5193 LPA Str. mutans, E. faecalis, and Str. Gordonii In vitro Biofilm formation inhibition. (QSI mechanism is suggested but not investigated). [52]
Lb. kefiranofaciens DD2 CFS Str. mutans and Str. sobrinus In vitro Antibiofilm activity through repression biofilm-associated
genes (ftf, comDE, brpA, and vicR).
[53]

Lb: Lactobacillus; C.: Clostridium; Staph.: Staphylococcus; L.: Listeria; B.: Bacillus; P.: Pseudomonas; Ent.: Enterococcus; Str.: Streptococcus; Pd.: Pediococcus; V.: Vibrio; W.: Weissella; CE: cell extract; CFS: cell-free supernatant; LPA: lipoteichoic acid; N/A: not available; EPS: exopolysaccharides; SaeRS: two-component signaling system; DKP: diketopiperazine; AI: autoinducer; QQ: quorum quenching; PQS: Pseudomonas quinolone signal; BIC: biofilm inhibitory compound; QSI: QS inhibitor.