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Article: Tamoxifen administration induces histopathologic changes within the lungs of Cre-recombinase-negative mice: A case report

Wyatt, Kara D / Sakamoto, Kaori / Watford, Wendy T

Laboratory animals. 2022 June, v. 56, no. 3

2022

Abstract: Tamoxifen is commonly used as a cancer treatment in humans and for inducing genetic alterations using Cre-lox mouse models in the research setting. However, the extent of tamoxifen off-target effects in animal research is underappreciated. Here, we ... ...

Abstract	Tamoxifen is commonly used as a cancer treatment in humans and for inducing genetic alterations using Cre-lox mouse models in the research setting. However, the extent of tamoxifen off-target effects in animal research is underappreciated. Here, we report significant changes in cellular infiltration in Cre-recombinase-negative mice treated with tamoxifen intraperitoneally. These changes were noted in the lungs, which were characterized by the presence of alveolitis, vasculitis, and pleuritis. Despite significant immunological changes in response to tamoxifen treatment, clinical symptoms were not observed. This study provides a cautionary note that tamoxifen treatment alone leads to histologic alterations that may obscure research interpretations and further highlights the need for the development of alternative mouse models for inducible Cre-mediated deletion.
Keywords	alveolitis ; animal research ; cancer therapy ; case studies ; histology ; histopathology ; laboratories ; mice ; pleurisy ; tamoxifen ; vasculitis
Language	English
Dates of publication	2022-06
Size	p. 297-303.
Publishing place	SAGE Publications
Document type	Article
ZDB-ID	391008-8
ISSN	1758-1117 ; 0023-6772
ISSN (online)	1758-1117
ISSN	0023-6772
DOI	10.1177/00236772211042968
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Influenza-induced Tpl2 expression within alveolar epithelial cells is dispensable for host viral control and anti-viral immunity.

Wyatt, Kara D / Sarr, Demba / Sakamoto, Kaori / Watford, Wendy T

PloS one

2022 Volume 17, Issue 1, Page(s) e0262832

Abstract: Tumor progression locus 2 (Tpl2) is a serine/threonine kinase that regulates the expression of inflammatory mediators in response to Toll-like receptors (TLR) and cytokine receptors. Global ablation of Tpl2 leads to severe disease in response to ... ...

Abstract	Tumor progression locus 2 (Tpl2) is a serine/threonine kinase that regulates the expression of inflammatory mediators in response to Toll-like receptors (TLR) and cytokine receptors. Global ablation of Tpl2 leads to severe disease in response to influenza A virus (IAV) infection, characterized by respiratory distress, and studies in bone marrow chimeric mice implicated Tpl2 in non-hematopoietic cells. Lung epithelial cells are primary targets and replicative niches of influenza viruses; however, the specific regulation of antiviral responses by Tpl2 within lung epithelial cells has not been investigated. Herein, we show that Tpl2 is basally expressed in primary airway epithelial cells and that its expression increases in both type I and type II airway epithelial cells (AECI and AECII) in response to influenza infection. We used Nkx2.1-cre to drive Tpl2 deletion within pulmonary epithelial cells to delineate epithelial cell-specific functions of Tpl2 during influenza infection in mice. Although modest increases in morbidity and mortality were attributed to cre-dependent deletion in lung epithelial cells, no alterations in host cytokine production or lung pathology were observed. In vitro, Tpl2 inhibition within the type I airway epithelial cell line, LET1, as well as genetic ablation in primary airway epithelial cells did not alter cytokine production. Overall, these findings establish that Tpl2-dependent defects in cells other than AECs are primarily responsible for the morbidity and mortality seen in influenza-infected mice with global Tpl2 ablation.
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Animals ; Cytokines/metabolism ; Disease Models, Animal ; Dogs ; Female ; Host Microbial Interactions/genetics ; Influenza A virus ; MAP Kinase Kinase Kinases/genetics ; MAP Kinase Kinase Kinases/metabolism ; Madin Darby Canine Kidney Cells ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Orthomyxoviridae Infections/blood ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/mortality ; Orthomyxoviridae Infections/virology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
Chemical Substances	Cytokines ; Proto-Oncogene Proteins ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; Map3k8 protein, mouse (EC 2.7.11.25)
Language	English
Publishing date	2022-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0262832
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Tumor Progression Locus 2 Protects against Acute Respiratory Distress Syndrome in Influenza A Virus-Infected Mice.

Latha, Krishna / Rao, Sanjana / Sakamoto, Kaori / Watford, Wendy T

Microbiology spectrum

2022 Volume 10, Issue 5, Page(s) e0113622

Abstract: Excessive inflammation in patients with severe influenza disease may lead to acute lung injury that results in acute respiratory distress syndrome (ARDS). ARDS is associated with alveolar damage and pulmonary edema that severely impair gas exchange, ... ...

