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Article: Notch-1 Signaling Modulates Macrophage Polarization and Immune Defense against

Keewan, Esra'a / Naser, Saleh A

2020 Volume 8, Issue 7

Abstract: Despite the extensive research on Notch signaling involvement in inflammation, its specific role in macrophage response in autoimmune disease and defense mechanisms against bacterial infection, such ... ...

Abstract	Despite the extensive research on Notch signaling involvement in inflammation, its specific role in macrophage response in autoimmune disease and defense mechanisms against bacterial infection, such as
Language	English
Publishing date	2020-07-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8071006
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Article: MiR-146a

Keewan, Esra'a / Naser, Saleh A

Gut pathogens

2020 Volume 12, Page(s) 48

Abstract: Background: MiR-146a, an effector mediator, targets Notch-1 and regulates the innate and adaptive immune systems response. Recently, we reported that Notch-1 signaling plays a key role in macrophage polarization and response during infection. We ... ...

Abstract	Background: MiR-146a, an effector mediator, targets Notch-1 and regulates the innate and adaptive immune systems response. Recently, we reported that Notch-1 signaling plays a key role in macrophage polarization and response during infection. We employed Methods: We determined the incidence of miR-146a Results: MiR-146a Conclusions: The data clearly associates miR-146a
Keywords	covid19
Language	English
Publishing date	2020-10-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2478277-4
ISSN	1757-4749
ISSN	1757-4749
DOI	10.1186/s13099-020-00387-0
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Article ; Online: The Role of Notch Signaling in Macrophages during Inflammation and Infection: Implication in Rheumatoid Arthritis?

Keewan, Esra'a / Naser, Saleh A

Cells

2020 Volume 9, Issue 1

Abstract: Notch signaling coordinates numerous cellular processes and has been implicated in many pathological conditions, including rheumatoid arthritis (RA). Although the role of Notch signaling in development, maturation, differentiation, and activation of ... ...

Abstract	Notch signaling coordinates numerous cellular processes and has been implicated in many pathological conditions, including rheumatoid arthritis (RA). Although the role of Notch signaling in development, maturation, differentiation, and activation of lymphocytes has been comprehensively reported, less is known about its role in myeloid cells. Certainly, limited data are available about the role of Notch signaling in macrophages during inflammation and infection. In this review, we discuss the recent advances pertaining to the role of Notch signaling in differentiation, activation, and metabolism of macrophages during inflammation and infection. We also highlight the reciprocal interplay between Notch signaling and other signaling pathways in macrophages under different inflammatory and infectious conditions including pathogenesis of RA. Finally, we discuss approaches that could consider Notch signaling as a potential therapeutic target against infection- and inflammation-driven diseases.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/complications ; Arthritis, Rheumatoid/pathology ; Humans ; Infections/complications ; Infections/pathology ; Inflammation/pathology ; Macrophages/metabolism ; Receptors, Notch/metabolism ; Signal Transduction
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2020-01-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9010111
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Article: Metabolic Reprogramming and Cell Adhesion in Acute Leukemia Adaptation to the CNS Niche.

Sharma, Nitesh D / Keewan, Esra'a / Matlawska-Wasowska, Ksenia

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 767510

Abstract: Involvement of the Central Nervous System (CNS) in acute leukemia confers poor prognosis and lower overall survival. Existing CNS-directed therapies are associated with a significant risk of short- or long-term toxicities. Leukemic cells can ... ...

Abstract	Involvement of the Central Nervous System (CNS) in acute leukemia confers poor prognosis and lower overall survival. Existing CNS-directed therapies are associated with a significant risk of short- or long-term toxicities. Leukemic cells can metabolically adapt and survive in the microenvironment of the CNS. The supporting role of the CNS microenvironment in leukemia progression and dissemination has not received sufficient attention. Understanding the mechanism by which leukemic cells survive in the nutrient-poor and oxygen-deprived CNS microenvironment will lead to the development of more specific and less toxic therapies. Here, we review the current literature regarding the roles of metabolic reprogramming in leukemic cell adhesion and survival in the CNS.
Language	English
Publishing date	2021-12-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.767510
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Article: The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia.

Keewan, Esra'a / Matlawska-Wasowska, Ksenia

Cancers

2021 Volume 13, Issue 16

Abstract: Cytokines are pleiotropic signaling molecules that execute an essential role in cell-to-cell communication through binding to cell surface receptors. Receptor binding activates intracellular signaling cascades in the target cell that bring about a wide ... ...

