LIVIVO - Search results -

Search results

Result 1 - 10 of total 23

Search options

Article ; Online: The matricellular protein thrombospondin-1 in lung inflammation and injury.

Tabary, Mohammadreza / Gheware, Atish / Peñaloza, Hernán F / Lee, Janet S

American journal of physiology. Cell physiology

2022 Volume 323, Issue 3, Page(s) C857–C865

Abstract: Matricellular proteins comprise a diverse group of molecular entities secreted into the extracellular space. They interact with the extracellular matrix (ECM), integrins, and other cell-surface receptors, and can alter matrix strength, cell attachment to ...

Abstract	Matricellular proteins comprise a diverse group of molecular entities secreted into the extracellular space. They interact with the extracellular matrix (ECM), integrins, and other cell-surface receptors, and can alter matrix strength, cell attachment to the matrix, and cell-cell adhesion. A founding member of this group is thrombospondin-1 (TSP-1), a high molecular-mass homotrimeric glycoprotein. Given the importance of the matrix and ECM remodeling in the lung following injury, TSP-1 has been implicated in a number of lung pathologies. This review examines the role of TSP-1 as a damage controller in the context of lung inflammation, injury resolution, and repair in noninfectious and infectious models. This review also discusses the potential role of TSP-1 in human diseases as it relates to lung inflammation and injury.
MeSH term(s)	Cell Adhesion ; Extracellular Matrix/metabolism ; Extracellular Matrix Proteins/metabolism ; Humans ; Pneumonia/metabolism ; Thrombospondin 1/metabolism ; Thrombospondins/metabolism
Chemical Substances	Extracellular Matrix Proteins ; Thrombospondin 1 ; Thrombospondins
Language	English
Publishing date	2022-08-01
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00182.2022
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Barriers to Access: Global Variability in Implementing Treatment Advances in Lung Cancer.

Febbraro, Michela / Gheware, Atish / Kennedy, Thomas / Jain, Deepali / de Moraes, Fabio Ynoe / Juergens, Rosalyn

American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting

2022 Volume 42, Page(s) 1–7

Abstract: Globally, lung cancer is the second most-diagnosed cancer and is the leading cause of cancer death. Advances in science and technology have contributed to improvements in primary cancer prevention, cancer diagnosis, and cancer therapy, leading to an ... ...

Abstract	Globally, lung cancer is the second most-diagnosed cancer and is the leading cause of cancer death. Advances in science and technology have contributed to improvements in primary cancer prevention, cancer diagnosis, and cancer therapy, leading to an increase in survival and improvement in quality of life. Many of these advances have been seen in high-income countries. Accessibility, availability, and affordability are key domains in barriers to access of care between countries and within countries. The impact of these domains, as they relate to molecular testing, radiation therapy, and systemic therapy, are discussed.
MeSH term(s)	Developing Countries ; Health Services Accessibility ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/epidemiology ; Lung Neoplasms/genetics ; Quality of Life
Language	English
Publishing date	2022-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2431126-1
ISSN	1548-8756 ; 1548-8748
ISSN (online)	1548-8756
ISSN	1548-8748
DOI	10.1200/EDBK_351021
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Obesity impairs cardiolipin-dependent mitophagy and therapeutic intercellular mitochondrial transfer ability of mesenchymal stem cells.

Sagar, Shakti / Faizan, Md Imam / Chaudhary, Nisha / Singh, Vandana / Singh, Praveen / Gheware, Atish / Sharma, Khushboo / Azmi, Iqbal / Singh, Vijay Pal / Kharya, Gaurav / Mabalirajan, Ulaganathan / Agrawal, Anurag / Ahmad, Tanveer / Sinha Roy, Soumya

Cell death & disease

2023 Volume 14, Issue 5, Page(s) 324

Abstract: Mesenchymal stem cell (MSC) transplantation alleviates metabolic defects in diseased recipient cells by intercellular mitochondrial transport (IMT). However, the effect of host metabolic conditions on IMT and thereby on the therapeutic efficacy of MSCs ... ...

