Pathogens

Editorial

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4 pages, 167 KiB

Open AccessEditorial

Pathogenesis of Fungal and Bacterial Microbes

by Jennifer Geddes-McAlister

Pathogens 2020, 9(8), 602; https://doi.org/10.3390/pathogens9080602 - 23 Jul 2020

Cited by 2 | Viewed by 2311

Abstract

The pathogenesis of fungal and bacterial microbes is a complex process involving distinct parameters, including virulence factors, nutrient sensing and availability, microbial signals, as well as host status and defense responses. Defining pathogenesis improves our understanding of how an organism causes diseases and [...] Read more.

The pathogenesis of fungal and bacterial microbes is a complex process involving distinct parameters, including virulence factors, nutrient sensing and availability, microbial signals, as well as host status and defense responses. Defining pathogenesis improves our understanding of how an organism causes diseases and provides insight into novel prospects to combat infection. The effects of pathogenic microbes have significant impact on diverse sectors, including health, agriculture, and economics, underscoring their immense importance in society. Articles in this Special Issue address unique aspects of microbial pathogenesis by exploring interactions between host and pathogen during infection, defining inflammatory immune responses, profiling the importance of essential microbial structures associated with virulence, and outlining critical considerations driving complex diseases. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

Research

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20 pages, 2886 KiB

Open AccessArticle

Enniatin Production Influences Fusarium avenaceum Virulence on Potato Tubers, but not on Durum Wheat or Peas

by Anas Eranthodi, Danielle Schneiderman, Linda J. Harris, Thomas E. Witte, Amanda Sproule, Anne Hermans, David P. Overy, Syama Chatterton, Jiajun Liu, Tao Li, Dianevys González-Peña Fundora, Weiquan Zhao and Nora A. Foroud

Pathogens 2020, 9(2), 75; https://doi.org/10.3390/pathogens9020075 - 21 Jan 2020

Cited by 24 | Viewed by 3714

Abstract

Fusarium avenaceum is a generalist pathogen responsible for diseases in numerous crop species. The fungus produces a series of mycotoxins including the cyclohexadepsipeptide enniatins. Mycotoxins can be pathogenicity and virulence factors in various plant–pathogen interactions, and enniatins have been shown to influence aggressiveness [...] Read more.

Fusarium avenaceum is a generalist pathogen responsible for diseases in numerous crop species. The fungus produces a series of mycotoxins including the cyclohexadepsipeptide enniatins. Mycotoxins can be pathogenicity and virulence factors in various plant–pathogen interactions, and enniatins have been shown to influence aggressiveness on potato tubers. To determine the role of these mycotoxins in other F. avenaceum–host interactions, ENNIATIN SYNTHASE 1 (ESYN1) disruption and overexpression mutants were generated and their ability to infect wheat and peas investigated. As a preliminary study, the transformants were screened for their ability to cause potato tuber necrosis and, consistent with a previous report, enniatin production increased necrotic lesion size on the tubers. By contrast, when the same mutants were assessed in their ability to cause disease in pea roots or durum wheat spikes, no changes in disease symptoms or virulence were observed. While it is known that, at least in the case of wheat, exogenously applied enniatins can cause tissue necrosis, this group of mycotoxins does not appear to be a key factor on its own in disease development on peas or durum wheat. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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15 pages, 2360 KiB

Open AccessEditor’s ChoiceArticle

Genetic Changes in Experimental Populations of a Hybrid in the Cryptococcus neoformans Species Complex

by Kelly Dong, Man You and Jianping Xu

Pathogens 2020, 9(1), 3; https://doi.org/10.3390/pathogens9010003 - 18 Dec 2019

Cited by 13 | Viewed by 2281

Abstract

Hybrids between Cryptococcus neoformans and Cryptococcus deneoformans are commonly found in patients and the environment. However, the genetic stability of these hybrids remains largely unknown. Here, we established mutation accumulation lines of a diploid C. neoformans × C. deneoformans laboratory hybrid and analyzed [...] Read more.

