Immune Subversion and Pathology Associated with Bacterial Infection

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 5339

Special Issue Editors


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Guest Editor
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
Interests: blood coagulation and complement activation in response to bacterial sepsis; haemostatic properties of the vessel wall; cell biology of tissue factor pathway inhibitor.

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Guest Editor
Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
Interests: humoral immune response to C. difficile infection; B cell repertoire analysis; NKT cells and regulation of humoral immunity

Special Issue Information

Dear Colleagues,

We are planning a Special Issue dedicated to the subversion of host immune responses and immunopathology caused by pathogenic bacteria. We expect to publish 12–15 original articles and reviews by September 2021. Of interest are studies aimed at understanding mechanisms by which pathogenic bacteria subvert and limit the host immune response. Articles that consider pathogen-associated virulence determinants that mediate effects on the immune system are encouraged, as are effects on innate and adaptive immunity. Short- and long-term immunopathology associated with bacterial infections are of particular interest and may include mechanisms underlying intravascular coagulation, cytokine storms and other host responses that drive sepsis and organ failure. Long-term immune sequelae, including autoimmune responses are welcomed. An in-depth understanding of the effects of bacterial pathogens on the host immune system will likely help in the identification of novel targets and therapies for the treatment of infectious disease and we seek to bring relevant concepts together in a Special Issue of Microorganisms.

Dr. Florea Lupu
Prof. Mark Lang
Guest Editors

Manuscript Submission Information

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Keywords

  • sepsis
  • inflammation
  • cytokines
  • innate immunity
  • adaptive immunity
  • hemostatic responses to pathogens
  • disseminated intravascular coagulation
  • complement activation
  • neutrophils
  • mononuclear phagocytes
  • pattern recognition receptors
  • mucosal defense
  • cell death in response to pathogens
  • phagocytosis of pathogens
  • biodefense and emerging pathogens
  • microRNA host responses to infection
  • intravital imaging of host responses to pathogens

Published Papers (2 papers)

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Research

13 pages, 2240 KiB  
Article
Insufficient Anthrax Lethal Toxin Neutralization Is Associated with Antibody Subclass and Domain Specificity in the Plasma of Anthrax-Vaccinated Individuals
by Kenneth Smith, Lori Garman, Kathleen Norris, Jennifer Muther, Angie Duke, Renata J. M. Engler, Michael R. Nelson, Limone C. Collins, Christina Spooner, Carla Guthridge and Judith A. James
Microorganisms 2021, 9(6), 1204; https://doi.org/10.3390/microorganisms9061204 - 2 Jun 2021
Cited by 2 | Viewed by 2391
Abstract
Anthrax vaccine adsorbed (AVA) is a significant line of defense against bioterrorist attack from Bacillus anthracis spores. However, in a subset of individuals, this vaccine may produce a suboptimal quantity of anti-protective antigen (PA), antibodies that are poorly neutralizing, and/or antibody titers that [...] Read more.
Anthrax vaccine adsorbed (AVA) is a significant line of defense against bioterrorist attack from Bacillus anthracis spores. However, in a subset of individuals, this vaccine may produce a suboptimal quantity of anti-protective antigen (PA), antibodies that are poorly neutralizing, and/or antibody titers that wane over time, necessitating annual boosters. To study individuals with such poor responses, we examine the properties of anti-PA in a subset of vaccinated individuals that make significant quantities of antibody but are still unable to neutralize toxin. In this cohort, characterized by poorly neutralizing antibody, we find that increased IgG4 to IgG1 subclass ratios, low antibody avidity, and insufficient antibody targeting domain 4 associate with improper neutralization. Thus, future vaccines and vaccination schedules should be formulated to improve these deficiencies. Full article
(This article belongs to the Special Issue Immune Subversion and Pathology Associated with Bacterial Infection)
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14 pages, 2318 KiB  
Article
Lipoteichoic Acid from Staphylococcus aureus Activates the Complement System via C3 Induction and CD55 Inhibition
by Bong Jun Jung, Hangeun Kim, Kyoung Ok Jang, Seongjae Kim and Dae Kyun Chung
Microorganisms 2021, 9(6), 1135; https://doi.org/10.3390/microorganisms9061135 - 24 May 2021
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Abstract
Staphylococcus aureus inhibits complement activity by secreting a variety of toxins. However, the underlying mechanism of complement component regulation by lipoteichoic acid (LTA), a cell wall component of S. aureus, has not been elucidated. In this study, we observed that aLTA (LTA [...] Read more.
Staphylococcus aureus inhibits complement activity by secreting a variety of toxins. However, the underlying mechanism of complement component regulation by lipoteichoic acid (LTA), a cell wall component of S. aureus, has not been elucidated. In this study, we observed that aLTA (LTA of S. aureus) increased C3 expression in THP-1 cells. The mechanism of aLTA-mediated C3 induction includes an aLTA-toll-like receptor (TLR) 2 interaction, interleukin 1 receptor associated kinase (IRAK) 2 recruitment, and nuclear factor kappa B (NF-kB) activation. In HepG2 cells, C3 protein production begins to increase from 3 h and increases steadily until 48 h. On the other hand, CD55 levels increased up to 6 h after aLTA treatment and started to decrease after 24 h and levels were decreased at 48 h by more than 50% compared to untreated cells. The expression of CD55 in HepG2 cells was shown to be regulated by IRAK-M induced by aLTA. Serum C3 levels increased in mice injected with aLTA, which resulted in an increase in the amount and activity of the membrane attack complex (MAC). We also observed that CD55 mRNA was increased in the liver 24 h after aLTA injection, but was decreased 48 h after injection. These results suggest that aLTA increases complement levels via induction of C3 and inhibition of CD55, which may cause associated MAC-mediated liver damage. Full article
(This article belongs to the Special Issue Immune Subversion and Pathology Associated with Bacterial Infection)
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