Abstract	Cytokines are pleiotropic signaling molecules that execute an essential role in cell-to-cell communication through binding to cell surface receptors. Receptor binding activates intracellular signaling cascades in the target cell that bring about a wide range of cellular responses, including induction of cell proliferation, migration, differentiation, and apoptosis. The Janus kinase and transducers and activators of transcription (JAK/STAT) signaling pathways are activated upon cytokines and growth factors binding with their corresponding receptors. The SOCS family of proteins has emerged as a key regulator of cytokine signaling, and SOCS insufficiency leads to constitutive activation of JAK/STAT signaling and oncogenic transformation. Dysregulation of SOCS expression is linked to various solid tumors with invasive properties. However, the roles of SOCS in hematological malignancies, such as leukemia, are less clear. In this review, we discuss the recent advances pertaining to SOCS dysregulation in leukemia development and progression. We also highlight the roles of specific SOCS in immune cells within the tumor microenvironment and their possible involvement in anti-tumor immunity. Finally, we discuss the epigenetic, genetic, and post-transcriptional modifications of SOCS genes during tumorigenesis, with an emphasis on leukemia.
Language	English
Publishing date	2021-08-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13164000
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Article ; Online: Changes in dietary habits and eating behaviors during COVID-19 induced confinement: A study from Jordan.

Alomari, Mahmoud A / Khabour, Omar F / Alzoubi, Karem H / Keewan, Esra'a

Human nutrition & metabolism

2022 Volume 30, Page(s) 200169

Abstract: Objective: This study aimed to evaluate dietary habits (DH) and eating behaviors (EB) among adults during confinement induced by COVID-19 in Jordan.: Method: In this cross-sectional study, an online survey designed to assess the change in DH and EB ... ...

Abstract	Objective: This study aimed to evaluate dietary habits (DH) and eating behaviors (EB) among adults during confinement induced by COVID-19 in Jordan. Method: In this cross-sectional study, an online survey designed to assess the change in DH and EB during April and May 2020 was distributed using various social media platforms. Results: The survey was completed by a total of 1844 adult (18-72 years) participants from the public in Jordan. The results indicated an increase (42.5-61.8%) in most of the DH and EB examined in the current study in the majority of participants. Among these changes, they have increased (p < 0.05) the prevalence of fruit and vegetable, immune boosters, water, and hot beverage consumption, as well as decreased (p < 0.05) eating in restaurants and fatty food consumption, indicating a positive change. Conversely, a larger (p < 0.05) proportion of participants reported increased consumption of high-calorie food and late-night eating, indicating a risky behavior for obesity and subsequent chronic complications. Additionally, age, sex, obesity, education, income, and type of job appeared to contribute (p < 0.05) to changes in DH and EB. Overall, confinement caused by COVID-19 appears to compel adults to adopt a specific DH and EB. Although most of these changes were positive, some were negative. Conclusion: This study provides essential information for designing subpopulation recommendations and developmental programs for adults under such conditions.
Language	English
Publishing date	2022-11-13
Publishing country	United States
Document type	Journal Article
ISSN	2666-1497
ISSN (online)	2666-1497
DOI	10.1016/j.hnm.2022.200169
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Article ; Online: Anti-TNF-α agents Modulate SARS-CoV-2 Receptors and Increase the Risk of Infection Through Notch-1 Signaling.

Keewan, Esra'a / Beg, Shazia / Naser, Saleh A

Frontiers in immunology

2021 Volume 12, Page(s) 641295

Abstract: Although millions of patients with underlining conditions are treated primarily with anti-TNF-α agents, little is known about the safety of this standard therapy during the coronavirus disease-2019 (COVID-19) pandemic. In this study, we investigated the ... ...

