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Virulent Factors, Morphology, Antibiotic Susceptibility
- The History, Biochemistry, and Potential of Quorum Sensing

One of the most important prospects of studying QS mechanisms is the idea of containing virulent factors in pathogens. There continues to be more studies being done on auto-inducer targeting molecules to fight against antibiotic resistance in industry and medicine. AI-2 mediated quorum sensing is common for activating virulent factors in enteric species. Cinnamaldehyde is one known molecule that disrupts AI-2 activity (1). While Cinnamaldehyde does not inhibit bacterial growth, it is able to inhibit AI-2 induced virulence factors in Vibrio spp., a common marine pathogen. Cinnamaldehyde inhibits the bio-film formation of a population, which makes the bacteria considerably more susceptible to stress and antibiotics. This suggests that molecules that target QS systems can be used themselves as a prophylactic, or in combination with an antibiotic to more efficiently kill pathogens. This is good news for the aquaculture industry, where Vibrio spp. infection is a large part of the economic loss. After years of overuse, Vibrio spp. has become resistant to common antibiotics used to prevent disease.

Molecules that mimic AHLs are also capable of inhibiting QS mediated phenotypes. It has been shown that N-nonanoyl-cyclopentylamide, an AHL-like molecule, is also capable of inhibiting virulence factors in Serratia marcescens (9). These new studies allude to a broad spectrum of molecules being used to inhibit microbial virulence. It may be possible to custom-make these molecules, targeting only specific systems and species. QS targeting molecules can be used in conjunction with antibiotics, rather than contributing to pathogen resistance by increasing the antibiotics being used.

Many pathogenic bacteria require the formation of bio-film colony morphology before they become virulent. These bacteria can often be beneficial to the host in a symbiotic relationship. However, bio-film can interfere with the host, starving it from oxygen and nutrients. Some marine plants have evolved to produce compounds that target QS systems responsible for bio-filming. The marine seaweed Delisea pulchra is one such host. D. pulchra has been shown to produce a halogenated furanone that interferes with bio-film formation on the level of quorum sensing (16).

The study of bio-filming bacteria is important in realizing how widespread quorum sensing systems are in bacteria. By studying marine sponges and invertebrates it is evident that most, if not all bacteria produce auto-inducers at some point in their life cycle (17). These studies also show that there is a sort of bio-cycle between growth stages in different species. That is to say, different bacteria species produce their auto-inducers at different life stages on the same host, which is indicative of the density-dependent nature of quorum sensing. Marine sponges appear to produce diketopiperazines (17) a molecule also shown to be produced by P. aeruginosa as an AHL system antagonist towards some bacteria (4). These molecules target the swarming motility in Serratia liquefaciens.

Swarming motility is a coordinated movement of bacteria across a substrate. Another example of multicellular activity in single-celled organisms, swarming motility is coordinated by quorum sensing. Reduced virulence was shown in Erwinia chrysanthemi when a null mutation was introduced to genes encoding for the AHLs responsible for swarming (10). Not much is known as to why some bacteria swarm, however the benefit has been demonstrated; antibiotic resistance. It's been suggested that alteration of LPS repels cationic antibiotics such as polymyxin and kanamycin in swarming Salmonella enterica. The proposed mechanism for resistance is addition of 4-amino-4-deoxy-L-arabinose to the lipid A of LPS, causing a more positively charged outer membrane. L-AraN is controlled under the QS pmrHFIJKLM operon, which is up-regulated in swarming cells (7).

By targeting QS systems, it may be possible to prevent microbial infection without the negative side effects of antibiotics. It has been shown that virulence can decrease a number of ways; mimic auto-inducers, or molecules that inhibit auto-inducer synthesis or deletion of genes that code for auto-inducers. Hopefully by controlling QS involved with population and morphology, virulent and parasitic phenotypes can be repressed for medical and industrial purposes.

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