Insights into Microbial Infections, Co-Infections, and Comorbidities

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 765

Special Issue Editors


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Guest Editor
1. Department of Life Sciences, School of Agriculture and Life Sciences, College of Agriculture and Environmental Sciences, Science Campus, University of South Africa, 28 Pioneer Avenue, Florida Park, Roodepoort 1709, South Africa
2. Department of Medical Microbiology, College of Health Sciences, School of Laboratory Medicine & Medical Sciences, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4001, South Africa
Interests: immunology; antimicrobial resistance; co-infections

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Guest Editor
College of Health Sciences, University of KwaZulu-Natal, Durban 4000, South Africa
Interests: human genetics; infectious diseases; epigenetics; polymorphisms
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Special Issue Information

Dear Colleagues,

Microbial infections and co-infections are major global health concerns, significantly contributing to disease burden and mortality worldwide. Co-infections—the simultaneous occurrence of two or more infections within a host—introduce unique challenges in understanding disease dynamics, progression, and management due to intricate pathogen–pathogen and pathogen–host interactions. These interactions often overlap with, impact on, or are impacted by comorbidities, particularly noncommunicable diseases (NCDs) such as cancer, cardiovascular diseases, and diabetes, as well as biological factors such as dysbiosis and genetics. These NCDs alter host susceptibility, immune responses, and treatment outcomes, further complicating the management of microbial infections.

This Special Issue aims to explore the multifaceted relationships between microbial infections, co-infections, and comorbidities, emphasizing biological and mechanistic insights, along with real-world applications. Topics of interest include the molecular, cellular, and immunological basis of pathogenesis; pathogen–pathogen and host–pathogen interactions during co-infections; and the role of comorbidities/biological factors and antimicrobial resistance in complicating treatment strategies. Research addressing the diagnostic challenges of detecting multiple infections and their interplay with NCDs is also highly relevant. Furthermore, the Special Issue welcomes studies on the ecological and biophysical, including exposomic and physiological, impacts of microbial communities in the context of these diseases, including their role in modulating host immune responses and influencing therapeutic outcomes.

We particularly encourage submissions that address the confluence of co-infections with comorbidities and that highlight innovative approaches to combating these health challenges, including novel diagnostic tools, therapeutic strategies, and public health interventions. Interdisciplinary studies that integrate microbiology, immunology, epidemiology, and clinical perspectives are strongly encouraged. The findings presented in this Special Issue aim to contribute to global efforts to reduce the burden of infectious diseases and improve health outcomes for patients with complex disease profiles.

Dr. Zilungile Mkhize-Kwitshana
Dr. Veron Ramsuran
Guest Editors

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Keywords

  • antimicrobial resistance
  • cancer
  • cardiovascular diseases
  • co-infections
  • comorbidities
  • complex disease profiles
  • diabetes
  • infection pathogenesis
  • immune modulation
  • microbiome and co-infections
  • noncommunicable diseases
  • pathogen interactions
  • pneumonia
  • pulmonary infections
  • sepsis
  • stress tolerance
  • therapeutics
  • vaccine development

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Published Papers (1 paper)

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Research

15 pages, 5904 KiB  
Article
The Vaginally Exposed Extracellular Vesicle of Gardnerella vaginalis Induces RANK/RANKL-Involved Systemic Inflammation in Mice
by Yoon-Jung Shin, Xiaoyang Ma, Ji-Su Baek and Dong-Hyun Kim
Microorganisms 2025, 13(4), 955; https://doi.org/10.3390/microorganisms13040955 - 21 Apr 2025
Viewed by 231
Abstract
Gardnerella vaginalis (GV), an opportunistic pathogen excessively proliferated in vaginal dysbiosis, causes systemic inflammation including vaginitis, neuroinflammation, and osteitis. To understand its systemic inflammation-triggering factor, we purified extracellular vesicles isolated from GV (gEVs) and examined their effect on the occurrence of vaginitis, osteitis, [...] Read more.
Gardnerella vaginalis (GV), an opportunistic pathogen excessively proliferated in vaginal dysbiosis, causes systemic inflammation including vaginitis, neuroinflammation, and osteitis. To understand its systemic inflammation-triggering factor, we purified extracellular vesicles isolated from GV (gEVs) and examined their effect on the occurrence of vaginitis, osteitis, and neuroinflammation in mice with and without ovariectomy (Ov). The gEVs consisted of lipopolysaccharide, proteins, and nucleic acid and induced TNF-α and RANKL expression in macrophage cells. When the gEVs were vaginally exposed in mice without Ov, they significantly induced RANK, RANKL, and TNF-α expression and NF-κB+ cell numbers in the vagina, femur, hypothalamus, and hippocampus, as observed in GV infection. The gEVs decreased time spent in the open field (OT) in the elevated plus maze test by 47.3%, as well as the distance traveled in the central area (DC) by 28.6%. In the open field test, they also decreased the time spent in the central area (TC) by 39.3%. Additionally, gEVs decreased spontaneous alteration (SA) in the Y-maze test by 33.8% and the recognition index (RI) in the novel object recognition test by 26.5%, while increasing the immobility time (IT) in the tail suspension test by 36.7%. In mice with OV (Ov), the gEVs also induced RANK, RANKL, and TNF-α expression and increased NF-κB+ cell numbers in the vagina, femur, hypothalamus, and hippocampus compared to vehicle-treated mice. When gEVs were exposed to mice with Ov, gEVs also reduced the DC, TC, OT, SA, and RI to 62.1%, 62.7%, 28.2%, 90.7%, and 85.4% of mice with Ov, respectively, and increased IT to 122.9% of mice with Ov. Vaginally exposed fluorescein-isothiocyanate-tagged gEVs were detected in the blood, femur, and hippocampus. These findings indicate that GV-derived gEVs may induce systemic inflammation through the activation of RANK/RANKL-involved NF-κB signaling, leading to systemic disorders including vaginitis, osteoporosis, depression, and cognitive impairment. Therefore, gEVs may be an important risk factor for vaginitis, osteoporosis, depression, and cognitive impairment in women. Full article
(This article belongs to the Special Issue Insights into Microbial Infections, Co-Infections, and Comorbidities)
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