Microbiology and Immunology最新文献

Y. Hiramatsu, M. Osada-Oka, Y. Horiguchi, “Bordet-Gengou Agar Medium Supplemented With Albumin-Containing Biologics for Cultivation of Bordetellae,” Microbiology and Immunology 63 (2019): 513–516.

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N. Onoda, Y. Hiramatsu, S. Teruya, K. Suzuki, Y. Horiguchi, “Identification of the Minimum Region of Bordetella pertussis Vag8 Required for Interaction With C1 Inhibitor,” Microbiology and Immunology 64 (2020): 570–573.

Figure 2a showed the wrong data and should be replaced with the new figure with the correct data. This correction does not affect the research's conclusion but is requested for accuracy. In addition, “(Figure 1a)” on the left column of page 572, lines 5 and 7, should be “(Figure 2a).”

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Ambient humidity, temperature, and ozone influence the viability of airborne viruses, but their synergistic effects are poorly understood, particularly regarding ozone with humidity/temperature changes. Therefore, we examined the inactivation of airborne influenza viruses and coronaviruses under combinations of low ambient ozone concentrations, relative humidity (RH) levels, and temperatures typical of daily life. Viral fluid was atomized in a closed chamber conditioned with different combinations of these factors. The atomized aerosol particles containing the virus were exposed to ambient air and then sampled for titration. Active virus levels in ambient air at 50%–85% RH with 15, 35, and 55 ppb ozone significantly decreased compared with those in ambient air with 0 ppb ozone, whereas those in ambient air at < 40% RH decreased only slightly, even with 100 ppb ozone. Viral gene copy numbers, assayed via quantitative real-time polymerase chain reaction, remained similar across all conditions. Inactivation increased with higher temperatures, although not at 15°C. These findings suggest that low concentrations of ambient ozone, when combined with high humidity and temperature, effectively inactivate airborne viruses, potentially influencing viral transmission in real-world environments.

Cover photograph: Heatmaps of correlations between different mediators in serum of etiological groups. Microbiol Immunol: 69:174-181. Article link here

The pathogenesis of enterotoxigenic Escherichia coli (ETEC) involves the colonization of hosts by colonization factors (CFs) and the secretion of enterotoxins. CFs, especially chaperone-usher fimbriae, mediate bacterial adhesion to host cells, with extensive genetic diversity observed among isolates. One ETEC strain, O169YN10, possessed a unique plasmid (pEntYN10) encoding three CFs, CS6, and two novel homologs of CS8 and F4 (CS6_O169, CS8_O169, and F4_O169). In this study, F4_O169 was found to play a major role in adhesion to multiple hosts, including human, bovine, and porcine epithelial cells, whereas the other two CSs were less functional. Inhibition assays using antibodies showed that FayG1, one of the two major paralogous adhesins of F4_O169, directly contributes to human cell adhesion. Despite the established function of FayG1, the FayG2 protein was not detected under the in vitro conditions. Comparative genomics revealed that FayG1 and FayG2 share low homology with other E. coli strains isolated from hosts, suggesting sporadic emergence from an unknown origin.

Hepatitis B virus (HBV) causes chronic hepatitis B, which can progress to liver cirrhosis and hepatocellular carcinoma. HBV has complex interactions with various cell organelles and proteins that ensure effective progeny virus production. We previously reported that a mitochondrial protein, TIMM29, should regulate the HBV life cycle through interactions with the HBV preS1 protein. Here, we established Halo-TIMM29wt-, Halo-TIMM29:∆99–192-, and Halo-TIMM29:92–194-expressing cells using TIMM29-knockout HB611 (TIMM29KO/HB611) cells, a stably HBV-producing cell line based on Huh6 cells. We found that HBV antigen expression and replication were downregulated in cells stably expressing full-length TIMM29, but not in those expressing TIMM29 deletion mutants. On the other hand, in the case of TIMM29-knockout C4 (TIMM29KO/C4), which is a human NTCP-expressing HepG2 cell line that is competent for HBV infection and amplification, these phenomena were not reproduced, except in full-length TIMM29 (Halo-TIMM29wt)-expressing cells. Using gene expression microarrays, we identified downregulation of ARRDC3 and BASP1 in TIMM29KO/HB611 and TIMM29KO/C4. It was suggested that TIMM29 localized at the mitochondrial inner membrane served as a signaling hub, orchestrating the activation of ARRDC3 and BASP1 expression to restrict HBV transcription. The expression of TIMM29 mutants in TIMM29KO/HB611 and TIMM29KO/C4 cells suggested that ARRDC3 was dependent on the HBV preS1-binding region of TIMM29 (amino acids 99–189). In contrast, BASP1 expression varied according to cell type, indicating additional regulatory mechanisms. Thus, this study should significantly advance our understanding of TIMM29-mediated inhibition of HBV amplification and lead to improvements in antiviral strategies and therapeutic interventions against HBV.

Supersulfides are molecular species characterized by catenated sulfur moieties, including low-molecular-weight and protein-bound supersulfides. Emerging evidence suggests that these molecules, abundantly present in diverse organisms, play essential roles far beyond their chemical properties, such as functions in energy metabolism, protein stabilization, and antiviral defense. Recent studies highlight their regulatory effects on pattern-recognition receptors (PRRs) and associated signaling pathways–such as nucleotide oligomerization domain-like receptor signaling, toll-like receptor signaling, and type I interferon receptor signaling–critical for innate immunity and inflammatory responses. Dysregulation of these pathways is implicated in a heterogeneous group of autoinflammatory diseases, including inflammasomopathies, relopathies, and type I interferonopathies, respectively. Notably, both endogenous and synthetic supersulfide donors have recently shown promising inhibitory effects on PRR signaling, offering their potential as targeted therapies for managing autoinflammatory conditions. This review summarizes the fundamental biology of supersulfides and typical autoinflammatory diseases, focusing on their roles in innate immune and inflammatory responses, while exploring their therapeutic potential in these diseases.