Special Issue "Toxins and Lung Infection"

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (4 November 2020).

Special Issue Editors

Prof. Dr. Rudolf Lucas
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Guest Editor
Vascular Biology Center, Division of Pulmonary Critical care MedicineMedical College of Georgia at Augusta University, 1460, Laney-Walker Blvd, Augusta, GA 30912, USA
Prof. Dr. Trinad Chakraborty
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Guest Editor
Justus-Liebig-University, Biomedical Research Centre Seltersberg, Schubertstr. 81, 35392 Giessen, Germany

Special Issue Information

Dear Colleagues,

The air-blood barrier in the lungs, formed by the alveoli together with the surrounding capillaries, is the primary exchange surface for the uptake of O2 from the alveolar space and the removal of CO2 from the blood. This vulnerable system requires that the alveoli remain relatively dry, as assured by vectorial sodium transport-driven alveolar liquid clearance, and that the alveolar-capillary barriers remain tight, regulated by adherens and tight junction proteins. Bacterial toxins are potent inducers of pulmonary inflammation and can impair alveolar fluid clearance, through vectorial sodium transport actions, and barrier function, through phosphorylation of tight and adherens junction proteins. These toxin actions can ultimately lead to lung disease, including acute lung injury and acute respiratory distress syndrome (ARDS). This Special Issue will focus on how G+/G- bacterial toxins, including the pore-forming toxins pneumolysin, listeriolysin-O, and alpha-toxin, as well as lipopolysaccharide (LPS), affect cellular processes involved in pathophysiology and resolution of lung disease and how their actions may be modulated. The reader will be provided with an overall view of what is presently known about the mode of action and functions of these toxins, and how they may be inhibited or even harnessed to promote the entry of other important biologically relevant proteins and substances.

Prof. Dr. Rudolf Lucas
Prof. Dr. Trinad Chakraborty
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (3 papers)

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Research

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Open AccessArticle
Exoenzyme Y Contributes to End-Organ Dysfunction Caused by Pseudomonas aeruginosa Pneumonia in Critically Ill Patients: An Exploratory Study
Toxins 2020, 12(6), 369; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12060369 - 04 Jun 2020
Cited by 3 | Viewed by 886
Abstract
Pseudomonas aeruginosa is an opportunistic pathogen that causes pneumonia in immunocompromised and intensive care unit (ICU) patients. During host infection, P. aeruginosa upregulates the type III secretion system (T3SS), which is used to intoxicate host cells with exoenzyme (Exo) virulence factors. Of the [...] Read more.
Pseudomonas aeruginosa is an opportunistic pathogen that causes pneumonia in immunocompromised and intensive care unit (ICU) patients. During host infection, P. aeruginosa upregulates the type III secretion system (T3SS), which is used to intoxicate host cells with exoenzyme (Exo) virulence factors. Of the four known Exo virulence factors (U, S, T and Y), ExoU has been shown in prior studies to associate with high mortality rates. Preclinical studies have shown that ExoY is an important edema factor in lung infection caused by P. aeruginosa, although its importance in clinical isolates of P. aeruginosa is unknown. We hypothesized that expression of ExoY would be highly prevalent in clinical isolates and would significantly contribute to patient morbidity secondary to P. aeruginosa pneumonia. A single-center, prospective observational study was conducted at the University of Alabama at Birmingham Hospital. Mechanically ventilated ICU patients with a bronchoalveolar lavage fluid culture positive for P. aeruginosa were included. Enrolled patients were followed from ICU admission to discharge and clinical P. aeruginosa isolates were genotyped for the presence of exoenzyme genes. Ninety-nine patients were enrolled in the study. ExoY was present in 93% of P. aeruginosa clinical isolates. Moreover, ExoY alone (ExoY+/ExoU) was present in 75% of P. aeruginosa isolates, compared to 2% ExoU alone (ExoY/ExoU+). We found that bacteria isolated from human samples expressed active ExoY and ExoU, and the presence of ExoY in clinical isolates was associated with end-organ dysfunction. This is the first study we are aware of that demonstrates that ExoY is important in clinical outcomes secondary to nosocomial pneumonia. Full article
(This article belongs to the Special Issue Toxins and Lung Infection)
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Review

