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Pathogens
Special Issues
Host Defense Against Bacteria
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Host Defense Against Bacteria

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (31 March 2017) | Viewed by 26164

Special Issue Editor

Dr. Sandip K. Datta

E-Mail Website
Guest Editor
Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Interests: host defense against Staphylococcus aureus

Special Issue Information

Dear Colleagues,

Anti-bacterial host defense encompasses a diverse and clinically important set of interactions between bacteria and their host. Bacteria can range from mutualistic microbiota to highly virulent pathogens. Different species and strains have evolved unique mechanisms to adapt to their host environment, and continual adaptation to environmental exposures such as antibiotics presents an ongoing challenge for medicine. Bacterial virulence strategies often reveal important mammalian immune mechanisms, which span all aspects of innate and adaptive immunity. For this Special Issue of Pathogens, we invite you to submit a review article related to host defense against bacteria that elucidates emerging paradigms regarding interactions between medically relevant bacteria and their human hosts.

Dr. Sandip K. Datta
Guest Editor

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 submissions that pass pre-check are 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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens 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 2700 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.

 

Keywords

  • bacteria
  • host defense
  • pathogen
  • microbiota
  • innate immunity
  • antibody
  • T cells
  • vaccine

Published Papers (4 papers)

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Research

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704 KiB  
Article
Molecular Typing of Staphylococcus aureus Isolated from Patients with Autosomal Dominant Hyper IgE Syndrome
by Inka Sastalla, Kelli W. Williams, Erik D. Anderson, Ian A. Myles, Jensen D. Reckhow, Marlene Espinoza-Moraga, Alexandra F. Freeman and Sandip K. Datta
Pathogens 2017, 6(2), 23; https://doi.org/10.3390/pathogens6020023 - 6 Jun 2017
Cited by 9 | Viewed by 5455
Abstract
Autosomal dominant hyper IgE syndrome (AD-HIES) is a primary immunodeficiency caused by a loss-of-function mutation in the Signal Transducer and Activator of Transcription 3 (STAT3). This immune disorder is clinically characterized by increased susceptibility to cutaneous and sinopulmonary infections, in particular with Candida [...] Read more.
Autosomal dominant hyper IgE syndrome (AD-HIES) is a primary immunodeficiency caused by a loss-of-function mutation in the Signal Transducer and Activator of Transcription 3 (STAT3). This immune disorder is clinically characterized by increased susceptibility to cutaneous and sinopulmonary infections, in particular with Candida and Staphylococcus aureus. It has recently been recognized that the skin microbiome of patients with AD-HIES is altered with an overrepresentation of certain Gram-negative bacteria and Gram-positive staphylococci. However, these alterations have not been characterized at the species- and strain-level. Since S. aureus infections are influenced by strain-specific expression of virulence factors, information on colonizing strain characteristics may provide insights into host-pathogen interactions and help guide management strategies for treatment and prophylaxis. The aim of this study was to determine whether the immunodeficiency of AD-HIES selects for unique strains of colonizing S. aureus. Using multi-locus sequence typing (MLST), protein A (spa) typing, and PCR-based detection of toxin genes, we performed a detailed analysis of the S. aureus isolates (n = 13) found on the skin of twenty-one patients with AD-HIES. We found a low diversity of sequence types, and an abundance of strains that expressed methicillin resistance, Panton-Valentine leukocidin (PVL), and staphylococcal enterotoxins K and Q (SEK, SEQ). Our results indicate that patients with AD-HIES may often carry antibiotic-resistant strains that harbor key virulence factors. Full article
(This article belongs to the Special Issue Host Defense Against Bacteria)
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4168 KiB  
Article
Modulation of Human Airway Barrier Functions during Burkholderia thailandensis and Francisella tularensis Infection
by Cornelia Blume, Jonathan David, Rachel E. Bell, Jay R. Laver, Robert C. Read, Graeme C. Clark, Donna E. Davies and Emily J. Swindle
Pathogens 2016, 5(3), 53; https://doi.org/10.3390/pathogens5030053 - 3 Aug 2016
Cited by 6 | Viewed by 4864
Abstract
The bronchial epithelium provides protection against pathogens from the inhaled environment through the formation of a highly-regulated barrier. In order to understand the pulmonary diseases melioidosis and tularemia caused by Burkholderia thailandensis and Fransicella tularensis, respectively, the barrier function of the human [...] Read more.
The bronchial epithelium provides protection against pathogens from the inhaled environment through the formation of a highly-regulated barrier. In order to understand the pulmonary diseases melioidosis and tularemia caused by Burkholderia thailandensis and Fransicella tularensis, respectively, the barrier function of the human bronchial epithelium were analysed. Polarised 16HBE14o- or differentiated primary human bronchial epithelial cells (BECs) were exposed to increasing multiplicities of infection (MOI) of B. thailandensis or F. tularensis Live Vaccine Strain and barrier responses monitored over 24–72 h. Challenge of polarized BECs with either bacterial species caused an MOI- and time-dependent increase in ionic permeability, disruption of tight junctions, and bacterial passage from the apical to the basolateral compartment. B. thailandensis was found to be more invasive than F. tularensis. Both bacterial species induced an MOI-dependent increase in TNF-α release. An increase in ionic permeability and TNF-α release was induced by B. thailandensis in differentiated BECs. Pretreatment of polarised BECs with the corticosteroid fluticasone propionate reduced bacterial-dependent increases in ionic permeability, bacterial passage, and TNF-α release. TNF blocking antibody Enbrel® reduced bacterial passage only. BEC barrier properties are disrupted during respiratory bacterial infections and targeting with corticosteroids or anti-TNF compounds may represent a therapeutic option. Full article
(This article belongs to the Special Issue Host Defense Against Bacteria)
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Review