Hybrids between Cryptococcus neoformans and Cryptococcus deneoformans are commonly found in patients and the environment. However, the genetic stability of these hybrids remains largely unknown. Here, we established mutation accumulation lines of a diploid C. neoformans × C. deneoformans laboratory hybrid and analyzed the genotypes at 33 markers distributed across all 14 chromosomes. Our analyses found that under standard culture conditions, heterozygosity at most loci was maintained over 800 mitotic generations, with an estimated 6.44 × 10⁻⁵ loss-of-heterozygosity (LoH) event per mitotic division. However, under fluconazole stress, the observed LoH frequency increased by > 50 folds for the two markers on Chromosome 1, all due to the loss of the fluconazole susceptible allele on this chromosome. Flow cytometry analyses showed that after the 40th transfer (120 days), 19 of the 20 lines maintained the original ploidy level (2N), while one line was between 2N and 3N. The combined flow cytometry, genotyping at 33 markers, and quantitative PCR analyses showed the allelic loss was compensated for by amplification of the resistant ERG11 allele in eight of the ten fluconazole-stress lines. Our results suggest that hybrids in C. neoformans species complex are generally stable but that they can undergo rapid adaptation to environmental stresses through LoH and gene duplication. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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17 pages, 2999 KiB

Open AccessArticle

Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition

by Nouman Amjad, Ruicheng Yang, Liang Li, Jiyang Fu, Bo Yang, Bojie Xu, Chen Tan, Huanchun Chen and Xiangru Wang

Pathogens 2019, 8(4), 268; https://doi.org/10.3390/pathogens8040268 - 27 Nov 2019

Cited by 13 | Viewed by 2457

Abstract

Meningitic Escherichia coli can traverse the host’s blood–brain barrier (BBB) and induce severe neuroinflammatory damage to the central nervous system (CNS). During this process, the host needs to reasonably balance the battle between bacteria and brain microvascular endothelial cells (BMECs) to minimize inflammatory [...] Read more.

Meningitic Escherichia coli can traverse the host’s blood–brain barrier (BBB) and induce severe neuroinflammatory damage to the central nervous system (CNS). During this process, the host needs to reasonably balance the battle between bacteria and brain microvascular endothelial cells (BMECs) to minimize inflammatory damage, but this quenching of neuroinflammatory responses at the BBB is unclear. MicroRNAs (miRNAs) are widely recognized as key negative regulators in many pathophysiological processes, including inflammatory responses. Our previous transcriptome sequencing revealed numbers of differential miRNAs in BMECs upon meningitic E. coli infection; we next sought to explore whether and how these miRNAs worked to modulate neuroinflammatory responses at meningitic E. coli entry of the BBB. Here, we demonstrated in vivo and in vitro that meningitic E. coli infection of BMECs significantly downregulated miR-19b-3p, which led to attenuated production of proinflammatory cytokines and chemokines via increasing the expression of TNFAIP3, a negative regulator of NF-κB signaling. Moreover, in vivo injection of miR-19b-3p mimics during meningitic E. coli challenge further aggravated the inflammatory damage to mice brains. These in vivo and in vitro findings indicate a novel quenching mechanism of the host by attenuating miR-19b-3p/TNFAIP3/NF-κB signaling in BMECs in response to meningitic E. coli, thus preventing CNS from further neuroinflammatory damage. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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16 pages, 3744 KiB

Open AccessArticle

Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade

by Lu Liu, Jixuan Li, Dong Huo, Zhong Peng, Ruicheng Yang, Jiyang Fu, Bojie Xu, Bo Yang, Huanchun Chen and Xiangru Wang

Pathogens 2019, 8(4), 254; https://doi.org/10.3390/pathogens8040254 - 22 Nov 2019

Cited by 7 | Viewed by 3211

Abstract

Bacterial meningitis is currently recognized as one of the most important life-threatening infections of the central nervous system (CNS) with high morbidity and mortality, despite the advancements in antimicrobial treatment. The disruption of blood–brain barrier (BBB) induced by meningitis bacteria is crucial for [...] Read more.