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Open AccessReview
Streptococcus pneumoniae and Its Virulence Factors H2O2 and Pneumolysin Are Potent Mediators of the Acute Chest Syndrome in Sickle Cell Disease
Toxins 2021, 13(2), 157; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13020157 - 17 Feb 2021
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Abstract
Sickle cell disease (SCD) is one of the most common autosomal recessive disorders in the world. Due to functional asplenia, a dysfunctional antibody response, antibiotic drug resistance and poor response to immunization, SCD patients have impaired immunity. A leading cause of hospitalization and [...] Read more.
Sickle cell disease (SCD) is one of the most common autosomal recessive disorders in the world. Due to functional asplenia, a dysfunctional antibody response, antibiotic drug resistance and poor response to immunization, SCD patients have impaired immunity. A leading cause of hospitalization and death in SCD patients is the acute chest syndrome (ACS). This complication is especially manifested upon infection of SCD patients with Streptococcus pneumoniae (Spn)—a facultative anaerobic Gram-positive bacterium that causes lower respiratory tract infections. Spn has developed increased rates of antibiotics resistance and is particularly virulent in SCD patients. The primary defense against Spn is the generation of reactive oxygen species (ROS) during the oxidative burst of neutrophils and macrophages. Paradoxically, Spn itself produces high levels of the ROS hydrogen peroxide (H2O2) as a virulence strategy. Apart from H2O2, Spn also secretes another virulence factor, i.e., the pore-forming exotoxin pneumolysin (PLY), a potent mediator of lung injury in patients with pneumonia in general and particularly in those with SCD. PLY is released early on in infection either by autolysis or bacterial lysis following the treatment with antibiotics and has a broad range of biological activities. This review will discuss recent findings on the role of pneumococci in ACS pathogenesis and on strategies to counteract the devastating effects of its virulence factors on the lungs in SCD patients. Full article
(This article belongs to the Special Issue Toxins and Lung Infection)
Open AccessReview
Impact of Bacterial Toxins in the Lungs
Toxins 2020, 12(4), 223; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12040223 - 02 Apr 2020
Cited by 6 | Viewed by 1381
Abstract
Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate lung barrier function and to impair host defense in order to promote infection. Although in general, these toxins [...] Read more.
Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate lung barrier function and to impair host defense in order to promote infection. Although in general, these toxins target common cellular signaling pathways and host compartments, toxin- and cell-specific effects have also been reported. Toxins can affect resident pulmonary cells involved in alveolar fluid clearance (AFC) and barrier function through impairing vectorial Na+ transport and through cytoskeletal collapse, as such, destroying cell-cell adhesions. The resulting loss of alveolar-capillary barrier integrity and fluid clearance capacity will induce capillary leak and foster edema formation, which will in turn impair gas exchange and endanger the survival of the host. Toxins modulate or neutralize protective host cell mechanisms of both the innate and adaptive immunity response during chronic infection. In particular, toxins can either recruit or kill central players of the lung’s innate immune responses to pathogenic attacks, i.e., alveolar macrophages (AMs) and neutrophils. Pulmonary disorders resulting from these toxin actions include, e.g., acute lung injury (ALI), the acute respiratory syndrome (ARDS), and severe pneumonia. When acute infection converts to persistence, i.e., colonization and chronic infection, lung diseases, such as bronchitis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) can arise. The aim of this review is to discuss the impact of bacterial toxins in the lungs and the resulting outcomes for pathogenesis, their roles in promoting bacterial dissemination, and bacterial survival in disease progression. Full article
(This article belongs to the Special Issue Toxins and Lung Infection)
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