Abstract	Excessive inflammation in patients with severe influenza disease may lead to acute lung injury that results in acute respiratory distress syndrome (ARDS). ARDS is associated with alveolar damage and pulmonary edema that severely impair gas exchange, leading to hypoxia. With no existing FDA-approved treatment for ARDS, it is important to understand the factors that lead to virus-induced ARDS development to improve prevention, diagnosis, and treatment. We have previously shown that mice deficient in the serine-threonine mitogen-activated protein kinase, Tpl2 (MAP3K8 or COT), succumb to infection with a typically low-pathogenicity strain of influenza A virus (IAV; HKX31, H3N2 [x31]). The goal of the current study was to evaluate influenza A virus-infected
MeSH term(s)	Animals ; Humans ; Mice ; Influenza A virus ; Influenza A Virus, H3N2 Subtype ; Lactate Dehydrogenases ; Neoplasms ; Protein Serine-Threonine Kinases ; Respiratory Distress Syndrome/genetics ; Respiratory Distress Syndrome/virology ; Orthomyxoviridae Infections/genetics ; MAP Kinase Kinase Kinases/genetics
Chemical Substances	Lactate Dehydrogenases (EC 1.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Map3k8 protein, mouse (EC 2.7.11.25) ; MAP Kinase Kinase Kinases (EC 2.7.11.25)
Language	English
Publishing date	2022-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.01136-22
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Article ; Online: Tamoxifen administration induces histopathologic changes within the lungs of Cre-recombinase-negative mice: A case report.

Wyatt, Kara D / Sakamoto, Kaori / Watford, Wendy T

Laboratory animals

2021 Volume 56, Issue 3, Page(s) 297–303

Abstract	Tamoxifen is commonly used as a cancer treatment in humans and for inducing genetic alterations using Cre-lox mouse models in the research setting. However, the extent of tamoxifen off-target effects in animal research is underappreciated. Here, we report significant changes in cellular infiltration in Cre-recombinase-negative mice treated with tamoxifen intraperitoneally. These changes were noted in the lungs, which were characterized by the presence of alveolitis, vasculitis, and pleuritis. Despite significant immunological changes in response to tamoxifen treatment, clinical symptoms were not observed. This study provides a cautionary note that tamoxifen treatment alone leads to histologic alterations that may obscure research interpretations and further highlights the need for the development of alternative mouse models for inducible Cre-mediated deletion.
MeSH term(s)	Animals ; Disease Models, Animal ; Integrases/genetics ; Lung ; Mice ; Mice, Transgenic ; Tamoxifen/adverse effects
Chemical Substances	Tamoxifen (094ZI81Y45) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2021-09-22
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	391008-8
ISSN	1758-1117 ; 0023-6772
ISSN (online)	1758-1117
ISSN	0023-6772
DOI	10.1177/00236772211042968
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Intestinal microbiota programming of alveolar macrophages influences severity of respiratory viral infection.

Ngo, Vu L / Lieber, Carolin M / Kang, Hae-Ji / Sakamoto, Kaori / Kuczma, Michal / Plemper, Richard K / Gewirtz, Andrew T

bioRxiv : the preprint server for biology

2024

Abstract: Susceptibility to respiratory virus infections (RVIs) varies widely across individuals. Because the gut microbiome impacts immune function, we investigated the influence of intestinal microbiota composition on RVI and determined that segmented ... ...

Abstract	Susceptibility to respiratory virus infections (RVIs) varies widely across individuals. Because the gut microbiome impacts immune function, we investigated the influence of intestinal microbiota composition on RVI and determined that segmented filamentous bacteria (SFB), naturally acquired or exogenously administered, protected mice against influenza virus (IAV) infection. Such protection, which also applied to respiratory syncytial virus and SARS-CoV-2, was independent of interferon and adaptive immunity but required basally resident alveolar macrophages (AM). In SFB-negative mice, AM were quickly depleted as RVI progressed. In contrast, AM from SFB-colonized mice were intrinsically altered to resist IAV-induced depletion and inflammatory signaling. Yet, AM from SFB-colonized mice were not quiescent. Rather, they directly disabled IAV via enhanced complement production and phagocytosis. Accordingly, transfer of SFB-transformed AM into SFB-free hosts recapitulated SFB-mediated protection against IAV. These findings uncover complex interactions that mechanistically link the intestinal microbiota with AM functionality and RVI severity. One sentence summary: Intestinal segmented filamentous bacteria reprogram alveolar macrophages promoting nonphlogistic defense against respiratory viruses.
Language	English
Publishing date	2024-01-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.21.558814
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Intestinal microbiota programming of alveolar macrophages influences severity of respiratory viral infection.

