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Article ; Online: Building an institutional K awardee program at UC Davis through utilization of CTSA resources.

Guo, Betty P / Rainwater, Julie / Neves, Stacey / Anuurad, Erdembileg / Wun, Ted / Berglund, Lars

Journal of clinical and translational science

2021 Volume 5, Issue 1, Page(s) e171

Abstract: NIH offers multiple mentored career development award mechanisms. By building on the UC Davis Clinical and Translational Science Center (CTSC) from its initial NIH funding in 2006, we created an institution-wide K scholar resource. We investigated ... ...

Abstract	NIH offers multiple mentored career development award mechanisms. By building on the UC Davis Clinical and Translational Science Center (CTSC) from its initial NIH funding in 2006, we created an institution-wide K scholar resource. We investigated subsequent NIH funding for K scholars and to what extent CTSC research resources were used. Using NIH RePORTER, we created a database of UC Davis investigators who obtained K01, K08, K23, K25, or K99, as well as institutional KL2 or K12 awards and tracked CTSC research resource use and subsequent funding success. Overall, 94 scholars completed K training between 2007 and 2020, of which 70 participated in one of four institutional, NIH-funded K programs. An additional 103 scholars completed a mentored clinical research training program. Of 94 K awardees, 61 (65%) later achieved NIH funding, with the majority receiving a subsequent individual K award. A higher proportion (73%) of funded scholars used CTSC resources compared to unfunded (48%). Biostatistics and Biomedical Informatics were most commonly used and 55% of scholars used one or more CTSC resource. We conclude that institutional commitment to create a K scholar platform and use of CTSC research resources is associated with high NIH funding rates for early career investigators.
Language	English
Publishing date	2021-08-13
Publishing country	England
Document type	Journal Article
ISSN	2059-8661
ISSN (online)	2059-8661
DOI	10.1017/cts.2021.839
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Article ; Online: Infection-generated electric field in gut epithelium drives bidirectional migration of macrophages.

Sun, Yaohui / Reid, Brian / Ferreira, Fernando / Luxardi, Guillaume / Ma, Li / Lokken, Kristen L / Zhu, Kan / Xu, Gege / Sun, Yuxin / Ryzhuk, Volodymyr / Guo, Betty P / Lebrilla, Carlito B / Maverakis, Emanual / Mogilner, Alex / Zhao, Min

PLoS biology

2019 Volume 17, Issue 4, Page(s) e3000044

Abstract: Many bacterial pathogens hijack macrophages to egress from the port of entry to the lymphatic drainage and/or bloodstream, causing dissemination of life-threatening infections. However, the underlying mechanisms are not well understood. Here, we report ... ...

Abstract	Many bacterial pathogens hijack macrophages to egress from the port of entry to the lymphatic drainage and/or bloodstream, causing dissemination of life-threatening infections. However, the underlying mechanisms are not well understood. Here, we report that Salmonella infection generates directional electric fields (EFs) in the follicle-associated epithelium of mouse cecum. In vitro application of an EF, mimicking the infection-generated electric field (IGEF), induces directional migration of primary mouse macrophages to the anode, which is reversed to the cathode upon Salmonella infection. This infection-dependent directional switch is independent of the Salmonella pathogenicity island 1 (SPI-1) type III secretion system. The switch is accompanied by a reduction of sialic acids on glycosylated surface components during phagocytosis of bacteria, which is absent in macrophages challenged by microspheres. Moreover, enzymatic cleavage of terminally exposed sialic acids reduces macrophage surface negativity and severely impairs directional migration of macrophages in response to an EF. Based on these findings, we propose that macrophages are attracted to the site of infection by a combination of chemotaxis and galvanotaxis; after phagocytosis of bacteria, surface electrical properties of the macrophage change, and galvanotaxis directs the cells away from the site of infection.
MeSH term(s)	Animals ; Bacterial Proteins ; Cell Movement/physiology ; Electric Conductivity ; Electricity ; Epithelium/immunology ; Epithelium/metabolism ; Female ; Gastrointestinal Tract/immunology ; Macrophages/microbiology ; Macrophages/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Phagocytosis ; Salmonella/pathogenicity ; Salmonella Infections/metabolism ; Salmonella Infections/physiopathology ; Taxis Response/physiology
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2019-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3000044
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Article: Rapid genetic analysis of Helicobacter pylori gastric mucosal colonization in suckling mice.

Guo, Betty P / Mekalanos, John J

Proceedings of the National Academy of Sciences of the United States of America

2002 Volume 99, Issue 12, Page(s) 8354–8359

Abstract: Previously described animal models for Helicobacter pylori infection have been limited by cumbersome host requirements (e.g., germ-free conditions or unusual species) or are applicable to only special subsets of H. pylori strains (e.g., fresh clinical ... ...

