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Article ; Online: Persister-mediated emergence of antimicrobial resistance in agriculture due to antibiotic growth promoters.

Thompson, Noah T / Kitzenberg, David A / Kao, Daniel J

AIMS microbiology

2023 Volume 9, Issue 4, Page(s) 738–756

Abstract: The creation and continued development of antibiotics have revolutionized human health and disease for the past century. The emergence of antimicrobial resistance represents a major threat to human health, and practices that contribute to the development ...

Abstract	The creation and continued development of antibiotics have revolutionized human health and disease for the past century. The emergence of antimicrobial resistance represents a major threat to human health, and practices that contribute to the development of this threat need to be addressed. Since the 1950s, antibiotics have been used in low doses to increase growth and decrease the feed requirement of animal-derived food sources. A consequence of this practice is the accelerated emergence of antimicrobial resistance that can influence human health through its distribution via animal food products. In the laboratory setting, sublethal doses of antibiotics promote the expansion of bacterial persister populations, a low energy, low metabolism phenotype characterized broadly by antibiotic tolerance. Furthermore, the induction of persister bacteria has been positively correlated with an increased emergence of antibiotic-resistant strains. This body of evidence suggests that the use of antibiotics in agriculture at subtherapeutic levels is actively catalyzing the emergence of antimicrobial-resistant bacteria through the expansion of bacterial persister populations, which is potentially leading to increased infections in humans and decreased antibiotic potency. There is an urgent need to address this debilitating effect on antibiotics and its influence on human health. In this review, we summarize the recent literature on the topic of emerging antimicrobial resistance and its association with bacterial persister populations.
Language	English
Publishing date	2023-11-13
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2471-1888
ISSN (online)	2471-1888
DOI	10.3934/microbiol.2023038
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Persister-mediated emergence of antimicrobial resistance in agriculture due to antibiotic growth promoters

Noah T Thompson / David A Kitzenberg / Daniel J Kao

AIMS Microbiology, Vol 9, Iss 4, Pp 738-

2023 Volume 756

Abstract	The creation and continued development of antibiotics have revolutionized human health and disease for the past century. The emergence of antimicrobial resistance represents a major threat to human health, and practices that contribute to the development of this threat need to be addressed. Since the 1950s, antibiotics have been used in low doses to increase growth and decrease the feed requirement of animal-derived food sources. A consequence of this practice is the accelerated emergence of antimicrobial resistance that can influence human health through its distribution via animal food products. In the laboratory setting, sublethal doses of antibiotics promote the expansion of bacterial persister populations, a low energy, low metabolism phenotype characterized broadly by antibiotic tolerance. Furthermore, the induction of persister bacteria has been positively correlated with an increased emergence of antibiotic-resistant strains. This body of evidence suggests that the use of antibiotics in agriculture at subtherapeutic levels is actively catalyzing the emergence of antimicrobial-resistant bacteria through the expansion of bacterial persister populations, which is potentially leading to increased infections in humans and decreased antibiotic potency. There is an urgent need to address this debilitating effect on antibiotics and its influence on human health. In this review, we summarize the recent literature on the topic of emerging antimicrobial resistance and its association with bacterial persister populations.
Keywords	resistance ; agriculture ; persistence ; tolerance ; antibiotics ; catalyze ; bacteria ; antimicrobial resistance ; antibiotic growth promoters ; subtherapeutic ; Microbiology ; QR1-502
Subject code	610
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	AIMS Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Adenosine Awakens Metabolism to Enhance Growth-Independent Killing of Tolerant and Persister Bacteria across Multiple Classes of Antibiotics.

Kitzenberg, David A / Lee, J Scott / Mills, Krista B / Kim, Ju-Sim / Liu, Lin / Vázquez-Torres, Andrés / Colgan, Sean P / Kao, Daniel J

mBio

2022 Volume 13, Issue 3, Page(s) e0048022

Abstract: Metabolic and growth arrest are primary drivers of antibiotic tolerance and persistence in clinically diverse bacterial pathogens. We recently showed that adenosine (ADO) suppresses bacterial growth under nutrient-limiting conditions. In the current ... ...

