Fusaric acid modulates Type Three Secretion System of Salmonella enterica serovar Typhimurium

Li, Jianfang; Sun, Wenzhao; Guo, Zhixing; Chen, Lu; Shen, Yuemao

doi:10.1016/j.bbrc.2014.05.044

Cited by 20 publications

(16 citation statements)

References 28 publications

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“…results that the inhibitory effect of fusaric acid cannot be overcome by overexpression of T3SS activator HilA, unlike the case of Csn-B [77]. Also, fusaric acid does not change the level of PgrH, an assembly protein for the needle complex, and does not interfere with the SicA/InfV transcriptional pathway for T3SS initiation.…”

Section: Fusaric Acidmentioning

confidence: 94%

“…Inhibition was dose-dependent with a calculated IC50 = 53.5 μm. In a gentamycin-protection assay, fusaric acid markedly inhibited Salmonella invasion into HeLa cells, with no toxicity toward the HeLa cells observed [77]. Figure 8.…”

Section: Fusaric Acidmentioning

confidence: 97%

“…Fusaric acid causes a variety of negative outcomes in plants, and it is thought to be a virulence factor in Fusarium wilt in banana, tomato, and cotton crops [73][74][75] and heavy decline disease in grapevine [76]. Fusaric acid was first studied as a potential inhibitor of the T3SS in S. enterica in 2014 as part of a screen of a small library [77]. In SDS-PAGE and Western blot analysis, fusaric acid potently inhibited secretion of SPI-1 effector proteins when cells were treated with 100 μm fusaric acid, without disrupting cell growth.…”

Section: Fusaric Acidmentioning

confidence: 99%

“…Without the ability to easily access samples of (-)-hopeaphenol and analogs to test for T3SS inhibitory activity, further development of this structural class as inhibitors will be difficult. Some studies attempting to elucidate the mechanism of action of fusaric acid gave conclusive results that the inhibitory effect of fusaric acid cannot be overcome by overexpression of T3SS activator HilA, unlike the case of Csn-B [77]. Also, fusaric acid does not change the level of PgrH, an assembly protein for the needle complex, and does not interfere with the SicA/InfV transcriptional pathway for T3SS initiation.…”

Section: (-)-Hopeaphenolmentioning

confidence: 99%

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Natural Product Type III Secretion System Inhibitors

Pendergrass

May

2019

Antibiotics

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Many known inhibitors of the bacterial type III secretion system (T3SS), a virulence factor used by pathogenic bacteria to infect host cells, are natural products. These compounds, produced by bacteria, fungi, and plants, may have developed as prophylactic treatments for potential attack by bacterial pathogens or as an attempt by symbiotic organisms to protect their hosts. Regardless, better understanding of the structures and mechanisms of action of these compounds may open opportunities for drug development against diseases caused by pathogens utilizing the T3SS. This review will cover selected known natural products of the T3SS and detail what is known of their origin and mechanism of action. These inhibitors highlight nature’s ability to modulate interactions between organisms at a cellular level.

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Section: Fusaric Acidmentioning

confidence: 94%

Section: Fusaric Acidmentioning

confidence: 97%

Section: Fusaric Acidmentioning

confidence: 99%

Section: (-)-Hopeaphenolmentioning

confidence: 99%

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Natural Product Type III Secretion System Inhibitors

Pendergrass

May

2019

Antibiotics

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“…T3SSs are highly conserved among Gram-negative bacteria [ 33 ]. Compounds 1 – 18 were assayed for their anti-T3SS activity of S. enterica Typhimurium UK-1 χ8956 in vitro, as previously described in our laboratory [ 34 , 35 , 36 ]. S. enterica Typhimurium UK-1 χ8956 was cultured in the LB media (tryptone 10 g, yeast extract 5 g, NaCl 10 g, ddH 2 O 1000 mL, pH 7.2) supplemented with 0.2% L-arabinose at 37 °C in the presence of a solvent control or the tested compounds at the final concentration of 100 μM [ 37 ], respectively.…”

Section: Methodsmentioning

confidence: 99%

8-Deoxy-Rifamycin Derivatives from Amycolatopsis mediterranei S699 ΔrifT Strain

Shi

Zhao

et al. 2020

Biomolecules

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Proansamycin X, a hypothetical earliest macrocyclic precursor in the biosynthesis of rifamycin, had never been isolated and identified. According to bioinformatics analysis, it was proposed that RifT (a putative NADH-dependent dehydrogenase) may be a candidate target responsible for the dehydrogenation of proansamycin X. In this study, the mutant strain Amycolatopsis mediterranei S699 ΔrifT was constructed by deleting the rifT gene. From this strain, eleven 8-deoxy-rifamycin derivatives (1–11) and seven known analogues (12–18) were isolated. Their structures were elucidated by extensive analysis of 1D and 2D NMR spectroscopic data and high-resolution ESI mass spectra. Compound 1 is a novel amide N-glycoside of seco-rifamycin. Compounds 2 and 3 feature conserved 11,12-seco-rifamycin W skeleton. The diverse post-modifications in the polyketide chain led to the production of 4–11. Compounds 2, 3, 5, 6, 13 and 15 exhibited antibacterial activity against Staphylococcus aureus (MIC (minimal inhibitory concentration) values of 10, 20, 20, 20, 40 and 20 μg/mL, respectively). Compounds 14, 15, 16, 17 and 18 showed potent antiproliferative activity against KG1 cells with IC50 (half maximal inhibitory concentration) values of 14.91, 44.78, 2.16, 18.67 and 8.07 μM, respectively.

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