Abstract	Previously described animal models for Helicobacter pylori infection have been limited by cumbersome host requirements (e.g., germ-free conditions or unusual species) or are applicable to only special subsets of H. pylori strains (e.g., fresh clinical isolates or animal-adapted derivatives). Here, we report that 5- to 6-day-old outbred CD-1 (ICR) suckling mice support 24-h colonization of all H. pylori strains tested (SS1, 26695 SmR-1, 43504 SmR-1, and G27 SmR-1), including lab-passaged strains that cannot be adapted for colonization of adult animals. Total colony-forming units (cfu) recovered from infection with lab-passaged strains did not differ from those with mouse-adapted SS1. We also tested this model's ability to detect colonization defects in strains carrying mutations in known virulence genes by coinfecting with wild-type H. pylori and measuring differential recovery. This competition assay identified colonization defects in several classes of known attenuated mutants, including those defective in acid resistance (ureA), metabolism (frdA), motility (motB), and chemotaxis (cheY). A mutant defective in copA (copper transporting P-type ATPase) is nonattenuated in adult and infant mice. Possibly because of the limited duration of infection, our model did not identify defects in vacuolating cytotoxin (vacA) or gamma-glutamyltranspeptidase (ggt) as attenuating, in contrast to results from other animal models. We also identified a new virulence gene (HP0507) encoding a conserved hypothetical protein, which is important for colonization in our model. The suckling mouse model offers a rapid method to identify colonization defects in any H. pylori strain and may have utility as a new tool for studying immunity to primary infection.
MeSH term(s)	Aging ; Amino Acid Sequence ; Animals ; Animals, Suckling ; DNA Primers ; Gastric Mucosa/microbiology ; Helicobacter pylori/growth & development ; Helicobacter pylori/isolation & purification ; Helicobacter pylori/pathogenicity ; Humans ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; Mutagenesis ; Mutation ; Sequence Alignment ; Sequence Homology, Amino Acid
Chemical Substances	DNA Primers
Language	English
Publishing date	2002-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.122244899
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Article: In situ immune response in brain and kidney during early relapsing fever borreliosis.

Andersson, Marie / Nordstrand, Annika / Shamaei-Tousi, Alireza / Jansson, Anna / Bergström, Sven / Guo, Betty P

Journal of neuroimmunology

2007 Volume 183, Issue 1-2, Page(s) 26–32

Abstract: Characterization of the host immune response during initial pathogenesis of relapsing fever neuroborreliosis would be a key to understanding Borrelia persistence and factors driving the inflammatory process. We analyzed immune cells in brain and kidney ... ...

Abstract	Characterization of the host immune response during initial pathogenesis of relapsing fever neuroborreliosis would be a key to understanding Borrelia persistence and factors driving the inflammatory process. We analyzed immune cells in brain and kidney with the highly invasive B. crocidurae during the first two weeks of murine infection. In both organs, microglia and/or macrophages predominated while T-cell changes were minimal. Compared to kidney, brain neutrophils infiltrated more rapidly and B-cells were essentially absent. Our results indicate that during early neuroborreliosis, brain defense is comprised primarily of innate immune cells while adaptive immunity plays a minor role.
MeSH term(s)	Animals ; Antigens, Differentiation/metabolism ; Borrelia Infections/complications ; Borrelia Infections/immunology ; Brain/immunology ; Immunohistochemistry/methods ; Kidney/immunology ; Macrophages/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neuropil/metabolism ; Relapsing Fever/etiology ; Relapsing Fever/immunology ; Spirochaetales/isolation & purification ; Time Factors
Chemical Substances	Antigens, Differentiation
Language	English
Publishing date	2007-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2006.11.004
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Article: Persistent brain infection and disease reactivation in relapsing fever borreliosis.

Larsson, Christer / Andersson, Marie / Pelkonen, Jenni / Guo, Betty P / Nordstrand, Annika / Bergström, Sven

Microbes and infection

2006 Volume 8, Issue 8, Page(s) 2213–2219

Abstract: Relapsing fever, an infection caused by Borrelia spirochetes, is generally considered a transient, self-limiting disease in humans. The present study reveals that murine infection by Borrelia duttonii can be reactivated after an extended time as a silent ...

