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Article ; Online: Take my breath away: studying pathogen invasion of the human lung using primary tissue models.

Dragan, Amanda L / Voth, Daniel E

Pathogens and disease

2021 Volume 79, Issue 4

Abstract: The human pulmonary environment is complex, containing a matrix of cells, including fibroblasts, epithelial cells, interstitial macrophages, alveolar macrophages and neutrophils. When confronted with foreign material or invading pathogens, these cells ... ...

Abstract	The human pulmonary environment is complex, containing a matrix of cells, including fibroblasts, epithelial cells, interstitial macrophages, alveolar macrophages and neutrophils. When confronted with foreign material or invading pathogens, these cells mount a robust response. Nevertheless, many bacterial pathogens with an intracellular lifecycle stage exploit this environment for replication and survival. These include, but are not limited to, Coxiella burnetii, Legionella pneumophila, Yersinia pestis, Mycobacterium tuberculosis and Staphylococcus aureus. Currently, few human disease-relevant model systems exist for studying host-pathogen interactions during these bacterial infections in the lung. Here, we present two novel infection platforms, human alveolar macrophages (hAMs) and human precision-cut lung slices (hPCLS), along with an up-to-date synopsis of research using said models. Additionally, alternative uses for these systems in the absence of pathogen involvement are presented, such as tissue banking and further characterization of the human lung environment. Overall, hAMs and hPCLS allow novel human disease-relevant investigations that other models, such as cell lines and animal models, cannot completely provide.
MeSH term(s)	Bacterial Infections/immunology ; Bacterial Infections/microbiology ; Bacterial Infections/pathology ; Coxiella burnetii/growth & development ; Coxiella burnetii/immunology ; Coxiella burnetii/pathogenicity ; Host-Pathogen Interactions/immunology ; Humans ; Legionella pneumophila/growth & development ; Legionella pneumophila/immunology ; Legionella pneumophila/pathogenicity ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Lung Diseases/immunology ; Lung Diseases/microbiology ; Lung Diseases/pathology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/microbiology ; Macrophages, Alveolar/pathology ; Microtomy ; Models, Biological ; Mycobacterium tuberculosis/growth & development ; Mycobacterium tuberculosis/immunology ; Mycobacterium tuberculosis/pathogenicity ; Primary Cell Culture ; Staphylococcus aureus/growth & development ; Staphylococcus aureus/immunology ; Staphylococcus aureus/pathogenicity ; Tissue Banks ; Tissue Culture Techniques ; Yersinia pestis/growth & development ; Yersinia pestis/immunology ; Yersinia pestis/pathogenicity
Language	English
Publishing date	2021-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1093/femspd/ftab016
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Editorial: Obligate intracellular bacteria: Evasion and adaptative tactics shaping the host-pathogen interface.

Simões, Isaura / Voth, Daniel E / Mota, Luís Jaime

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 965554

MeSH term(s)	Bacteria ; Host-Pathogen Interactions
Language	English
Publishing date	2022-07-14
Publishing country	Switzerland
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.965554
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Article ; Online: Breathe In, Breathe Out: Metabolic Regulation of Lung Macrophages in Host Defense Against Bacterial Infection.

Andrews, J Tucker / Voth, Daniel E / Huang, Stanley Ching-Cheng / Huang, Lu

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 934460

Abstract: Lung macrophages are substantially distinct from other tissue-resident macrophages. They act as frontier sentinels of the alveolar-blood interface and are constantly exposed to various pathogens. Additionally, they precisely regulate immune responses ... ...

Abstract	Lung macrophages are substantially distinct from other tissue-resident macrophages. They act as frontier sentinels of the alveolar-blood interface and are constantly exposed to various pathogens. Additionally, they precisely regulate immune responses under homeostatic and pathological conditions to curtail tissue damage while containing respiratory infections. As a highly heterogeneous population, the phenotypes and functions of lung macrophages with differing developmental ontogenies are linked to both intrinsic and extrinsic metabolic processes. Importantly, targeting these metabolic pathways greatly impacts macrophage functions, which in turn leads to different disease outcomes in the lung. In this review, we will discuss underlying metabolic regulation of lung macrophage subsets and how metabolic circuits, together with epigenetic modifications, dictate lung macrophage function during bacterial infection.
MeSH term(s)	Bacterial Infections/pathology ; Humans ; Immunity ; Lung/microbiology ; Macrophages ; Macrophages, Alveolar
Language	English
Publishing date	2022-07-08
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.934460
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Article ; Online: Coxiella burnetii: international pathogen of mystery.

Dragan, Amanda L / Voth, Daniel E

Microbes and infection

2019 Volume 22, Issue 3, Page(s) 100–110

Abstract: Coxiella burnetii is an intracellular bacterium that causes acute and chronic Q fever. This unique pathogen has been historically challenging to study due to obstacles in genetically manipulating the organism and the inability of small animal models to ... ...