Abstract	Although millions of patients with underlining conditions are treated primarily with anti-TNF-α agents, little is known about the safety of this standard therapy during the coronavirus disease-2019 (COVID-19) pandemic. In this study, we investigated the effect of anti-TNF-α monoclonal antibodies on the cellular entry mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and increasing the risk of COVID-19 development. We focused on the expression of angiotensin-converting enzyme II (ACE2), type II transmembrane serine proteases (TMPRSS2)/TNF-α converting enzyme (TACE) ratio. We also investigated the involvement of Notch-1 signaling and its downstream influence on IL-6, myeloid cell leukemia sequence-1(MCL-1) in the anti-TNF-α mode of action and increased the susceptibility to
MeSH term(s)	ADAM17 Protein/metabolism ; Angiotensin-Converting Enzyme 2/metabolism ; Animals ; COVID-19/immunology ; COVID-19/transmission ; COVID-19/virology ; Disease Susceptibility ; Disease Transmission, Infectious ; Humans ; Interleukin-6/metabolism ; Macrophages/immunology ; Mycobacterium avium/physiology ; Receptor, Notch1/metabolism ; Risk ; SARS-CoV-2/physiology ; Serine Endopeptidases/metabolism ; Signal Transduction ; THP-1 Cells ; Tuberculosis, Avian/immunology ; Tumor Necrosis Factor-alpha/antagonists & inhibitors
Chemical Substances	Interleukin-6 ; NOTCH1 protein, human ; Receptor, Notch1 ; Tumor Necrosis Factor-alpha ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-) ; ADAM17 Protein (EC 3.4.24.86)
Language	English
Publishing date	2021-05-06
Publishing country	Switzerland
Document type	Journal Article ; 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.2021.641295
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Article: Are Fried Foods Unhealthy? The Dietary Peroxidized Fatty Acid, 13-HPODE, Induces Intestinal Inflammation In Vitro and In Vivo.

Keewan, Esra'a / Narasimhulu, Chandrakala Aluganti / Rohr, Michael / Hamid, Simran / Parthasarathy, Sampath

Antioxidants (Basel, Switzerland)

2020 Volume 9, Issue 10

Abstract: Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder characterized by progressive inflammation and the erosion of the gut mucosa. Although the exact cause of IBD is unknown, multiple factors contribute to its complex pathogenesis. Diet is ... ...

Abstract	Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder characterized by progressive inflammation and the erosion of the gut mucosa. Although the exact cause of IBD is unknown, multiple factors contribute to its complex pathogenesis. Diet is one such factor and a strong correlation exists between the western-style, high fat diets (HFDs) and IBD incidence rates. In this study, we propose that the peroxidized fatty acid components of HFDs could contribute to inflammation of the gut. The inflammatory nature of peroxidized linoleic acid (13-HPODE), was confirmed in vitro by analyzing pro-inflammatory gene expression in Caco-2 cells via RT-PCR and ELISA. Additionally, peroxide induced apoptosis was tested by Annexin-V fluorescent staining, while permeability was tested by FITC-dextran flux and TEER. The 13-HPODE-induced inflammation of intestinal epithelium was evaluated in vivo by analyzing pro-inflammatory cytokines under acute and chronic conditions after feeding 13-HPODE to C57BL/6J mice. Our data show that 13-HPODE significantly induced pro-inflammatory gene expression of TNF-α and MCP-1 in vitro, most notably in differentiated Caco-2 cells. Further, acute and chronic 13-HPODE treatments of mice similarly induced pro-inflammatory cytokine expression in the epithelium of both the proximal and distal small intestines, resident immune cells in Peyer's patches and peritoneal macrophages. The results of this study not only confirm the pro-inflammatory properties of peroxidized fats on the gut mucosa, but for the first time demonstrate their ability to differentially induce pro-inflammatory gene expression and influence permeability in the intestinal epithelium and mucosal cells. Collectively, our results suggest that the immunogenic properties of HFD's in the gut may be partly caused by peroxide derivatives, providing potential insight into how these diets contribute to exacerbations of IBD.
Language	English
Publishing date	2020-09-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9100926
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Article ; Online: The dietary peroxidized lipid, 13-HPODE, promotes intestinal inflammation by mediating granzyme B secretion from natural killer cells.

Rohr, Michael / Narasimhulu, Chandrakala Aluganti / Keewan, Esra'a / Hamid, Simran / Parthasarathy, Sampath

Food & function

2020 Volume 11, Issue 11, Page(s) 9526–9534

Abstract: It is well known that consumption of a high-fat diet (HFD) promotes intestinal inflammation despite little being known about causative factors. Recent evidence implicates dietary peroxidized lipids (POLs), which are typically formed from the oxidation of ...