Ngo, Vu L / Lieber, Carolin M / Kang, Hae-Ji / Sakamoto, Kaori / Kuczma, Michal / Plemper, Richard K / Gewirtz, Andrew T

Cell host & microbe

2024 Volume 32, Issue 3, Page(s) 335–348.e8

Abstract	Susceptibility to respiratory virus infections (RVIs) varies widely across individuals. Because the gut microbiome impacts immune function, we investigated the influence of intestinal microbiota composition on RVI and determined that segmented filamentous bacteria (SFB), naturally acquired or exogenously administered, protected mice against influenza virus (IAV) infection. Such protection, which also applied to respiratory syncytial virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was independent of interferon and adaptive immunity but required basally resident alveolar macrophages (AMs). In SFB-negative mice, AMs were quickly depleted as RVI progressed. In contrast, AMs from SFB-colonized mice were intrinsically altered to resist IAV-induced depletion and inflammatory signaling. Yet, AMs from SFB-colonized mice were not quiescent. Rather, they directly disabled IAV via enhanced complement production and phagocytosis. Accordingly, transfer of SFB-transformed AMs into SFB-free hosts recapitulated SFB-mediated protection against IAV. These findings uncover complex interactions that mechanistically link the intestinal microbiota with AM functionality and RVI severity.
MeSH term(s)	Animals ; Mice ; Macrophages, Alveolar ; Gastrointestinal Microbiome ; Phagocytosis ; Interferons ; Bacteria ; Virus Diseases
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2024.01.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Dual oxidase 1 is dispensable during

Gupta, Tuhina / Sarr, Demba / Fantone, Kayla / Ashtiwi, Nuha Milad / Sakamoto, Kaori / Quinn, Frederick D / Rada, Balázs

Frontiers in immunology

2023 Volume 14, Page(s) 1044703

Abstract: Introduction: Mycobacterium tuberculosis: Methods: Duox1-deficient (Duox1 KO) and wild-type (WT) mice were infected with Mtb aerosols and bacterial titers, lung pathology, cytokines and immune cell recruitment were assessed.: Results and discussion! ...

Abstract	Introduction: Mycobacterium tuberculosis Methods: Duox1-deficient (Duox1 KO) and wild-type (WT) mice were infected with Mtb aerosols and bacterial titers, lung pathology, cytokines and immune cell recruitment were assessed. Results and discussion: Mtb titers in the lung, spleen and liver were not different 30 days after infection between WT and Duox1 KO mice. Duox1 did not affect lung histology assessed at days 0, 30, and 90 post-Mtb infection. Mtb-infected Duox1 KO animals exhibited enhanced production of certain cytokines and chemokines in the airway; however, this response was not associated with significantly higher numbers of macrophages or neutrophils in the lung. B cell numbers were lower, while apoptosis was higher in the pulmonary lesions of Mtb-infected Duox1 KO mice compared to infected WT animals. Taken together, these data demonstrate that while Duox1 might influence leukocyte recruitment to inflammatory cell aggregates, Duox1 is dispensable for the overall clinical course of Mtb lung infection in a mouse model.
MeSH term(s)	Animals ; Humans ; Mice ; Cytokines/metabolism ; Dual Oxidases/genetics ; Hydrogen Peroxide/metabolism ; Lung/pathology ; Tuberculosis/immunology
Chemical Substances	Cytokines ; Dual Oxidases (EC 1.11.1.-) ; Hydrogen Peroxide (BBX060AN9V) ; hypothiocyanite ion (63296-34-4) ; Duox1 protein, mouse (EC 1.6.3.1)
Language	English
Publishing date	2023-03-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1044703
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Article ; Online: A rapid, parasite-dependent cellular response to Dirofilaria immitis in the Mongolian jird (Meriones unguiculatus).

Evans, Christopher C / Day, Katherine M / Chu, Yi / Garner, Bridget / Sakamoto, Kaori / Moorhead, Andrew R

Parasites & vectors

2021 Volume 14, Issue 1, Page(s) 25

Abstract: Background: The Mongolian jird (Meriones unguiculatus) has long been recognized as a permissive host for the filarial parasite Brugia malayi; however, it is nonpermissive to another filarial parasite, canine heartworm (Dirofilaria immitis). By ... ...

