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Gi, Mia,Jeong, Junhui,Lee, Keehoon,Lee, Kang-Mu,Toyofuku, Masanori,Yong, Dong Eun,Yoon, Sang Sun,Choi, Jae Young American Society for Microbiology 2014 Antimicrobial Agents and Chemotherapy Vol.58 No.12
<P><I>Pseudomonas aeruginosa</I>, a Gram-negative bacterium of clinical significance, produces elastase as a predominant exoprotease. Here, we screened a library of chemical compounds currently used for human medication and identified diethylene triamine penta-acetic acid (DTPA, pentetic acid) as an agent that suppresses the production of elastase. Elastase activity found in the prototype <I>P. aeruginosa</I> strain PAO1 was significantly decreased when grown with a concentration as low as 20 μM DTPA. Supplementation with Zn<SUP>2+</SUP> or Mn<SUP>2+</SUP> ions restored the suppressive effect of DTPA, suggesting that the DTPA-mediated decrease in elastase activity is associated with ion-chelating activity. In DTPA-treated PAO1 cells, transcription of the elastase-encoding <I>lasB</I> gene and levels of the <I>Pseudomonas</I> quinolone signal (PQS), a molecule that mediates <I>P. aeruginosa</I> quorum sensing (QS), were significantly downregulated, reflecting the potential involvement of the PQS QS system in DTPA-mediated elastase suppression. Biofilm formation was also decreased by DTPA treatment. When A549 alveolar type II-like adenocarcinoma cells were infected with PAO1 cells in the presence of DTPA, A549 cell viability was substantially increased. Furthermore, the intranasal delivery of DTPA to PAO1-infected mice alleviated the pathogenic effects of PAO1 cells in the animals. Together, our results revealed a novel function for a known molecule that may help treat <I>P. aeruginosa</I> airway infection.</P>
Serotonin regulates glucose-stimulated insulin secretion from pancreatic β cells during pregnancy
Ohara-Imaizumi, Mica,Kim, Hail,Yoshida, Masashi,Fujiwara, Tomonori,Aoyagi, Kyota,Toyofuku, Yukiko,Nakamichi, Yoko,Nishiwaki, Chiyono,Okamura, Tadashi,Uchida, Toyoyoshi,Fujitani, Yoshio,Akagawa, Kimio National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.48
<P>In preparation for the metabolic demands of pregnancy, beta cells in the maternal pancreatic islets increase both in number and in glucose-stimulated insulin secretion (GSIS) per cell. Mechanisms have been proposed for the increased beta cell mass, but not for the increased GSIS. Because serotonin production increases dramatically during pregnancy, we tested whether flux through the ionotropic 5-HT3 receptor (Htr3) affects GSIS during pregnancy. Pregnant Htr3a(-/-) mice exhibited impaired glucose tolerance despite normally increased cell mass, and their islets lacked the increase in GSIS seen in islets from pregnant wild-type mice. Electrophysiological studies showed that activation of Htr3 decreased the resting membrane potential in beta cells, which increased Ca2+ uptake and insulin exocytosis in response to glucose. Thus, our data indicate that serotonin, acting in a paracrine/autocrine manner through Htr3, lowers the beta cell threshold for glucose and plays an essential role in the increased GSIS of pregnancy.</P>
Biological and Chemical Approaches for Controlling Harmful Microcystis Blooms
Kim Wonjae,Park Yerim,Jung Jaejoon,Jeon Che Ok,Toyofuku Masanori,Lee Jiyoung,Park Woojun 한국미생물학회 2024 The journal of microbiology Vol.62 No.3
The proliferation of harmful cyanobacterial blooms dominated by Microcystis aeruginosa has become an increasingly serious problem in freshwater ecosystems due to climate change and eutrophication. Microcystis-blooms in freshwater generate compounds with unpleasant odors, reduce the levels of dissolved O2, and excrete microcystins into aquatic ecosystems, potentially harming various organisms, including humans. Various chemical and biological approaches have thus been developed to mitigate the impact of the blooms, though issues such as secondary pollution and high economic costs have not been adequately addressed. Red clays and H2O2 are conventional treatment methods that have been employed worldwide for the mitigation of the blooms, while novel approaches, such as the use of plant or microbial metabolites and antagonistic bacteria, have also recently been proposed. Many of these methods rely on the generation of reactive oxygen species, the inhibition of photosynthesis, and/or the disruption of cellular membranes as their mechanisms of action, which may also negatively impact other freshwater microbiota. Nevertheless, the underlying molecular mechanisms of anticyanobacterial chemicals and antagonistic bacteria remain unclear. This review thus discusses both conventional and innovative approaches for the management of M. aeruginosa in freshwater bodies.
Kang, Sujin,Okuno, Tatsusada,Takegahara, Noriko,Takamatsu, Hyota,Nojima, Satoshi,Kimura, Tetsuya,Yoshida, Yuji,Ito, Daisuke,Ohmae, Saori,You, Dong-Ju,Toyofuku, Toshihiko,Jang, Myoung Ho,Kumanogoh, Ats Williams Wilkins 2012 JOURNAL OF IMMUNOLOGY Vol.188 No.3
<P>The intestinal immune system is constantly challenged by commensal bacteria; therefore, it must maintain quiescence via several regulatory mechanisms. Although intestinal macrophages (Ms) have been implicated in repression of excessive inflammation, it remains unclear how their functions are regulated during inflammation. In this study, we report that semaphorin 7A (Sema7A), a GPI-anchored semaphorin expressed in intestinal epithelial cells (IECs), induces IL-10 production by intestinal M?s to regulate intestinal inflammation. Sema7A-deficient mice showed severe signs of dextran sodium sulfate-induced colitis due to reduced intestinal IL-10 levels. We further identified CX3CR1(+)MHC class II(int)F4/80(hi)CD11b(hi) M?s as the main producers of IL-10 via αvβ1 integrin in response to Sema7A. Notably, Sema7A was predominantly expressed on the basolateral side of IECs, and its expression pattern was responsible for protective effects against dextran sodium sulfate-induced colitis and IL-10 production by M?s during interactions between IECs and M?s. Furthermore, we determined that the administration of recombinant Sema7A proteins ameliorated the severity of colitis, and these effects were diminished by IL-10-blocking Abs. Therefore, our findings not only indicate that Sema7A plays crucial roles in suppressing intestinal inflammation through αvβ1 integrin, but also provide a novel mode of IL-10 induction via interactions between IECs and M?s.</P>