Abstract	It is well known that consumption of a high-fat diet (HFD) promotes intestinal inflammation despite little being known about causative factors. Recent evidence implicates dietary peroxidized lipids (POLs), which are typically formed from the oxidation of polyunsaturated fatty acid double bonds, as potential contributors due to their enrichment in HFDs, ability to be formed during gastrointestinal transit, and immunogenic and cytotoxic properties. 13-HPODE, the most common dietary POL, demonstrates pro-inflammatory activity in a variety of immune cells, especially Natural Killer (NK) cells whose role in mediating intestinal inflammation remains unclear. Therefore, we set out to investigate how 13-HPODE and other POLs modulate NK-cell activity in the context of intestinal inflammation. We not only found that NK cells fully decompose exogenous 13-HPODE, but that direct treatment stimulates TNF-α and MCP1 expression as well as Granzyme B (GZMB) secretion in a dose-dependent manner. Similar results were observed upon incubation of NK cells with oxidized, but not-unoxidized, low-density lipoproteins. Secretory products from 13-HPODE-treated NK cells were able to induce Caco2 intestinal cell inflammation in the same way as exogenous GZMB with greater sensitivity in undifferentiated compared to differentiated cells. Results were recapitulated in 13-HPODE-fed mice, demonstrating both spatial and temporal patterns of elevated GZMB expression that favored acute treatments in the distal intestinal epithelium. Collectively, our results suggest that that HFD-derived POLs, like 13-HPODE, potentially contribute to intestinal inflammation by stimulating the secretion of pro-inflammatory granzymes by resident NK cells, ultimately revealing a more direct role for diet in modulating gut homeostasis and the immune environment.
MeSH term(s)	Animals ; Caco-2 Cells/metabolism ; Dietary Fats/adverse effects ; Granzymes/metabolism ; Humans ; Inflammation/chemically induced ; Inflammation/metabolism ; Intestinal Diseases/chemically induced ; Intestinal Diseases/metabolism ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Killer Cells, Natural/metabolism ; Linoleic Acids/pharmacology ; Lipid Peroxides/pharmacology ; Male ; Mice ; Mice, Inbred C57BL
Chemical Substances	Dietary Fats ; Linoleic Acids ; Lipid Peroxides ; 13-hydroperoxy-9,11-octadecadienoic acid (23017-93-8) ; GZMB protein, human (EC 3.4.21.-) ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2020-10-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/d0fo02328k
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Article: The dietary peroxidized lipid, 13-HPODE, promotes intestinal inflammation by mediating granzyme B secretion from natural killer cells

Rohr, Michael / Narasimhulu, Chandrakala Aluganti / Keewan, Esra'a / Hamid, Simran / Parthasarathy, Sampath

Food & function. 2020 Nov. 18, v. 11, no. 11

2020

Abstract	It is well known that consumption of a high-fat diet (HFD) promotes intestinal inflammation despite little being known about causative factors. Recent evidence implicates dietary peroxidized lipids (POLs), which are typically formed from the oxidation of polyunsaturated fatty acid double bonds, as potential contributors due to their enrichment in HFDs, ability to be formed during gastrointestinal transit, and immunogenic and cytotoxic properties. 13-HPODE, the most common dietary POL, demonstrates pro-inflammatory activity in a variety of immune cells, especially Natural Killer (NK) cells whose role in mediating intestinal inflammation remains unclear. Therefore, we set out to investigate how 13-HPODE and other POLs modulate NK-cell activity in the context of intestinal inflammation. We not only found that NK cells fully decompose exogenous 13-HPODE, but that direct treatment stimulates TNF-α and MCP1 expression as well as Granzyme B (GZMB) secretion in a dose-dependent manner. Similar results were observed upon incubation of NK cells with oxidized, but not-unoxidized, low-density lipoproteins. Secretory products from 13-HPODE-treated NK cells were able to induce Caco2 intestinal cell inflammation in the same way as exogenous GZMB with greater sensitivity in undifferentiated compared to differentiated cells. Results were recapitulated in 13-HPODE-fed mice, demonstrating both spatial and temporal patterns of elevated GZMB expression that favored acute treatments in the distal intestinal epithelium. Collectively, our results suggest that that HFD-derived POLs, like 13-HPODE, potentially contribute to intestinal inflammation by stimulating the secretion of pro-inflammatory granzymes by resident NK cells, ultimately revealing a more direct role for diet in modulating gut homeostasis and the immune environment.
Keywords	cytotoxicity ; dose response ; environment ; gastrointestinal transit ; high fat diet ; homeostasis ; inflammation ; intestinal mucosa ; low density lipoprotein ; mice ; natural killer cells ; oxidation ; polyunsaturated fatty acids ; secretion
Language	English
Dates of publication	2020-1118
Size	p. 9526-9534.
Publishing place	The Royal Society of Chemistry
Document type	Article
Note	NAL-light
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/d0fo02328k
Database	NAL-Catalogue (AGRICOLA)

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