Abstract	Metabolic and growth arrest are primary drivers of antibiotic tolerance and persistence in clinically diverse bacterial pathogens. We recently showed that adenosine (ADO) suppresses bacterial growth under nutrient-limiting conditions. In the current study, we show that despite the growth-suppressive effect of ADO, extracellular ADO enhances antibiotic killing in both Gram-negative and Gram-positive bacteria by up to 5 orders of magnitude. The ADO-potentiated antibiotic activity is dependent on purine salvage and is paralleled with a suppression of guanosine tetraphosphate synthesis and the massive accumulation of ATP and GTP. These changes in nucleoside phosphates coincide with transient increases in rRNA transcription and proton motive force. The potentiation of antibiotic killing by ADO is manifested against bacteria grown under both aerobic and anaerobic conditions, and it is exhibited even in the absence of alternative electron acceptors such as nitrate. ADO potentiates antibiotic killing by generating proton motive force and can occur independently of an ATP synthase. Bacteria treated with an uncoupler of oxidative phosphorylation and NADH dehydrogenase-deficient bacteria are refractory to the ADO-potentiated killing, suggesting that the metabolic awakening induced by this nucleoside is intrinsically dependent on an energized membrane. In conclusion, ADO represents a novel example of metabolite-driven but growth-independent means to reverse antibiotic tolerance. Our investigations identify the purine salvage pathway as a potential target for the development of therapeutics that may improve infection clearance while reducing the emergence of antibiotic resistance.
MeSH term(s)	Adenosine/pharmacology ; Adenosine Triphosphate/metabolism ; Anti-Bacterial Agents/pharmacology ; Escherichia coli/genetics ; Guanosine Triphosphate ; Microbial Sensitivity Tests ; NADH Dehydrogenase/metabolism ; Nucleosides/pharmacology ; Salmonella enterica/metabolism
Chemical Substances	Anti-Bacterial Agents ; Nucleosides ; Guanosine Triphosphate (86-01-1) ; Adenosine Triphosphate (8L70Q75FXE) ; NADH Dehydrogenase (EC 1.6.99.3) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2022-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.00480-22
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Article: Creatine kinase in ischemic and inflammatory disorders.

Kitzenberg, David / Colgan, Sean P / Glover, Louise E

Clinical and translational medicine

2016 Volume 5, Issue 1, Page(s) 31

Abstract: The creatine/phosphocreatine pathway plays a conserved and central role in energy metabolism. Compartmentalization of specific creatine kinase enzymes permits buffering of local high energy phosphates in a thermodynamically favorable manner, enabling ... ...

Abstract	The creatine/phosphocreatine pathway plays a conserved and central role in energy metabolism. Compartmentalization of specific creatine kinase enzymes permits buffering of local high energy phosphates in a thermodynamically favorable manner, enabling both rapid energy storage and energy transfer within the cell. Augmentation of this metabolic pathway by nutritional creatine supplementation has been shown to elicit beneficial effects in a number of diverse pathologies, particularly those that incur tissue ischemia, hypoxia or oxidative stress. In these settings, creatine and phosphocreatine prevent depletion of intracellular ATP and internal acidification, enhance post-ischemic recovery of protein synthesis and promote free radical scavenging and stabilization of cellular membranes. The creatine kinase energy system is itself further regulated by hypoxic signaling, highlighting the existence of endogenous mechanisms in mammals that can enhance creatine metabolism during oxygen deprivation to promote tissue resolution and homeostasis. Here, we review recent insights into the creatine kinase pathway, and provide rationale for dietary creatine supplementation in human ischemic and inflammatory pathologies.
Language	English
Publishing date	2016-08-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2697013-2
ISSN	2001-1326
ISSN	2001-1326
DOI	10.1186/s40169-016-0114-5
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Article ; Online: Essential role for epithelial HIF-mediated xenophagy in control of Salmonella infection and dissemination.

Dowdell, Alexander S / Cartwright, Ian M / Kitzenberg, David A / Kostelecky, Rachael E / Mahjoob, Omemh / Saeedi, Bejan J / Welch, Nichole / Glover, Louise E / Colgan, Sean P

Cell reports

2022 Volume 40, Issue 13, Page(s) 111409

Abstract: The intestinal mucosa exists in a state of "physiologic hypoxia," where oxygen tensions are markedly lower than those in other tissues. Intestinal epithelial cells (IECs) have evolved to maintain homeostasis in this austere environment through oxygen- ... ...