Abstract	Coxiella burnetii is an intracellular bacterium that causes acute and chronic Q fever. This unique pathogen has been historically challenging to study due to obstacles in genetically manipulating the organism and the inability of small animal models to fully mimic human Q fever. Here, we review the current state of C. burnetii research, highlighting new approaches that allow the mechanistic study of infection in disease relevant settings.
MeSH term(s)	Animals ; Coxiella burnetii/pathogenicity ; Cytoplasm/microbiology ; Disease Models, Animal ; Global Health ; Humans ; Macrophages/microbiology ; Q Fever/microbiology
Language	English
Publishing date	2019-09-28
Publishing country	France
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2019.09.001
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Zs.A 5014: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Coxiella burnetii: A Pathogenic Intracellular Acidophile.

Shaw, Edward I / Voth, Daniel E

Microbiology (Reading, England)

2018 Volume 165, Issue 1, Page(s) 1–3

Abstract: Coxiella burnetii is an obligate intracellular pathogen that causes acute and chronic Q fever. C. burnetii grows within a eukaryotic host cell in a vacuole highly similar to a phagolysosome. Found worldwide, this environmentally stable pathogen is ... ...

Abstract	Coxiella burnetii is an obligate intracellular pathogen that causes acute and chronic Q fever. C. burnetii grows within a eukaryotic host cell in a vacuole highly similar to a phagolysosome. Found worldwide, this environmentally stable pathogen is maintained in nature via chronic infection of ruminants. Aerosol-mediated infection of humans results in infection and usurpation of alveolar macrophages through mechanisms using a bacterial Type 4B Secretion System and secreted effector proteins. Advances in axenic culture and genetic systems are changing our understanding of the pathogen's physiology and intimate molecular manipulations of host cells during infection.
MeSH term(s)	Acids/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Bacterial Secretion Systems/genetics ; Bacterial Secretion Systems/metabolism ; Coxiella burnetii/classification ; Coxiella burnetii/genetics ; Coxiella burnetii/isolation & purification ; Coxiella burnetii/metabolism ; Genome, Bacterial ; Humans ; Hydrogen-Ion Concentration ; Phylogeny ; Q Fever/microbiology ; Vacuoles/chemistry ; Vacuoles/microbiology
Chemical Substances	Acids ; Bacterial Proteins ; Bacterial Secretion Systems
Language	English
Publishing date	2018-11-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1180712-x
ISSN	1465-2080 ; 1350-0872
ISSN (online)	1465-2080
ISSN	1350-0872
DOI	10.1099/mic.0.000707
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Ud II Zs.140: Show issues

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Article ; Online: Coxiella burnetii Requires Host Eukaryotic Initiation Factor 2α Activity for Efficient Intracellular Replication.

Brann, Katelynn R / Fullerton, Marissa S / Voth, Daniel E

Infection and immunity

2020 Volume 88, Issue 7

Abstract: ... Coxiella ... ...

Abstract	Coxiella burnetii
MeSH term(s)	Activating Transcription Factor 6/metabolism ; Bacterial Secretion Systems ; Coxiella burnetii/physiology ; Eukaryotic Initiation Factor-2/metabolism ; Histones/metabolism ; Host-Pathogen Interactions ; Humans ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/microbiology ; Protein Transport ; Q Fever/metabolism ; Q Fever/microbiology ; Transcription Factor CHOP/metabolism
Chemical Substances	ATF6 protein, human ; Activating Transcription Factor 6 ; Bacterial Secretion Systems ; DDIT3 protein, human ; Eukaryotic Initiation Factor-2 ; Histones ; Transcription Factor CHOP (147336-12-7)
Language	English
Publishing date	2020-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00096-20
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Zs.A 684: Show issues

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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: MicroRNAs Contribute to Host Response to

Sachan, Madhur / Brann, Katelynn R / Fullerton, Marissa S / Voth, Daniel E / Raghavan, Rahul

Infection and immunity

2022 Volume 91, Issue 1, Page(s) e0019922

Abstract: MicroRNAs (miRNAs), a class of small noncoding RNAs, are critical to gene regulation in eukaryotes. They are involved in modulating a variety of physiological processes, including the host response to intracellular infections. Little is known about miRNA ...

Abstract	MicroRNAs (miRNAs), a class of small noncoding RNAs, are critical to gene regulation in eukaryotes. They are involved in modulating a variety of physiological processes, including the host response to intracellular infections. Little is known about miRNA functions during infection by Coxiella burnetii, the causative agent of human Q fever. This bacterial pathogen establishes a large replicative vacuole within macrophages by manipulating host processes such as apoptosis and autophagy. We investigated miRNA expression in C. burnetii-infected macrophages and identified several miRNAs that were down- or upregulated during infection. We further explored the functions of miR-143-3p, an miRNA whose expression is downregulated in macrophages infected with C. burnetii, and show that increasing the abundance of this miRNA in human cells results in increased apoptosis and reduced autophagy-conditions that are unfavorable to C. burnetii intracellular growth. In sum, this study demonstrates that C. burnetii infection elicits a robust miRNA-based host response, and because miR-143-3p promotes apoptosis and inhibits autophagy, downregulation of miR-143-3p expression during C. burnetii infection likely benefits the pathogen.
MeSH term(s)	Humans ; Coxiella burnetii/physiology ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Host-Pathogen Interactions/genetics ; Q Fever/genetics ; Q Fever/metabolism ; Macrophages/microbiology ; Vacuoles/microbiology
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/iai.00199-22
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Zs.A 684: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Characterization of Early Stages of Human Alveolar Infection by the Q Fever Agent

Dragan, Amanda L / Kurten, Richard C / Voth, Daniel E

Infection and immunity

2019 Volume 87, Issue 5

Abstract: Human Q fever is caused by the intracellular bacterial ... ...