Bacterial meningitis is currently recognized as one of the most important life-threatening infections of the central nervous system (CNS) with high morbidity and mortality, despite the advancements in antimicrobial treatment. The disruption of blood–brain barrier (BBB) induced by meningitis bacteria is crucial for the development of bacterial meningitis. However, the complete mechanisms involving in the BBB disruption remain to be elucidated. Here, we found meningitic Escherichia coli induction of angiopoietin-like 4 (ANGPTL4) in brain microvascular endothelial cells (BMECs) contributes to BBB disruption via ARHGAP5/RhoA/MYL5 signaling cascade, by the demonstration that ANGPTL4 was significantly upregulated in meningitis E. coli infection of BMECs as well as mice, and treatment of the recombinant ANGPTL4 protein led to an increased permeability of the BBB in vitro and in vivo. Moreover, we found that ANGPTL4 did not affect the expression of tight junction proteins involved in BBB disruption, but it increased the expression of MYL5, which was found to have a negative role on the regulation of barrier function during meningitic E. coli infection, through the activation of RhoA signaling pathway. To our knowledge, this is the first report demonstrating the disruption of BBB induced by ANGPTL4 through the ARHGAP5/RhoA/MYL5 pathway, which largely supports the involvement of ANGPTL4 during meningitic E. coli invasion and further expands the theoretical basis for the mechanism of bacterial meningitis. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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Review

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16 pages, 969 KiB

Open AccessEditor’s ChoiceReview

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

by Matthias Kretschmer, Djihane Damoo, Armin Djamei and James Kronstad

Pathogens 2020, 9(1), 19; https://doi.org/10.3390/pathogens9010019 - 24 Dec 2019

Cited by 65 | Viewed by 10732

Abstract

Chloroplasts play a central role in plant immunity through the synthesis of secondary metabolites and defense compounds, as well as phytohormones, such as jasmonic acid and salicylic acid. Additionally, chloroplast metabolism results in the production of reactive oxygen species and nitric oxide as [...] Read more.

Chloroplasts play a central role in plant immunity through the synthesis of secondary metabolites and defense compounds, as well as phytohormones, such as jasmonic acid and salicylic acid. Additionally, chloroplast metabolism results in the production of reactive oxygen species and nitric oxide as defense molecules. The impact of viral and bacterial infections on plastids and chloroplasts has been well documented. In particular, bacterial pathogens are known to introduce effectors specifically into chloroplasts, and many viral proteins interact with chloroplast proteins to influence viral replication and movement, and plant defense. By contrast, clear examples are just now emerging for chloroplast-targeted effectors from fungal and oomycete pathogens. In this review, we first present a brief overview of chloroplast contributions to plant defense and then discuss examples of connections between fungal interactions with plants and chloroplast function. We then briefly consider well-characterized bacterial effectors that target chloroplasts as a prelude to discussing the evidence for fungal effectors that impact chloroplast activities. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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22 pages, 1888 KiB

Open AccessEditor’s ChoiceReview

The Role of Pseudomonas aeruginosa Lipopolysaccharide in Bacterial Pathogenesis and Physiology

by Steven M. Huszczynski, Joseph S. Lam and Cezar M. Khursigara

Pathogens 2020, 9(1), 6; https://doi.org/10.3390/pathogens9010006 - 19 Dec 2019

Cited by 103 | Viewed by 13891

Abstract

The major constituent of the outer membrane of Gram-negative bacteria is lipopolysaccharide (LPS), which is comprised of lipid A, core oligosaccharide, and O antigen, which is a long polysaccharide chain extending into the extracellular environment. Due to the localization of LPS, it is [...] Read more.