Abstract	The intestinal mucosa exists in a state of "physiologic hypoxia," where oxygen tensions are markedly lower than those in other tissues. Intestinal epithelial cells (IECs) have evolved to maintain homeostasis in this austere environment through oxygen-sensitive transcription factors, including hypoxia-inducible factors (HIFs). Using an unbiased chromatin immunoprecipitation (ChIP) screen for HIF-1 targets, we identify autophagy as a major pathway induced by hypoxia in IECs. One important function of autophagy is to defend against intracellular pathogens, termed "xenophagy." Analysis reveals that HIF is a central regulator of autophagy and that in vitro infection of IECs with Salmonella Typhimurium results in induction of HIF transcriptional activity that tracks with the clearance of intracellular Salmonella. Work in vivo demonstrates that IEC-specific deletion of HIF compromises xenophagy and exacerbates bacterial dissemination. These results reveal that the interaction between hypoxia, HIF, and xenophagy is an essential innate immune component for the control of intracellular pathogens.
MeSH term(s)	Humans ; Hypoxia/metabolism ; Intestinal Mucosa/metabolism ; Macroautophagy ; Oxygen/metabolism ; Salmonella Infections/metabolism ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-09-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111409
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Article ; Online: Forward Genetic Approach to Uncover Stress Resistance Genes in Mice - A High-throughput Screen in ES Cells.

Ludwig, Michael / Kitzenberg, David / Chick, Wallace S

Journal of visualized experiments : JoVE

2015 , Issue 105

Abstract: Phenotype-driven genetic screens in mice is a powerful technique to uncover gene functions, but are often hampered by extremely high costs, which severely limits its potential. We describe here the use of mouse embryonic stem (ES) cells as surrogate ... ...

Abstract	Phenotype-driven genetic screens in mice is a powerful technique to uncover gene functions, but are often hampered by extremely high costs, which severely limits its potential. We describe here the use of mouse embryonic stem (ES) cells as surrogate cells to screen for a phenotype of interest and subsequently introduce these cells into a host embryo to develop into a living mouse carrying the phenotype. This method provides (1) a cost effective, high-throughput platform for genetic screen in mammalian cells; (2) a rapid way to identify the mutated genes and verify causality; and (3) a short-cut to develop mouse mutants directly from these selected ES cells for whole animal studies. We demonstrated the use of paraquat (PQ) to select resistant mutants and identify mutations that confer oxidative stress resistance. Other stressors or cytotoxic compounds may also be used to screen for resistant mutants to uncover novel genetic determinants of a variety of cellular stress resistance.
Language	English
Publishing date	2015-11-11
Publishing country	United States
Document type	Journal Article
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/53062
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Article ; Online: Dietary restriction in C. elegans: recent advances.

Cypser, James R / Kitzenberg, David / Park, Sang-Kyu

Experimental gerontology

2013 Volume 48, Issue 10, Page(s) 1014–1017

Abstract: The nematode Caenorhabditis elegans continues to serve as a useful model of life extension caused by dietary restriction. Using this model, downstream effectors of dietary restriction-induced longevity have been elucidated, including neuropeptides and ... ...

Abstract	The nematode Caenorhabditis elegans continues to serve as a useful model of life extension caused by dietary restriction. Using this model, downstream effectors of dietary restriction-induced longevity have been elucidated, including neuropeptides and cell-surface receptors. Although it remains possible that different forms of dietary restriction may utilize both specific and overlapping mechanisms to promote longevity, the nematode model has revealed roles for autophagy, metabolic energy-sensing and the hypoxic response. The nematode has also been used to identify specific tissues required for life extension via DR, including coelomocytes, intestine, and neurons.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/physiology ; Caloric Restriction ; DNA-Binding Proteins/physiology ; Gene Expression/physiology ; Longevity/physiology ; Neuropeptides/physiology ; Organ Specificity/physiology ; Signal Transduction/physiology ; Stress, Physiological/physiology ; TOR Serine-Threonine Kinases/physiology ; Transcription Factors/physiology
Chemical Substances	Caenorhabditis elegans Proteins ; DNA-Binding Proteins ; Neuropeptides ; Transcription Factors ; skn-1 protein, C elegans (148733-36-2) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2013-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	390992-x
ISSN	1873-6815 ; 0531-5565
ISSN (online)	1873-6815
ISSN	0531-5565
DOI	10.1016/j.exger.2013.02.018
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Zs.A 579: Show issues

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Article ; Online: Movement decline across lifespan of Caenorhabditis elegans mutants in the insulin/insulin-like signaling pathway.

Newell Stamper, Breanne L / Cypser, James R / Kechris, Katerina / Kitzenberg, David Alan / Tedesco, Patricia M / Johnson, Thomas E

Aging cell

2017 Volume 17, Issue 1

Abstract: Research in aging biology has identified several pathways that are molecularly conserved across species that extend lifespan when mutated. The insulin/insulin-like signaling (IIS) pathway is one of the most widely studied of these. It has been assumed ... ...

