Journal of Microbiology

Journal Article

Potent antibacterial and antibiofilm activities of TICbf-14, a peptide with increased stability against trypsin: Liping Wang , Xiaoyun Liu , Xinyue Ye , Chenyu Zhou , Wenxuan Zhao , Changlin Zhou , Lingman Ma; J. Microbiol. 2022;60(1):89-99. Published online December 29, 2021; DOI: https://doi.org/10.1007/s12275-022-1368-9

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The poor stability of peptides against trypsin largely limits their development as potential antibacterial agents. Here, to obtain a peptide with increased trypsin stability and potent antibacterial activity, TICbf-14 derived from the cationic peptide Cbf-14 was designed by the addition of disulfide-bridged hendecapeptide (CWTKSIPPKPC) loop. Subsequently, the trypsin stability and antimicrobial and antibiofilm activities of this peptide were evaluated. The possible mechanisms underlying its mode of action were also clarified. The results showed that TICbf-14 exhibited elevated trypsin inhibitory activity and effectively mitigated lung histopathological damage in bacteria-infected mice by reducing the bacterial counts, further inhibiting the systemic dissemination of bacteria and host inflammation. Additionally, TICbf-14 significantly repressed bacterial swimming motility and notably inhibited biofilm formation. Considering the mode of action, we observed that TICbf-14 exhibited a potent membrane-disruptive mechanism, which was attributable to its destructive effect on ionic bridges between divalent cations and LPS of the bacterial membrane. Overall, TICbf-14, a bifunctional peptide with both antimicrobial and trypsin inhibitory activity, is highly likely to become an ideal candidate for drug development against bacteria.

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Modified polymeric biomaterials with antimicrobial and immunomodulating properties
Katarzyna Szałapata, Mateusz Pięt, Martyna Kasela, Marcin Grąz, Justyna Kapral-Piotrowska, Aleksandra Mordzińska-Rak, Elżbieta Samorek, Paulina Pieniądz, Jolanta Polak, Monika Osińska-Jaroszuk, Roman Paduch, Bożena Pawlikowska-Pawlęga, Anna Malm, Anna Jar
Scientific Reports.2024;[Epub] CrossRef
Epinecidin-1, a marine antifungal peptide, inhibits Botrytis cinerea and delays gray mold in postharvest peaches
Li Fan, Yingying Wei, Yi Chen, Shu Jiang, Feng Xu, Chundan Zhang, Hongfei Wang, Xingfeng Shao
Food Chemistry.2023; 403: 134419. CrossRef

Research Support, Non-U.S. Gov'ts

A small hairpin RNA targeting myeloid cell leukemia-1 enhances apoptosis in host macrophages infected with Mycobacterium tuberculosis: Fei-yu Wang , Yu-qing Zhang , Xin-min Wang , Chan Wang , Xiao-fang Wang , Jiang-dong Wu , Fang Wu , Wan-jiang Zhang , Le Zhang; J. Microbiol. 2016;54(4):330-337. Published online April 1, 2016; DOI: https://doi.org/10.1007/s12275-016-5627-5

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Abstract

Myeloid cell leukemia-1 (Mcl-1) plays an important role in various cell survival pathways. Some studies indicated that the expression of Mcl-1 was upregulated in host cells during infection with the virulent Mycobacterium tuberculosis strain, H37Rv. The present study was designed to investigate the effect of inhibiting Mcl-1 expression both in vivo and in vitro on apoptosis of host macrophages infected with M. tuberculosis using a small hairpin (sh)RNA. Mcl-1 expression was detected by the real time-polymerase chain reaction, western blotting, and immunohistochemistry. Flow cytometry and transmission electron microscopy were used to measure host macrophage apoptosis. We found elevated Mcl-1 levels in host macrophages infected with M. tuberculosis H37Rv. The expression of Mcl-1 was downregulated efficiently in H37Rv-infected host macrophages using shRNA. Knockdown of Mcl-1 enhanced the extent of apoptosis in H37Rv-infected host macrophages significantly. The increased apoptosis correlated with a decrease in M. tuberculosis colony forming units recovered from H37Rv-infected cells that were treated with Mcl-1-shRNA. Reducing Mcl-1 accumulation by shRNA also reduced accumulation of the anti-apoptotic gene, Bcl-2, and increased expression of the pro-apoptotic gene, Bax, in H37Rv-infected host macrophages. Our results showed that specific knockdown of Mcl-1 expression increased apoptosis of host macrophages significantly and decreased the intracellular survival of a virulent strain of M. tuberculosis. These data indicate that interference with Mcl-1 expression may provide a new avenue for tuberculosis therapy.

