User:HelenaHysong/Delftia tsuruhatensis

Delftia tsuruhatensis is a Gram-negative, rod shaped, catalase- and oxidase-positive, motile bacterium from the Comamonadaceae family. It was isolated from a domestic wastewater treatment plant in Japan. Delftia tsuruhatensis is an opportunistic and emergent pathogen. All documented infections are healthcare-associated.

Metabolism
Delftia tsuruhatensis can degrade phenolic compounds and aniline, which are often pollutants of soil and water.

Morphology
Cells are slightly curved, short rod-shaped cells that occur singly or in pairs. Cells are 0.7-1.2 μm wide and 2.4-4.0 μm long.

Biofilm interactions
Delftia tsuruhatensis’s anti-quorum sensing capabilities against the highly drug resistant bacteria P. aeruginosa holds possible implications for designing novel therapeutic drugs. Quorum sensing mechanisms are responsible for biofilm production, virulence, and antibiotic resistance; therefore, quorum sensing inhibition is potentially a critical pathway for attenuating the harmfulness of drug resistant bacteria. While D. tsuruhatensis’s inhibition is well established by current literature, little agreement exists regarding the precise mechanism employed by the bacteria to achieve these effects.

Bacterial resistance is outpacing the development of new antibiotics, engendering the design of novel therapeutic approaches to fighting these multi-drug resistant bacteria. The ability of bacteria to form biofilms contributes to their antibiotic resistance. Furthermore, these biofilms are able to participate in a cell-to-cell signaling mechanism, quorum sensing (QS), that can increase the pathogen’s virulence. Certain bacterial species have demonstrated an ability to inhibit quorum sensing during bacterial competition. Since QS plays a role in biofilm formation, this ability to inhibit QS can serve as a model for designing new therapeutics to fight multi-drug resistant bacteria.

Pseudomonas aeruginosa is a highly infectious bacterial pathogen that grows in biofilms and possesses high antibiotic resistance in clinical settings; therefore, it has commonly been used as a model for understanding the role of QS and biofilm production in antibiotic resistance and virulence. D. tsuruhatensis has been shown to be able to significantly inhibit QS, suppress biofilm formation, and attenuate virulence in P. carotovorum and Chromobacterium violaceum without damaging individual bacterial cells. While many studies have conferred the ability of D. tsuruhatensis to attenuate virulence through QS and biofilm inhibition, an agreement has yet to be reached as to the exact mechanism the bacteria uses to achieve this effect.

Inhibition of quorum sensing
Bacterial species like Pseudomonas aeruginosa are able to participate in a cell-to-cell signaling mechanism called quorum sensing by sending out small diffusible molecules. Pesci et al. discovered that there are at least three different signaling molecules that P. aeruginosa uses to achieve quorum sensing. D. tsuruhatensis 11304 ethyl acetate extract was also shown to possess quorum sensing inhibition properties against P. aeruginosa and the widely used quorum sensinsing indicator strain Chromobacterium violaceum CV026. In this case, a novel long-chain dihydroxy-N-octadecanoylhomoserine lactone was isolated and speculated to be the agent responsible for interfering with the N-acyl-homoserine lactones (AHL)s of the quorum sensing bacteria. In another study, it was demonstrated that the Delftia tsuruhatensis VM4 strain is able to quench Pectobacterium carotovorum’s quorum sensing ability. The enzyme thought to be responsible for degrading N-acyl-homoserine lactones (AHL), a quorum sensing signaling molecule, was isolated from VM4 using anionic-exchange column chromatography and was identified to be 82 kDa with a multiple amino acid sequence alignment tool. In yet another study, fractionation and mass spectrometry identified 1,2-benzenedicarboxylic acid to be responsible for D. tsuruhatensis SJ01’s ability to interfere with the cell-to-cell signaling mechanism of CV026 by 98% with just 0.1 mg/ml of extract. Although quorum sensing inhibition by multiple D. tsuruhatensis strains has been demonstrated decisively, due to dissension regarding the causative agent, future studies should be directed at identifying the mechanistic principles governing this ability.

Suppression of biofilm production
It has been established that QS systems play a role in biofilm formation in P. aeruginosa. This relationship perhaps explains in part how D. tsuruhatensis 11304 ethyl acetate extract was able to restrict P. aeruginosa MMA83’s ability to form biofilm; however, it is noteworthy that the 11304 strain was unable to disturb existing biofilm. In an alternative, but perhaps related, fashion, D. tsuruhatensis SJ01 was able to decrease biofilm formation in P. aeruginosa PAO1 and P. aeruginosa PAH by decreasing the swarming mobility of the P. aeruginosa strains. It is clear that QS plays a vital role in biofilm production, so it is no surprise that D. tsuruhatensis’s ability to inhibit QS can in turn suppress biofilm production; however, further research needs to be conducted to determine an understanding of the precise mechanisms that guide this relationship.

Link to antibiotic resistance
P. aeruginosa in biofilm were shown to have an increased antibiotic resistance. ndvB-dependent β-(1→3)-linked cyclic glucans discovered in P. aeruginosa were linked to biofilm antibiotic resistance. A novel substance, furanone C-30, was shown to significantly reduce biofilm production in P. aeruginosa by targeting genes associated with QS. Moreover, this compound made P. aeruginosa 2-3 times more susceptible to antibiotics following biofilm reduction.

Attenuation of virulence
It was established that a cell-to-cell signaling molecule in P. aeruginosa controls the production of a major virulence factor, LasB elastase. D. tsuruhatensis anti-quorum sensing properties attenuated virulence of P. carotovorum and P. aeruginosa.