Abstract	Relapsing fever, an infection caused by Borrelia spirochetes, is generally considered a transient, self-limiting disease in humans. The present study reveals that murine infection by Borrelia duttonii can be reactivated after an extended time as a silent infection in the brain, with no bacteria appearing in the blood and spirochete load comparable to the numbers in an infected tick. The host cerebral gene expression pattern is indistinguishable from that of uninfected animals, indicating that persistent bacteria are not recognized by the immune system nor cause noticeable tissue damage. Silent infection can be reactivated by immunosuppression, inducing spirochetemia comparable to that of initial densities. B. duttonii has never been found in any host except man and the tick vector. We therefore propose the brain to be a possible natural reservoir of the spirochete. The view of relapsing fever as an acute disease should be extended to include in some cases prolonged persistence, a feature characteristic of the related spirochetal infections Lyme disease and syphilis.
MeSH term(s)	Animals ; Bacteremia ; Borrelia/classification ; Borrelia/isolation & purification ; Brain/microbiology ; Brain Chemistry ; Brain Diseases/microbiology ; Colony Count, Microbial ; Disease Models, Animal ; Gene Expression Profiling ; Immunosuppression ; Male ; Mice ; Mice, Inbred C57BL ; Relapsing Fever/microbiology ; Serotyping
Language	English
Publishing date	2006-07
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2006.04.007
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Article ; Online: Relapsing fever Borrelia binds to neolacto glycans and mediates rosetting of human erythrocytes.

Guo, Betty P / Teneberg, Susann / Münch, Robert / Terunuma, Daiyo / Hatano, Ken / Matsuoka, Koji / Angström, Jonas / Borén, Thomas / Bergström, Sven

Proceedings of the National Academy of Sciences of the United States of America

2009 Volume 106, Issue 46, Page(s) 19280–19285

Abstract: A hallmark of acute relapsing fever borreliosis is severe bacteremia. Some Borrelia species, such as B. duttonii and B. crocidurae, associate with erythrocytes and induce aggregation recognized as erythrocyte rosetting. Erythrocyte rosettes contribute to ...

Abstract	A hallmark of acute relapsing fever borreliosis is severe bacteremia. Some Borrelia species, such as B. duttonii and B. crocidurae, associate with erythrocytes and induce aggregation recognized as erythrocyte rosetting. Erythrocyte rosettes contribute to disease severity by increased tissue invasiveness (such as invasion of CNS and encephalitis), hemorrhaging, and reduced blood flow in affected microcapillaries. Here we report that relapsing fever Borrelia binds to neolacto (Galbeta4GlcNAcbeta3Galbeta4Glcbeta1)-carrying glycoconjugates that are present on human erythrocytes. This interaction is of low affinity but is compensated for by the multivalency of neo-lacto-oligosaccharides on the erythrocyte cell surface. Hence, the protein-carbohydrate interaction is dependent on multivalent neolacto-glycans to mediate binding.
MeSH term(s)	Borrelia/immunology ; Epitopes/immunology ; Erythrocytes/immunology ; Erythrocytes/microbiology ; Globosides/immunology ; Humans ; Polysaccharides/immunology ; Relapsing Fever/immunology ; Relapsing Fever/microbiology ; Rosette Formation/methods
Chemical Substances	Epitopes ; Globosides ; Polysaccharides ; paragloboside (56573-54-7)
Language	English
Publishing date	2009-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0905470106
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Article: Molecular cloning and characterization of two Helicobacter pylori genes coding for plasminogen-binding proteins.

Jönsson, Klas / Guo, Betty P / Monstein, Hans-Jürg / Mekalanos, John J / Kronvall, Göran

Proceedings of the National Academy of Sciences of the United States of America

2004 Volume 101, Issue 7, Page(s) 1852–1857

Abstract: Helicobacter pylori binds a number of host cell proteins, including the plasma protein plasminogen, which is the proenzyme of the serine protease plasmin. Two H. pylori plasminogen-binding proteins have been described; however, no genes were identified. ... ...

Abstract	Helicobacter pylori binds a number of host cell proteins, including the plasma protein plasminogen, which is the proenzyme of the serine protease plasmin. Two H. pylori plasminogen-binding proteins have been described; however, no genes were identified. Here we report the use of a phage display library to clone two genes from the H. pylori CCUG 17874 genome that mediate binding to plasminogen. DNA sequence analysis of one of these genes revealed 96.6% homology with H. pylori 26695 HP0508. A subsequent database search revealed that the amino acid sequence of a lysine-rich C-terminal segment of HP0508 is identical to the C terminus of HP0863. Recombinant proteins expressed from HP0508 and HP0863 bound plasminogen specifically and in a lysine-dependent manner. We designate these genes pgbA and pgbB, respectively. These proteins are expressed by a variety of H. pylori strains, have surface-exposed domains, and do not inhibit plasminogen activation. These results indicate that pgbA and pgbB may allow H. pylori to coat its exterior with plasminogen, which subsequently can be activated to plasmin. The surface acquisition of protease activity may enhance the virulence of H. pylori.
MeSH term(s)	Amino Acid Sequence ; Bacterial Proteins/chemistry ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Carrier Proteins/chemistry ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cloning, Molecular ; Computational Biology ; Fibrinolysin/metabolism ; Genes, Bacterial/genetics ; Helicobacter pylori/genetics ; Lysine/metabolism ; Molecular Sequence Data ; Plasminogen/metabolism ; Protein Binding ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism
Chemical Substances	Bacterial Proteins ; Carrier Proteins ; Recombinant Proteins ; plasminogen-binding protein, bacteria ; Plasminogen (9001-91-6) ; Fibrinolysin (EC 3.4.21.7) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2004-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0307329101
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Article: Complications of pregnancy and transplacental transmission of relapsing-fever borreliosis.

