## 4 Antimicrobial Agents
### Antiquorum Sensing Molecules  
QS is a cell-cell interaction mechanism in the microbial groups to harvest a coordinated effort on regulating the genes related to virulence, biofilm formation, antibiotic tolerance, and survival. The QS mechanism is brought by a set of two proteins in Gram-negative bacteria. One of these is an autoinducer (AI) which leads to signaling molecule production, while the other one acts in response to the AI [57]. In contrast to Gram-positive bacteria that use secreted autoinducing peptides (AIPs) such as Als for QS, Gram-negative bacteria employ homoserine lactones (HSL). In addition, unlike Gram-negative bacteria that use a regulator-type protein as an autoinducer sensor, Gram-positive bacteria employ two-component adaptive response proteins for sensing AIs. This mechanism of signaling is stimulated by a phosphorylation/dephosphorylation cascade [58]. Cyclic di-GMP (c-di-GMP) is also known as a secondary messenger since it is responsible for controlling several functions such as motility, cell cycle, differentiation, developmental transitions, adhesion, aggregation, biofilm production, and virulence in various pathogens. In several Gram-negative bacteria such as _Escherichia coli_, _Gluconacetobacter xylinus_, _P. aeruginosa_, and _Salmonella enterica_, c-di-GMP plays a significant role in the shift in between motile to sessile lifestyle, construction of three-dimensional (3D) biofilms, and during biofilm dispersal [59; 60; 61]. Many natural and synthetic compounds act as anti-QS molecules that target various QS signaling molecules (Table 3). A natural compound such as garlic was able to reduce the virulence factors progression and decrease the QS signal production in _P. aeruginosa_ in a mouse urinary tract infection (UTI) model [62]. In another study by [PERSON] et al., it was reported that garlic extracts inhibit biofilm production in six clinical isolates of bacteria [57]. Besides, through the rigorous design and screening, all the biological com \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Name of the Compound** & **Type** & **Mode of Action** & **Effective Against** & **Reference** \\ \hline Triton X-100 & surfactant & autolysis, targeting EPS & _S. aureus_ & [31; 32] \\ \hline Tween 80 & surfactant & N/A & _P. aeruginosa_, _S. aureus_ & [30] \\ \hline Quaternary ammonium & & & & \\ compounds & & & & \\ \hline Poloxamer containing & & & & \\ non-ionic surfactant & & & & \\ \hline Rhamolipids & bio-surfactant & N/A & _S. aureus_, _Salmonella Entertitials_, & \\  & & & & _ Listeria monocytogenes_ & [36] \\ \hline EDTA & chelators & damage to cell wall & _P. aeruginosa_ & [40] \\ \hline Chitosan & biomaterial & membrane damage & _P. aeruginosa_ & [41] \\ \hline Secondary metabolite & & & & \\ from _Cirus limonoids_ & secondary metabolite & quorum sensing & _Vibrio havevyi_ & [42] \\ \hline Cyclo(1-Tyr-l-Leu) & secondary metabolite & inhibit EPS & _S. epidermidis_ & [43] \\ \hline Cahuitamycins & secondary metabolite & N/A & _A. humantii_ & [44] \\ \hline Phlorotannin & secondary metabolite & damaging membrane & & \\  & & & & \\ \hline \(\alpha\)-amylase & enzyme & degrade EPS & MRSA & [46] \\ \hline Polyamine nonspermidine & polyamine & interacts with EPS & _B. subtilis_, _E. coli_ and _S. aureus_ & [47] \\ \hline D-amino acids & amino acid & target YqxM & _E. coli_, _S. aureus_ & [48] \\ \hline N-acetylcysteine/NAC & amino acid & degrade EPS polysaccharide & Rapidly growing & \\  & & & & Mycobacterium & [49] \\ \hline Esp (Serine protease) & enzymes & degrade EPS protein content & _S. aureus_ & [50] \\ \hline DNase I & enzymes & degrade cDNA & _E. coli_, _S. aureus_ & [51] \\ \hline tea-tree oil & secondary metabolite & metabolism & _S. aureus_ & [52] \\ \hline Protease from _P. aeruginosa_ & enzymes & degrade EPS protein content & _S. aureus_ & [53] \\ \hline \hline \end{tabular}
\end{table} 
Table 2: Different types of antimicrobial agents and their mode of action.