Journal of Microbiology

Review

Microbiome-Mucosal Immunity Nexus: Driving Forces in Respiratory Disease Progression: Young Chae Park, Soo Yeon Choi, Yunah Cha, Hyeong Won Yoon, Young Min Son; J. Microbiol. 2024;62(9):709-725. Published online September 6, 2024; DOI: https://doi.org/10.1007/s12275-024-00167-4

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The importance of the complex interplay between the microbiome and mucosal immunity, particularly within the respiratory tract, has gained significant attention due to its potential implications for the severity and progression of lung diseases. Therefore, this review summarizes the specific interactions through which the respiratory tract-specific microbiome influences mucosal immunity and ultimately impacts respiratory health. Furthermore, we discuss how the microbiome affects mucosal immunity, considering tissue-specific variations, and its capacity in respiratory diseases containing asthma, chronic obstructive pulmonary disease, and lung cancer. Additionally, we investigate the external factors which affect the relationship between respiratory microbiome and mucosal immune responses. By exploring these intricate interactions, this review provides valuable insights into the potential for microbiome-based interventions to modulate mucosal immunity and alleviate the severity of respiratory diseases.

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Bacteria and fungi of the lung: allies or enemies?
Enrico Garaci, Marilena Pariano, Emilia Nunzi, Claudio Costantini, Marina Maria Bellet, Cinzia Antognelli, Matteo Antonio Russo, Luigina Romani
Frontiers in Pharmacology.2024;[Epub] CrossRef

Journal Article

Vibrio vulnificus PlpA facilitates necrotic host cell death induced by the pore forming MARTX toxin: Changyi Cho , Sanghyeon Choi , Myung Hee Kim , Byoung Sik Kim; J. Microbiol. 2022;60(2):224-233. Published online February 1, 2022; DOI: https://doi.org/10.1007/s12275-022-1448-x

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Abstract

Opportunistic pathogen Vibrio vulnificus causes severe systemic infection in humans with high mortality. Although multiple exotoxins have been characterized in V. vulnificus, their interactions and potential synergistic roles in pathogen-induced host cell death have not been investigated previously. By employing a series of multiple exotoxin deletion mutants, we investigated whether specific exotoxins of the pathogen functioned together to achieve severe and rapid necrotic cell death. Human epithelial cells treated with V. vulnificus with a plpA deletion background exhibited an unusually prolonged cell blebbing, suggesting the importance of PlpA, a phospholipase A2, in rapid necrotic cell death by this pathogen. Additional deletion of the rtxA gene encoding the multifunctional autoprocessing repeats-in-toxin (MARTX) toxin did not result in necrotic cell blebs. However, if the rtxA gene was engineered to produce an effector-free MARTX toxin, the cell blebbing was observed, indicating that the pore forming activity of the MARTX toxin is sufficient, but the MARTX toxin effector domains are not necessary, for the blebbing. When a recombinant PlpA was treated on the blebbed cells, the blebs were completely disrupted. Consistent with this, MARTX toxin-pendent rapid release of cytosolic lactate dehydrogenase was significantly delayed in the plpA deletion background. Mutations in other exotoxins such as elastase, cytolysin/hemolysin, and/or extracellular metalloprotease did not affect the bleb formation or disruption. Together, these findings indicate that the pore forming MARTX toxin and the phospholipase A2, PlpA, cooperate sequentially to achieve rapid necrotic cell death by inducing cell blebbing and disrupting the blebs, respectively.

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Genome-wide phenotypic profiling of transcription factors and identification of novel targets to control the virulence of Vibrio vulnificus
Dayoung Sung, Garam Choi, Minji Ahn, Hokyung Byun, Tae Young Kim, Hojun Lee, Zee-Won Lee, Ji Yong Park, Young Hyun Jung, Ho Jae Han, Sang Ho Choi
Nucleic Acids Research.2024;[Epub] CrossRef
Vibrio-infecting bacteriophages and their potential to control biofilm
Ana Cevallos-Urena, Jeong Yeon Kim, Byoung Sik Kim
Food Science and Biotechnology.2023; 32(12): 1719. CrossRef
Pathogenic Mechanism of Vibrio Vulnificus Infection
Kun Lu, Yang Li, Rui Chen, Hua Yang, Yong Wang, Wei Xiong, Fang Xu, Qijun Yuan, Haihui Liang, Xian Xiao, Renqiang Huang, Zhipeng Chen, Chunou Tian, Songqing Wang
Future Microbiology.2023; 18(6): 373. CrossRef
Functional conservation of specialized ribosomes bearing genome-encoded variant rRNAs in Vibrio species
Younkyung Choi, Eunkyoung Shin, Minho Lee, Ji-Hyun Yeom, Kangseok Lee, Bashir Sajo Mienda
PLOS ONE.2023; 18(12): e0289072. CrossRef
Complex regulatory networks of virulence factors in Vibrio vulnificus
Garam Choi, Sang Ho Choi
Trends in Microbiology.2022; 30(12): 1205. CrossRef
MARTX toxin of Vibrio vulnificus induces RBC phosphatidylserine exposure that can contribute to thrombosis
Han Young Chung, Yiying Bian, Kyung-Min Lim, Byoung Sik Kim, Sang Ho Choi
Nature Communications.2022;[Epub] CrossRef

Histological Alterations and Immune Response Induced by Pet Toxin During Colonization with Enteroaggregative Escherichia coli (EAEC) in a Mouse Model: Teresita Sainz , Julia Perez , Ma. Cristina Fresan , Veronica Flores , Luis Jimenez , Ulises Hernandez , Ismael Herrera , Carlos Eslava; J. Microbiol. 2002;40(2):91-97.

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Abstract: Enteroaggregative E. coli (EAEC) is an important aethiological causal agent of diarrhea in people of developed and undeveloped countries. Different in vitro and in vivo models have been proposed to study the pathogenic and immune mechanisms of EAEC infection. The aim of this study was to analyze whether BALB/c mice could be used as an animal model to study EAEC pathogenesis. Six-week-old BALB/c mice were inoculated with EAEC strain 042 (O44:H18) nalidixic acid resistant, and re-inoculated ten days after. Mice feces were monitored for the presence of the EAEC strain over a period of 20 days. Bacteria were enumerated on MacConkey agar containing 100 ug of nalidixic acid per ml. Results showed that 35% of the animals were colonized for 3 days, 15% for 5 and 10% for more than 7 days. After re-inoculation only 16% of the animals remained colonized for more than 3 days. During the necropsy, the intestinal fluid of some of the infected animals presented mucus and blood. Six of these fluids showed the presence of IgA antibodies against Pet toxin and IgG antibodies raised against the toxin were also detected in the animal serum. Histopathologic evidence confirms the stimulation of mucus hypersecretion, an increased amount of goblet cells and the presence of bacterial aggregates in the apical surfaces of intestinal epithelial cells. Edema was present in the submucosa. These results suggest that BALB/c mice could be used as an animal model for the in vivo study of EAEC infection.

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