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Phytomedicines Targeting Antibiotic Resistance through Quorum Sensing and Biofilm Formation Associated with Acne Vulgaris
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Isa A. Lambrechts, Namrita Lall
RNAIII plays a role in the transcription of several virulent factors associated with the bacteria. RNAIII contains the hld gene that codes for the phenol-soluble modulin, a delta toxin. These delta toxins play a role in the detachment of bacteria from the biofilm. This detachment could spread the bacteria, establish biofilms and release virulence factors such as hemolysins, protease and lipase enzymes associated with quorum sensing and various diseases. In addition, the RNAIII gene has been found to prevent the translation of the repressor of toxin protein (Rot) that results in the upregulation of enzymes such as lipase and protease involved in acne vulgaris (Le and Otto, 2015; Vuong et al., 2003; Kong, Vuong, and Otto, 2006).
Quorum sensing inhibitors: a patent review (2014–2018)
Published in Expert Opinion on Therapeutic Patents, 2018
Xin Chen, Likun Zhang, Mingxiang Zhang, Huayu Liu, Panrui Lu, Kejiang Lin
The Agr system is also an essential component of QS. Agr systems exists in Gram-positive bacteria, with the system in S. aureus being a classic example. The Agr locus consists two transcripts, RNA II and RNA III [57]. AgrD produces Pro-AIP which is then processed, modified and transported out by AgrB. AgrC is then activated and binds to AIP while AIP accumulates in the extracellular environment and reaches a certain threshold level when the bacterial density is high [58]. AgrC and AgrA together constitute a two-component system, which activates RNAII and RNAIII after itself is activated [59]. RNAII is transcribed to agr operon while RNAIII decreases the expression of surface adhesins and increases the production of capsule, toxins, and proteases 41 (Figure 6 and Table 4).
Quorum sensing pathways in Gram-positive and -negative bacteria: potential of their interruption in abating drug resistance
Published in Journal of Chemotherapy, 2019
Shafiul Haque, Dinesh K. Yadav, Shekhar C. Bisht, Neelam Yadav, Vineeta Singh, Kashyap Kumar Dubey, Arshad Jawed, Mohd Wahid, Sajad Ahmad Dar
Salicylideneaniline is another small peptide virulence factor inhibitor of T3SS in EPEC without influencing motility and expression of flagellin.246 Additionally, micromolar concentrations of INP002 and INP008 can hinder T3SS secretion in Yersinia pseudotuberculosis.247 Though, the exact molecular targets of salicylideneaniline, INP002 and INP008 are equivocal. Molecules targeting the toxin genes by inhibiting its transcription regulators or inhibiting the toxins directly have attracted the attention. For example, virstatin was found to inhibit transcription regulator ToxT in V. cholerae.248 Virstatin ceases the expression of cholera toxin and toxin co-regulated pilus, which are accountable for secretory diaorrhea and attachment of V. cholerae to human intestinal wall.248 Similarly, compound peptide toxin has been shown to bind with cholera toxins.249 Essentially, RNAIII-activating protein controls the expression of α-toxin and serine protease in S. aureus.250 The RNAIII-activating protein is inhibited by RNAIII-activating protein inhibitor peptide (RIP), which also inhibits biofilm formation, α-toxin production and serine protease expression in S. aureus.251 Though, in vivo proteolysis of RIP could confine its potential in the therapeutic application.251 Hamamelitannin is also reported to restrain RNAIII-activating protein,251 however, its biological property in presence of esterases is questionable. Several other small molecules have also been reported to inhibit bacterial virulence factor.252,253