Abstract	Research in aging biology has identified several pathways that are molecularly conserved across species that extend lifespan when mutated. The insulin/insulin-like signaling (IIS) pathway is one of the most widely studied of these. It has been assumed that extending lifespan also extends healthspan (the period of life with minimal functional loss). However, data supporting this assumption conflict and recent evidence suggest that life extension may, in and of itself, extend the frail period. In this study, we use Caenorhabditis elegans to further probe the link between lifespan and healthspan. Using movement decline as a measure of health, we assessed healthspan across the entire lifespan in nine IIS pathway mutants. In one series of experiments, we studied healthspan in mass cultures, and in another series, we studied individuals longitudinally. We found that long-lived mutants display prolonged mid-life movement and do not prolong the frailty period. Lastly, we observed that early-adulthood movement was not predictive of late-life movement or survival, within identical phenotypes. Overall, these observations show that extending lifespan does not prolong the period of frailty. Both genotype and a stochastic component modulate aging, and movement late in life is more variable than early-life movement.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Insulin/metabolism ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Longevity/genetics ; Mutation/genetics ; Receptor, Insulin/genetics ; Receptor, Insulin/metabolism ; Signal Transduction/genetics
Chemical Substances	Caenorhabditis elegans Proteins ; Insulin ; Insulin-Like Growth Factor I (67763-96-6) ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2017-12-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12704
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Zs.A 6581: Show issues

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Article: Forward genetic approach to uncover stress resistance genes in mice — a high-throughput screen in es cells

Ludwig, Michael / Kitzenberg, David / Chick, Wallace S

Journal of visualized experiments. 2015 Nov. 11, , no. 105

2015

Abstract	Phenotype-driven genetic screens in mice is a powerful technique to uncover gene functions, but are often hampered by extremely high costs, which severely limits its potential. We describe here the use of mouse embryonic stem (ES) cells as surrogate cells to screen for a phenotype of interest and subsequently introduce these cells into a host embryo to develop into a living mouse carrying the phenotype. This method provides (1) a cost effective, high-throughput platform for genetic screen in mammalian cells; (2) a rapid way to identify the mutated genes and verify causality; and (3) a short-cut to develop mouse mutants directly from these selected ES cells for whole animal studies. We demonstrated the use of paraquat (PQ) to select resistant mutants and identify mutations that confer oxidative stress resistance. Other stressors or cytotoxic compounds may also be used to screen for resistant mutants to uncover novel genetic determinants of a variety of cellular stress resistance.
Keywords	cost effectiveness ; cytotoxicity ; embryo (animal) ; mice ; mutants ; mutation ; oxidative stress ; paraquat ; phenotype ; resistance genes ; stress tolerance
Language	English
Dates of publication	2015-1111
Size	p. e53062.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/53062
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Oral vitamin B

Kelly, Caleb J / Alexeev, Erica E / Farb, Linda / Vickery, Thad W / Zheng, Leon / Eric L, Campbell / Kitzenberg, David A / Battista, Kayla D / Kominsky, Douglas J / Robertson, Charles E / Frank, Daniel N / Stabler, Sally P / Colgan, Sean P

Gut microbes

2019 Volume 10, Issue 6, Page(s) 654–662

Abstract: ... Vitamin ... ...

Abstract	Vitamin B
MeSH term(s)	Administration, Oral ; Animals ; Bacteroides/drug effects ; Bacteroides/growth & development ; Cecum/chemistry ; Colitis/chemically induced ; Colitis/diet therapy ; Corrinoids/analysis ; Dextran Sulfate/toxicity ; Dietary Supplements/analysis ; Fatty Acids, Volatile/analysis ; Feces/chemistry ; Feces/microbiology ; Gastrointestinal Microbiome/drug effects ; Mice, Inbred C57BL ; Vitamin B 12/administration & dosage ; Vitamin B 12/pharmacology ; Vitamin B Complex/administration & dosage ; Vitamin B Complex/pharmacology
Chemical Substances	Corrinoids ; Fatty Acids, Volatile ; Vitamin B Complex (12001-76-2) ; Dextran Sulfate (9042-14-2) ; Vitamin B 12 (P6YC3EG204)
Language	English
Publishing date	2019-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1949-0984
ISSN (online)	1949-0984
DOI	10.1080/19490976.2019.1597667
Database	MEDical Literature Analysis and Retrieval System OnLINE

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