The major constituent of the outer membrane of Gram-negative bacteria is lipopolysaccharide (LPS), which is comprised of lipid A, core oligosaccharide, and O antigen, which is a long polysaccharide chain extending into the extracellular environment. Due to the localization of LPS, it is a key molecule on the bacterial cell wall that is recognized by the host to deploy an immune defence in order to neutralize invading pathogens. However, LPS also promotes bacterial survival in a host environment by protecting the bacteria from these threats. This review explores the relationship between the different LPS glycoforms of the opportunistic pathogen Pseudomonas aeruginosa and the ability of this organism to cause persistent infections, especially in the genetic disease cystic fibrosis. We also discuss the role of LPS in facilitating biofilm formation, antibiotic resistance, and how LPS may be targeted by new antimicrobial therapies. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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59 pages, 2178 KiB

Open AccessEditor’s ChoiceReview

Lyme Disease Frontiers: Reconciling Borrelia Biology and Clinical Conundrums

by Vladimir V. Bamm, Jordan T. Ko, Iain L. Mainprize, Victoria P. Sanderson and Melanie K. B. Wills

Pathogens 2019, 8(4), 299; https://doi.org/10.3390/pathogens8040299 - 16 Dec 2019

Cited by 27 | Viewed by 16959

Abstract

Lyme disease is a complex tick-borne zoonosis that poses an escalating public health threat in several parts of the world, despite sophisticated healthcare infrastructure and decades of effort to address the problem. Concepts like the true burden of the illness, from incidence rates [...] Read more.

Lyme disease is a complex tick-borne zoonosis that poses an escalating public health threat in several parts of the world, despite sophisticated healthcare infrastructure and decades of effort to address the problem. Concepts like the true burden of the illness, from incidence rates to longstanding consequences of infection, and optimal case management, also remain shrouded in controversy. At the heart of this multidisciplinary issue are the causative spirochetal pathogens belonging to the Borrelia Lyme complex. Their unusual physiology and versatile lifestyle have challenged microbiologists, and may also hold the key to unlocking mysteries of the disease. The goal of this review is therefore to integrate established and emerging concepts of Borrelia biology and pathogenesis, and position them in the broader context of biomedical research and clinical practice. We begin by considering the conventions around diagnosing and characterizing Lyme disease that have served as a conceptual framework for the discipline. We then explore virulence from the perspective of both host (genetic and environmental predispositions) and pathogen (serotypes, dissemination, and immune modulation), as well as considering antimicrobial strategies (lab methodology, resistance, persistence, and clinical application), and borrelial adaptations of hypothesized medical significance (phenotypic plasticity or pleomorphy). Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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10 pages, 769 KiB

Open AccessReview

Tasked with a Challenging Objective: Why Do Neutrophils Fail to Battle Pseudomonas aeruginosa Biofilms

by Jennifer Geddes-McAlister, Abirami Kugadas and Mihaela Gadjeva

Pathogens 2019, 8(4), 283; https://doi.org/10.3390/pathogens8040283 - 04 Dec 2019

Cited by 14 | Viewed by 4428

Abstract

Multidrug-resistant (MDR) bacterial infections are a leading cause of mortality, affecting approximately 250,000 people in Canada and over 2 million people in the United States, annually. The lack of efficacy of antibiotic-based treatments is often caused by inability of the drug to penetrate [...] Read more.

Multidrug-resistant (MDR) bacterial infections are a leading cause of mortality, affecting approximately 250,000 people in Canada and over 2 million people in the United States, annually. The lack of efficacy of antibiotic-based treatments is often caused by inability of the drug to penetrate bacterial biofilms in sufficient concentrations, posing a major therapeutic challenge. Here, we review the most recent information about the architecture of Pseudomonas aeruginosa biofilms in vivo and describe how advances in imaging and mass spectroscopy analysis bring about novel therapeutic options and challenge existing dogmas. Full article

(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)

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