Abstract	Human Q fever is caused by the intracellular bacterial pathogen
MeSH term(s)	Coxiella burnetii/pathogenicity ; Host-Pathogen Interactions/immunology ; Humans ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/microbiology ; Macrophages, Alveolar/pathology ; Q Fever/immunology ; Q Fever/microbiology ; Q Fever/physiopathology
Language	English
Publishing date	2019-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00028-19
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 684: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: ThANKs for the repeat: Intracellular pathogens exploit a common eukaryotic domain.

Voth, Daniel E

Cellular logistics

2011 Volume 1, Issue 4, Page(s) 128–132

Abstract: Bacterial pathogens are renowned cell biologists that subvert detrimental host responses by manipulating eukaryotic protein function. A select group of pathogens use a specialized type IV secretion system (T4SS) as a conduit to deliver an arsenal of ... ...

Abstract	Bacterial pathogens are renowned cell biologists that subvert detrimental host responses by manipulating eukaryotic protein function. A select group of pathogens use a specialized type IV secretion system (T4SS) as a conduit to deliver an arsenal of proteins into the host cytosol where they interact with host proteins. The translocated "effectors" have garnered increased attention because they uncover novel aspects of host-pathogen interactions at the subcellular level. This review presents a group of effectors termed Anks that possess eukaryotic-like ankyrin repeat domains that mediate proteinprotein interactions and are critical for effector function. Interestingly, most known prokaryotic Anks are produced by bacteria that devote much of their time to replicating inside eukaryotic cells. Ank proteins represent a fascinating and versatile family of effectors exploited by bacterial pathogens and are proving useful as tools to study eukaryotic cell biology.
Language	English
Publishing date	2011-07-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2682440-1
ISSN	2159-2799 ; 2159-2780
ISSN (online)	2159-2799
ISSN	2159-2780
DOI	10.4161/cl.1.4.18738
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Article ; Online: Neurotransmitter System-Targeting Drugs Antagonize Growth of the Q Fever Agent, Coxiella burnetii, in Human Cells.

Fullerton, Marissa S / Colonne, Punsiri M / Dragan, Amanda L / Brann, Katelynn R / Kurten, Richard C / Voth, Daniel E

mSphere

2021 Volume 6, Issue 4, Page(s) e0044221

Abstract: Coxiella burnetii is a highly infectious, intracellular, Gram-negative bacterial pathogen that causes human Q fever, an acute flu-like illness that can progress to chronic endocarditis. C. burnetii is transmitted to humans via aerosols and has long been ... ...

Abstract	Coxiella burnetii is a highly infectious, intracellular, Gram-negative bacterial pathogen that causes human Q fever, an acute flu-like illness that can progress to chronic endocarditis. C. burnetii is transmitted to humans via aerosols and has long been considered a potential biological warfare agent. Although antibiotics, such as doxycycline, effectively treat acute Q fever, a recently identified antibiotic-resistant strain demonstrates the ability of C. burnetii to resist traditional antimicrobials, and chronic disease is extremely difficult to treat with current options. These findings highlight the need for new Q fever therapeutics, and repurposed drugs that target eukaryotic functions to prevent bacterial replication are of increasing interest in infectious disease. To identify this class of anti-C. burnetii therapeutics, we screened a library of 727 FDA-approved or late-stage clinical trial compounds using a human macrophage-like cell model of infection. Eighty-eight compounds inhibited bacterial replication, including known antibiotics, antipsychotic or antidepressant treatments, antihistamines, and several additional compounds used to treat a variety of conditions. The majority of identified anti-C. burnetii compounds target host neurotransmitter system components. Serotoninergic, dopaminergic, and adrenergic components are among the most highly represented targets and potentially regulate macrophage activation, cytokine production, and autophagy. Overall, our screen identified multiple host-directed compounds that can be pursued for potential use as anti-C. burnetii drugs.
MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Coxiella burnetii/drug effects ; Coxiella burnetii/genetics ; Coxiella burnetii/growth & development ; High-Throughput Screening Assays/methods ; Host-Pathogen Interactions/drug effects ; Humans ; Neurotransmitter Agents/antagonists & inhibitors ; Pharmaceutical Preparations/analysis ; Pharmacology ; Q Fever/drug therapy ; Q Fever/microbiology ; Small Molecule Libraries/pharmacology ; THP-1 Cells
Chemical Substances	Anti-Bacterial Agents ; Neurotransmitter Agents ; Pharmaceutical Preparations ; Small Molecule Libraries
Language	English
Publishing date	2021-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-5042
ISSN (online)	2379-5042
DOI	10.1128/mSphere.00442-21
Database	MEDical Literature Analysis and Retrieval System OnLINE

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