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Tolerance of Listeria monocytogenes to biocides used in food processing environments
Sanelisiwe Thinasonke Duze, Musa Marimani, Mrudula Patel
Food Microbiology.2021; 97: 103758. CrossRef
Regulatory role and mechanism of the inhibition of the Mcl-1 pathway during apoptosis and polarization of H37Rv-infected macrophages
Ling Han, Yang Lu, Xiaofang Wang, Shujun Zhang, Yingzi Wang, Fang Wu, Wanjiang Zhang, Xinmin Wang, Le Zhang
Medicine.2020; 99(42): e22438. CrossRef
Current and emerging therapies to combat persistent intracellular pathogens
Philip Arandjelovic, Marcel Doerflinger, Marc Pellegrini
Current Opinion in Pharmacology.2019; 48: 33. CrossRef
PPARγ is critical for Mycobacterium tuberculosis induction of Mcl-1 and limitation of human macrophage apoptosis
Eusondia Arnett, Ashlee M. Weaver, Kiersten C. Woodyard, Maria J. Montoya, Michael Li, Ky V. Hoang, Andrew Hayhurst, Abul K. Azad, Larry S. Schlesinger, Thomas R. Hawn
PLOS Pathogens.2018; 14(6): e1007100. CrossRef
Effect of gap junctions on RAW264.7 macrophages infected with H37Rv
Yang Lu, Xin-min Wang, Pu Yang, Ling Han, Ying-zi Wang, Zhi-hong Zheng, Fang Wu, Wan-jiang Zhang, Le Zhang
Medicine.2018; 97(35): e12125. CrossRef

Innate signaling mechanisms controlling Mycobacterium chelonae-mediated CCL2 and CCL5 expression in macrophages: Yi Sak Kim , Ji Hye Kim , Minjeong Woo , Tae-sung Kim Kim , Kyung Mok Sohn , Young-Ha Lee , Eun-Kyeong Jo , Jae-Min Yuk; J. Microbiol. 2015;53(12):864-874. Published online December 2, 2015; DOI: https://doi.org/10.1007/s12275-015-5348-1

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Abstract

Mycobacterium chelonae (Mch) is an atypical rapidly growing mycobacterium (RGM) that belongs to the M. chelonae complex, which can cause a variety of human infections. During this type of mycobacterial infection, macrophagederived chemokines play an important role in the mediation of intracellular communication and immune surveillance by which they orchestrate cellular immunity. However, the intracellular signaling pathways involved in the macrophage- induced chemokine production during Mch infections remain unknown. Thus, the present study aimed to determine the molecular mechanisms by which Mch activates the gene expressions of chemokine (C-C motif) ligand 2 (CCL2) and CCL5 in murine bone marrow-derived macrophages (BMDMs) and in vivo mouse model. Toll-like receptor 2 (TLR2)-deficient mice showed increased bacterial burden in spleen and lung and decreased protein expression of CCL2 and CCL5 in serum. Additionally, Mch infection triggered the mRNA and protein expression of CCL2 and CCL5 in BMDMs via TLR2 and myeloid differentiation primary response gene 88 (MyD88) signaling and that it rapidly activated nuclear factor (NF)-κB signaling, which is required for the Mch-induced expressions of CCL2 and CCL5 in BMDMs. Moreover, while the innate receptor Dectin-1 was only partly involved in the Mch-induced expression of the CCL2 and CCL5 chemokines in BMDMs, the generation of intracellular reactive oxygen species (ROS) was an important contributor to these processes. Taken together, the present data indicate that the TLR2, MyD88, and NF-κB pathways, Dectin-1 signaling, and intracellular ROS generation contribute to the Mch-mediated expression of chemokine genes in BMDMs.