Larsson, Christer / Andersson, Marie / Guo, Betty P / Nordstrand, Annika / Hagerstrand, Inga / Carlsson, Sara / Bergstrom, Sven

The Journal of infectious diseases

2006 Volume 194, Issue 10, Page(s) 1367–1374

Abstract: Relapsing-fever borreliosis caused by Borrelia duttonii is a common cause of complications of pregnancy, miscarriage, and neonatal death in sub-Saharan Africa. We established a murine model of gestational relapsing fever infection for the study of the ... ...

Abstract	Relapsing-fever borreliosis caused by Borrelia duttonii is a common cause of complications of pregnancy, miscarriage, and neonatal death in sub-Saharan Africa. We established a murine model of gestational relapsing fever infection for the study of the pathological development of these complications. We demonstrate that B. duttonii infection during pregnancy results in intrauterine growth retardation, as well as placental damage and inflammation, impaired fetal circulation, and decreased maternal hemoglobin levels. We show that spirochetes frequently cross the maternal-fetal barrier, resulting in congenital infection. Furthermore, we compared the severity of infection in pregnant and nonpregnant mice and show that pregnancy has a protective effect. This model closely parallels the consequences of human gestational infection, and our results provide insight into the mechanisms behind the complications of pregnancy that have been reported in human relapsing-fever infection.
MeSH term(s)	Animals ; Bacteremia ; Borrelia ; Disease Models, Animal ; Female ; Fetal Diseases/microbiology ; Fetal Diseases/pathology ; Fetal Growth Retardation ; Fetal Weight ; Hemoglobins/analysis ; Histocytochemistry ; Infectious Disease Transmission, Vertical ; Mice ; Mice, Inbred C3H ; Placenta/microbiology ; Placenta/pathology ; Placental Circulation ; Pregnancy ; Pregnancy Complications, Infectious/microbiology ; Pregnancy Complications, Infectious/pathology ; Relapsing Fever/microbiology ; Relapsing Fever/pathology ; Relapsing Fever/transmission
Chemical Substances	Hemoglobins
Language	English
Publishing date	2006-11-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1086/508425
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Article: Relapsing fever Borrelia binds to neolacto glycans and mediates rosetting of human erythrocytes

Guo, Betty P / Teneberg, Susann / MÃ¼nch, Robert / Terunuma, Daiyo / Hatano, Ken / Matsuoka, Koji / ÃngstrÃ¶m, Jonas / BorÃ©n, Thomas / BergstrÃ¶m, Sven

Proceedings of the National Academy of Sciences of the United States of America. 2009 Nov. 17, v. 106, no. 46

2009

Abstract	A hallmark of acute relapsing fever borreliosis is severe bacteremia. Some Borrelia species, such as B. duttonii and B. crocidurae, associate with erythrocytes and induce aggregation recognized as erythrocyte rosetting. Erythrocyte rosettes contribute to disease severity by increased tissue invasiveness (such as invasion of CNS and encephalitis), hemorrhaging, and reduced blood flow in affected microcapillaries. Here we report that relapsing fever Borrelia binds to neolacto (GalÎ²4GlcNAcÎ²3GalÎ²4GlcÎ²1)-carrying glycoconjugates that are present on human erythrocytes. This interaction is of low affinity but is compensated for by the multivalency of neo-lacto-oligosaccharides on the erythrocyte cell surface. Hence, the protein-carbohydrate interaction is dependent on multivalent neolacto-glycans to mediate binding.
Keywords	Borrelia ; Lyme disease ; bacteremia ; blood flow ; disease severity ; encephalitis ; erythrocytes ; fever ; glycoconjugates ; humans ; polysaccharides
Language	English
Dates of publication	2009-1117
Size	p. 19280-19285.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0905470106
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