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965 KiB  
Review
Interactions between Neutrophils and Pseudomonas aeruginosa in Cystic Fibrosis
by Balázs Rada
Pathogens 2017, 6(1), 10; https://doi.org/10.3390/pathogens6010010 - 9 Mar 2017
Cited by 64 | Viewed by 13809
Abstract
Cystic fibrosis (CF) affects 70,000 patients worldwide. Morbidity and mortality in CF is largely caused by lung complications due to the triad of impaired mucociliary clearance, microbial infections and chronic inflammation. Cystic fibrosis airway inflammation is mediated by robust infiltration of polymorphonuclear neutrophil [...] Read more.
Cystic fibrosis (CF) affects 70,000 patients worldwide. Morbidity and mortality in CF is largely caused by lung complications due to the triad of impaired mucociliary clearance, microbial infections and chronic inflammation. Cystic fibrosis airway inflammation is mediated by robust infiltration of polymorphonuclear neutrophil granulocytes (PMNs, neutrophils). Neutrophils are not capable of clearing lung infections and contribute to tissue damage by releasing their dangerous cargo. Pseudomonas aeruginosa is an opportunistic pathogen causing infections in immunocompromised individuals. P. aeruginosa is a main respiratory pathogen in CF infecting most patients. Although PMNs are key to attack and clear P. aeruginosa in immunocompetent individuals, PMNs fail to do so in CF. Understanding why neutrophils cannot clear P. aeruginosa in CF is essential to design novel therapies. This review provides an overview of the antimicrobial mechanisms by which PMNs attack and eliminate P. aeruginosa. It also summarizes current advances in our understanding of why PMNs are incapable of clearing P. aeruginosa and how this bacterium adapts to and resists PMN-mediated killing in the airways of CF patients chronically infected with P. aeruginosa. Full article
(This article belongs to the Special Issue Host Defense Against Bacteria)
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Other

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1 pages, 153 KiB  
Erratum
Erratum: Blume, C., et al. Modulation of Human Airway Barrier Functions during Burkholderia thailandensis and Francisella tularensis Infection Running Title: Airway Barrier Functions during Bacterial Infections. Pathogens 2016, 5, 53
by Cornelia Blume, Jonathan David, Rachel E. Bell, Jay R. Laver, Robert C. Read, Graeme C. Clark, Donna E. Davies and Emily J. Swindle
Pathogens 2020, 9(12), 987; https://doi.org/10.3390/pathogens9120987 - 26 Nov 2020
Cited by 1 | Viewed by 1058
Abstract
There is an error in the title [...] Full article
(This article belongs to the Special Issue Host Defense Against Bacteria)
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