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The Rise of Non-Tuberculosis Mycobacterial Lung Disease
Champa N. Ratnatunga, Viviana P. Lutzky, Andreas Kupz, Denise L. Doolan, David W. Reid, Matthew Field, Scott C. Bell, Rachel M. Thomson, John J. Miles
Frontiers in Immunology.2020;[Epub] CrossRef
A Comparative Analysis of Edwardsiella tarda-Induced Transcriptome Profiles in RAW264.7 Cells Reveals New Insights into the Strategy of Bacterial Immune Evasion
Huili Li, Boguang Sun, Xianhui Ning, Shuai Jiang, Li Sun
International Journal of Molecular Sciences.2019; 20(22): 5724. CrossRef
Abnormal Microglia and Enhanced Inflammation-Related Gene Transcription in Mice with Conditional Deletion ofCtcfinCamk2a-Cre-Expressing Neurons
Bryan E. McGill, Ruteja A. Barve, Susan E. Maloney, Amy Strickland, Nicholas Rensing, Peter L. Wang, Michael Wong, Richard Head, David F. Wozniak, Jeffrey Milbrandt
The Journal of Neuroscience.2018; 38(1): 200. CrossRef

Review

REVIEW] Perturbation of Pulmonary Immune Functions by Carbon Nanotubes and Susceptibility to Microbial Infection: Brent E. Walling , Gee W. Lau; J. Microbiol. 2014;52(3):227-234. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-3695-y

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Abstract

Occupational and environmental pulmonary exposure to carbon nanotubes (CNT) is considered to be a health risk with a very low threshold of tolerance as determined by the United States Center for Disease Control. Immortalized airway epithelial cells exposed to CNTs show a diverse range of effects including reduced viability, impaired proliferation, and elevated reactive oxygen species generation. Additionally, CNTs inhibit internalization of targets in multiple macrophage cell lines. Mice and rats exposed to CNTs often develop pulmonary granulomas and fibrosis. Furthermore, CNTs have immunomodulatory properties in these animal models. CNTs themselves are proinflammatory and can exacerbate the allergic response. However, CNTs may also be immunosuppressive, both locally and systemically. Studies that examined the relationship of CNT exposure prior to pulmonary infection have reached different conclusions. In some cases, pre-exposure either had no effect or enhanced clearance of infections while other studies showed CNTs inhibited clearance. Interestingly, most studies exploring this relationship use pathogens which are not considered primary pulmonary pathogens. Moreover, harmony across studies is difficult as different types of CNTs have dissimilar biological effects. We used Pseudomonas aeruginosa as model pathogen to study how helical multi-walled carbon nanotubes (HCNTs) affected internalization and clearance of the pulmonary pathogen. The results showed that, although HCNTs can inhibit internalization through multiple processes, bacterial clearance was not altered, which was attributed to an enhanced inflammatory response caused by pre-exposure to HCNTs. We compare and contrast our findings in relation to other studies to gauge the modulation of pulmonary immune response by CNTs.

Citations

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Activation of Kruppel-like factor 6 by multi-walled carbon nanotubes in a diameter-dependent manner in THP-1 macrophages in vitro and bronchoalveolar lavage cells in vivo
Fengmei Song, Xiaomin Tang, Weichao Zhao, Chaobo Huang, Xuyan Dai, Yi Cao
Environmental Science: Nano.2023; 10(3): 855. CrossRef
Comparative analysis of lung and blood transcriptomes in mice exposed to multi-walled carbon nanotubes
Timur O. Khaliullin, Naveena Yanamala, Mackenzie S. Newman, Elena R. Kisin, Liliya M. Fatkhutdinova, Anna A. Shvedova
Toxicology and Applied Pharmacology.2020; 390: 114898. CrossRef
Non-Malignant Respiratory Illnesses in Association with Occupational Exposure to Asbestos and Other Insulating Materials: Findings from the Alberta Insulator Cohort
Subhabrata Moitra, Ali Farshchi Tabrizi, Kawtar Idrissi Machichi, Samineh Kamravaei, Noushin Miandashti, Linda Henderson, Manali Mukherjee, Fadi Khadour, Muhammad T. Naseem, Paige Lacy, Lyle Melenka
International Journal of Environmental Research and Public Health.2020; 17(19): 7085. CrossRef
The curious case of how mimicking physiological complexity in in vitro models of the human respiratory system influences the inflammatory responses. A preliminary study focused on gold nanoparticles
Dania Movia, Luisana Di Cristo, Roaa Alnemari, Joseph E. McCarthy, Hanane Moustaoui, Marc Lamy de la Chapelle, Jolanda Spadavecchia, Yuri Volkov, Adriele Prina‐Mello
Journal of Interdisciplinary Nanomedicine.2017; 2(2): 110. CrossRef
Molecular microbiology in antibacterial research
You-Hee Cho
Journal of Microbiology.2014; 52(3): 185. CrossRef

