Acyl-homoserine lactones suppresses IEC-6 cell proliferation and increase permeability of isolated rat colon

Joe, Ga-Hyun; Andoh, Midori; Nomura, Mikako; Iwaya, Hitoshi; Lee, Jae-Sung; Shimizu, Hidehisa; Tsuji, Youhei; Maseda, Hideaki; Miyazaki, Hitoshi; Hara, Hiroshi; Ishizuka, Satoshi

doi:10.1080/09168451.2014.882748

Cited by 4 publications

(2 citation statements)

References 20 publications

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“…7) However, we previously found that relatively low concentrations of 3-oxo-C 12 -HSL between 10 and 30 μM can induce the apoptosis of undifferentiated Caco-2 cells, and increase the mucosal permeability of the isolated rat colon. 8,9) Similar levels of 3-oxo-C 12 -HSL can be generated in culture supernatants of the P. aeruginosa PT149 strain without biofilm formation. 10) Therefore, 3-oxo-C 12 -HSL can affect intestinal epithelial cells at much lower concentrations than those found in biofilms.…”

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confidence: 96%

Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone

Shimizu

Baba

Taguchi

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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The signal molecule, 3-oxo-C12-homoserine lactone (3-oxo-C12-HSL), is similar to a mammalian hormone in bacteria. Although most studies have examined the effects of high 3-oxo-C12-HSL concentrations (>200 μM) on mammalian cellular functions because ~600 μM 3-oxo-C12-HSL can be secreted in biofilms of Pseudomonas aeruginosa grown in vitro, we previously showed that a low 3-oxo-C12-HSL concentration (30 μM) induces the apoptosis of undifferentiated Caco-2 cells through suppressing Akt activity. Here, we found that a low concentration of 3-oxo-C12-HSL-activated ERK1/2 in undifferentiated Caco-2 cells. Incubating cells with the ERK pathway inhibitor U0126 for 30 min alleviated the mucin 3 (MUC3) expression suppressed by 3-oxo-C12-HSL, and the upregulation of MUC3 expression induced by a 48-h incubation with U0126-reduced cell death. Thus, altered MUC3 expression caused by long-term attenuated ERK1/2 activity might correlate with the death of undifferentiated Caco-2 cells induced by 3-oxo-C12-HSL.

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confidence: 96%

Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone

Shimizu

Baba

Taguchi

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…Notably, quorum sensing was previously considered to be a bacteria-to-bacteria signaling mechanism to shape community structure, but now there is evidence indicating that QS may also be involved in the inter-kingdom signaling among symbiotic microbiota, pathogenic microbiota and the host [64][65][66]. Examples include a host synthesis of QSmimics to communicate with bacteria [67] and host responses to bacterial QS signals [68][69][70]. Moreover, bacteria have also been reported to sense and respond to host signals (e.g., hormones [71]).…”

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confidence: 99%

Electrochemical reverse engineering: A systems-level tool to probe the redox-based molecular communication of biology

Liu

Kim

et al. 2017

Free Radical Biology and Medicine

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The intestine is the site of digestion and forms a critical interface between the host and the outside world. This interface is composed of host epithelium and a complex microbiota which is "connected" through an extensive web of chemical and biological interactions that determine the balance between health and disease for the host. This biology and the associated chemical dialogues occur within a context of a steep oxygen gradient that provides the driving force for a variety of reduction and oxidation (redox) reactions. While some redox couples (e.g., catecholics) can spontaneously exchange electrons, many others are kinetically "insulated" (e.g., biothiols) allowing the biology to set and control their redox states far from equilibrium. It is well known that within cells, such non-equilibrated redox couples are poised to transfer electrons to perform reactions essential to immune defense (e.g., transfer from NADH to O for reactive oxygen species, ROS, generation) and protection from such oxidative stresses (e.g., glutathione-based reduction of ROS). More recently, it has been recognized that some of these redox-active species (e.g., HO) cross membranes and diffuse into the extracellular environment including lumen to transmit redox information that is received by atomically-specific receptors (e.g., cysteine-based sulfur switches) that regulate biological functions. Thus, redox has emerged as an important modality in the chemical signaling that occurs in the intestine and there have been emerging efforts to develop the experimental tools needed to probe this modality. We suggest that electrochemistry provides a unique tool to experimentally probe redox interactions at a systems level. Importantly, electrochemistry offers the potential to enlist the extensive theories established in signal processing in an effort to "reverse engineer" the molecular communication occurring in this complex biological system. Here, we review our efforts to develop this electrochemical tool for in vitro redox-probing.

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Assessing Pseudomonas aeruginosa Autoinducer Effects on Mammalian Epithelial Cells

Everett

Gabrilska

Rumbaugh

et al. 2017

Methods in Molecular Biology

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The human mucosal environment in the gut is rich with interactions between microbiota and mammalian epithelia. Microbes such as the Gram-negative bacterium Pseudomonas aeruginosa may use quorum sensing to communicate with other microorganisms and mammalian cells to alter gene expression. Here, we present methodologies to evaluate the effects of P. aeruginosa N-(3-oxo-dodecanoyl)-L-homoserine lactone (3O-C-HSL) on Caco-2 cell monolayers. First, we describe a method for assessing barrier function and permeability of epithelial cells when exposed to 3O-C-HSL by measuring transepithelial electrical resistance (TER) and paracellular flow using fluorescently labeled dextran. Secondly, we detail methods to investigate the effect of 3O-C-HSL on protein-protein interactions of epithelial junction proteins. Lastly, we will detail imaging techniques to visualize Caco-2 barrier disruption following exposure to 3O-C-HSL through the use of confocal laser scanning microscopy (CLSM) and a super resolution technique, stimulated emission depletion (STED) microscopy, to achieve nanoscale visualization of Caco-2 monolayers.

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Acyl-homoserine lactones suppresses IEC-6 cell proliferation and increase permeability of isolated rat colon

Cited by 4 publications

References 20 publications

Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone

Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone

Electrochemical reverse engineering: A systems-level tool to probe the redox-based molecular communication of biology

Assessing Pseudomonas aeruginosa Autoinducer Effects on Mammalian Epithelial Cells

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