Abstract	Background: The Mongolian jird (Meriones unguiculatus) has long been recognized as a permissive host for the filarial parasite Brugia malayi; however, it is nonpermissive to another filarial parasite, canine heartworm (Dirofilaria immitis). By elucidating differences in the early response to infection, we sought to identify mechanisms involved in the species-specific clearance of these parasites. We hypothesized that the early clearance of D. immitis in intraperitoneal infection of the jird is immune mediated and parasite species dependent. Methods: Jird peritoneal exudate cells (PECs) were isolated and their attachment to parasite larvae assessed in vitro under various conditions: D. immitis and B. malayi cultured separately, co-culture of both parasites, incubation before addition of cells, culture of heat-killed parasites, and culture with PECs isolated from jirds with mature B. malayi infection. The cells attaching to larvae were identified by immunohistochemistry. Results: In vitro cell attachment to live D. immitis was high (mean = 99.6%) while much lower for B. malayi (mean = 5.56%). This species-specific attachment was also observed when both filarial species were co-cultured, with no significant change from controls (U Conclusions: These results suggest a strongly species-dependent response from which B. malayi could not confer protection by proxy in co-culture. The changes in cell attachment following heat-killing and pre-incubation suggest a role for excretory/secretory products in host immune evasion and/or antigenicity. The nature of this attachment is the subject of ongoing study and may provide insight into filarial host specificity.
MeSH term(s)	Animals ; Cell Adhesion ; Cell Biology ; Dirofilaria immitis/immunology ; Dirofilaria immitis/metabolism ; Gerbillinae/immunology ; Gerbillinae/parasitology ; Larva/immunology ; Larva/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Male
Language	English
Publishing date	2021-01-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2409480-8
ISSN	1756-3305 ; 1756-3305
ISSN (online)	1756-3305
ISSN	1756-3305
DOI	10.1186/s13071-020-04455-x
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Article ; Online: CtpB Facilitates

Shey-Njila, Oliver / Hikal, Ahmed F / Gupta, Tuhina / Sakamoto, Kaori / Yahyaoui Azami, Hind / Watford, Wendy T / Quinn, Frederick D / Karls, Russell K

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: Copper is required for aerobic respiration ... ...

Abstract	Copper is required for aerobic respiration by
MeSH term(s)	Animals ; Copper/metabolism ; Mice ; Mice, Inbred DBA ; Mycobacterium tuberculosis/metabolism ; Phagosomes/metabolism ; Tuberculosis/microbiology
Chemical Substances	Copper (789U1901C5)
Language	English
Publishing date	2022-05-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105713
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Article ; Online: Local pulmonary immune responses in domestic cats naturally infected with Cytauxzoon felis.

Frontera-Acevedo, Karelma / Sakamoto, Kaori

Veterinary immunology and immunopathology

2015 Volume 163, Issue 1-2, Page(s) 1–7

Abstract: Cytauxzoonosis is a hemoprotozoal disease of cats and wild felids in the South and Southeastern United States caused by Cytauxzoon felis. Although the causative agent has been recognized since the seventies, no study has examined the local immune ... ...

Abstract	Cytauxzoonosis is a hemoprotozoal disease of cats and wild felids in the South and Southeastern United States caused by Cytauxzoon felis. Although the causative agent has been recognized since the seventies, no study has examined the local immune response in affected organs, such as the lung, and compared them to the lungs of uninfected domestic cats. Previous studies have suggested that the histopathologic findings in the lungs of C. felis-infected cats are caused by the release of pro-inflammatory mediators, such as cytokines and increased production of inducible nitric oxide synthase (iNOS), by the infected macrophages. Our laboratory had previously found an upregulation of the adhesion molecule CD18, which can stimulate the release of these pro-inflammatory mediators. The objective of this study was to characterize local pulmonary immune responses in cats naturally infected with C. felis. Immunohistochemistry was performed to detect tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, iNOS, and major histocompatibility complex (MHC) II in 19 lungs from affected cats that died between 2005 and 2013. Results showed increased expression of all of these molecules when compared to lungs from uninfected, healthy cats. Furthermore, MHC II is expressed in the endothelium of C. felis naturally infected cats. These results support that there is a marked, local, pro-inflammatory immune response that can contribute to the pathogenesis of cytauxzoonosis in the lungs.
MeSH term(s)	Animals ; Cat Diseases/immunology ; Cat Diseases/parasitology ; Cat Diseases/pathology ; Cats ; Genes, MHC Class II/physiology ; Interleukin-1beta/analysis ; Lung/chemistry ; Lung/immunology ; Lung/pathology ; Nitric Oxide Synthase Type II/analysis ; Theileria/immunology ; Theileria/parasitology ; Theileriasis/immunology ; Theileriasis/pathology ; Tumor Necrosis Factor-alpha/analysis
Chemical Substances	Interleukin-1beta ; Tumor Necrosis Factor-alpha ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2015-01-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	754160-0
ISSN	1873-2534 ; 0165-2427
ISSN (online)	1873-2534
ISSN	0165-2427
DOI	10.1016/j.vetimm.2014.10.012
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