Research Support, Non-U.S. Gov't

Nucleotide-Binding Oligomerization Domain 2 (Nod2) Is Dispensable for the Innate Immune Responses of Macrophages against Yersinia enterocolitica: Yu-Jin Jeong , Chang-Hwan Kim , Eun-Jung Song , Min-Jung Kang , Jee-Cheon Kim , Sang-Muk Oh , Kyung-Bok Lee , Jong-Hwan Park; J. Microbiol. 2012;50(3):489-495. Published online June 30, 2012; DOI: https://doi.org/10.1007/s12275-012-1534-6

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Abstract: Nucleotide-binding oligomerization domain 2 (Nod2) is a cytosolic sensor for muramyl dipeptide, a component of bacterial peptidoglycan. In this study, we have examined whether Nod2 mediates the immune response of macrophages against Yersinia enterocolitica. Bone-marrow-derived macrophages (BMDMs) were isolated from WT and Nod2-deficient mice and were infected with various strains of Y. enterocolitica. ELISA showed that the production of IL-6 and TNF-α in BMDMs infected with Y. enterocolitica was not affected by the Nod2 deficiency. iNOS mRNA expression was induced in both WT and Nod2-deficienct BMDMs in response to Y. enterocolitica, beginning 2 h after infection. Nitric oxide (NO) production by Y. enterocolitica did not differ between WT and Nod2-deficient BMDMs. Western blot analysis revealed that Y. enterocolitica induces activation of NF-κB, p38, and ERK MAPK through a Nod2-independent pathway. Neither LDH release by Y. enterocolitica nor the phagocytic activity of the macrophages was altered by Nod2 deficiency. An in vivo experiment showed that bacterial clearance ability and production of IL-6 and KC in serum were comparable in WT and Nod2-deficient mice infected with Y. enterocolitica. These findings suggest that Nod2 may not be critical for initiating the innate immune response of macrophages against Yersinia infection.

Journal Article

Screening-Level Assays for Potentially Human-Infectious Environmental Legionella spp.: Helen Y. Buse , Abby Brehm , Jorge W. Santo Domingo , Nicholas J. Ashbolt; J. Microbiol. 2011;49(2):200-207. Published online May 3, 2011; DOI: https://doi.org/10.1007/s12275-011-0233-z

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Abstract: In spite of the fact that various Legionella species are isolated from nonclinical water settings, there is no standard method to determine whether environmental legionellae may be infectious to humans. Here we provide a screening-level approach based on an in vivo murine (A/J mouse) model and three in vitro proliferation assays using Acanthamoeba polyphaga, and THP-1 human and J774 murine macrophage cell lines to identify potentially human-infectious legionellae. As an initial demonstration the infectivity potential of three clinical (Legionella pneumophila, L. longbeacheae, and L. micdadei) and three environmental (L. dumoffii, L. maceachernii, and L. sainthelensi) legionellae were evaluated. A/J mice were intranasally infected and by 6 h post infection (p.i.), there were significant bacterial titers in the lungs. L. pneumophila, L. dumoffii, and L. micdadei densities were higher than L. longbeacheae, L. maceacherni, and L. sainthelensi at 24 h p.i. However, only L. pneumophila and L. micdadei persisted in the lungs after 48 h, indicating that the other isolates were rapidly cleared. Results from the in vitro assays showed that only L. pneumophila significantly multiplied within A. polyphaga, THP-1 and J774 cells after 72 h, but lysis of any of the in vitro hosts also flagged the strains for potential concern (e.g. L. dumoffii and L. micdadei). The results demonstrate the value of using multiple approaches to assess the potential level of pathogenicity of Legionella strains isolated from different environmental matrices.

Protective Effects of Antoxidant Enzymes of Candida albicans against Oxidative Killing by Macrophages: Kim, Hye Jin , Na, Byoung Kuk , Kim, Moon Bo , Choi, Duk Young , Song, Chul Yong; J. Microbiol. 1999;37(2):117-122.

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Abstract: Protective roles of antioxidant enzymes, copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and catalase of Candida albicans against exogenous reactive oxygens and oxidative killing by macrophages were investigated. The initial growth of C. albicans was inhibited by reactive, oxygen-producing chemicals such as hydrogen peroxide, pyrogallol, and paraquat, but it was restored as the production of antioxidant enzymes were increased. The growth inhibition of C. albicans by reactive, oxygen-producing chemicals was reduced by treating the purified candidal SOD and catalase. Also, in the presence of SOD and catalase, the oxidative killing of C. albicans by macrophages was significantly inhibited. These results suggest that antioxidant enzymes, CuZnSOD, MnSOD, and catalase of C. albicans may play important roles in the protection of C. albicans not only from exogenous oxidative stress but also from oxidative killing by macrophages.

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