Abstract	Mesenchymal stem cell (MSC) transplantation alleviates metabolic defects in diseased recipient cells by intercellular mitochondrial transport (IMT). However, the effect of host metabolic conditions on IMT and thereby on the therapeutic efficacy of MSCs has largely remained unexplored. Here we found impaired mitophagy, and reduced IMT in MSCs derived from high-fat diet (HFD)-induced obese mouse (MSC-Ob). MSC-Ob failed to sequester their damaged mitochondria into LC3-dependent autophagosomes due to decrease in mitochondrial cardiolipin content, which we propose as a putative mitophagy receptor for LC3 in MSCs. Functionally, MSC-Ob exhibited diminished potential to rescue mitochondrial dysfunction and cell death in stress-induced airway epithelial cells. Pharmacological modulation of MSCs enhanced cardiolipin-dependent mitophagy and restored their IMT ability to airway epithelial cells. Therapeutically, these modulated MSCs attenuated features of allergic airway inflammation (AAI) in two independent mouse models by restoring healthy IMT. However, unmodulated MSC-Ob failed to do so. Notably, in human (h)MSCs, induced metabolic stress associated impaired cardiolipin-dependent mitophagy was restored upon pharmacological modulation. In summary, we have provided the first comprehensive molecular understanding of impaired mitophagy in obese-derived MSCs and highlight the importance of pharmacological modulation of these cells for therapeutic intervention. A MSCs obtained from (HFD)-induced obese mice (MSC-Ob) show underlying mitochondrial dysfunction with a concomitant decrease in cardiolipin content. These changes prevent LC3-cardiolipin interaction, thereby reducing dysfunctional mitochondria sequestration into LC3-autophagosomes and thus impaired mitophagy. The impaired mitophagy is associated with reduced intercellular mitochondrial transport (IMT) via tunneling nanotubes (TNTs) between MSC-Ob and epithelial cells in co-culture or in vivo. B Pyrroloquinoline quinone (PQQ) modulation in MSC-Ob restores mitochondrial health, cardiolipin content, and thereby sequestration of depolarized mitochondria into the autophagosomes to alleviate impaired mitophagy. Concomitantly, MSC-Ob shows restoration of mitochondrial health upon PQQ treatment (MSC-ObPQQ). During co-culture with epithelial cells or transplantation in vivo into the mice lungs, MSC-ObPQQ restores IMT and prevents epithelial cell death. C Upon transplantation in two independent allergic airway inflammatory mouse models, MSC-Ob failed to rescue the airway inflammation, hyperactivity, metabolic changes in epithelial cells. D PQQ modulated MSCs restored these metabolic defects and restored lung physiology and airway remodeling parameters.
MeSH term(s)	Mice ; Animals ; Humans ; Cardiolipins/metabolism ; Mitophagy ; Mitochondria/metabolism ; Disease Models, Animal ; Mesenchymal Stem Cells/metabolism ; Inflammation/metabolism ; Obesity/metabolism
Chemical Substances	Tunneling Nanotubes ; Cardiolipins
Language	English
Publishing date	2023-05-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-05810-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: MiR-326-mediated overexpression of NFIB offsets TGF-β induced epithelial to mesenchymal transition and reverses lung fibrosis.

Pattnaik, Bijay / Negi, Vinny / Chaudhuri, Rituparna / Desiraju, Koundinya / Faizan, Md Imam / Akhtar, Areej / Ansari, Md Sufyan / Shakir, Md / Gheware, Atish / Prakash, Y S / Guleria, Randeep / Ghosh, Balaram / Agrawal, Anurag / Ahmad, Tanveer

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 12, Page(s) 357

Abstract: Idiopathic Pulmonary Fibrosis (IPF) is a progressively fatal and incurable disease characterized by the loss of alveolar structures, increased epithelial-mesenchymal transition (EMT), and aberrant tissue repair. In this study, we investigated the role of ...

Abstract	Idiopathic Pulmonary Fibrosis (IPF) is a progressively fatal and incurable disease characterized by the loss of alveolar structures, increased epithelial-mesenchymal transition (EMT), and aberrant tissue repair. In this study, we investigated the role of Nuclear Factor I-B (NFIB), a transcription factor critical for lung development and maturation, in IPF. Using both human lung tissue samples from patients with IPF, and a mouse model of lung fibrosis induced by bleomycin, we showed that there was a significant reduction of NFIB both in the lungs of patients and mice with IPF. Furthermore, our in vitro experiments using cultured human lung cells demonstrated that the loss of NFIB was associated with the induction of EMT by transforming growth factor beta (TGF-β). Knockdown of NFIB promoted EMT, while overexpression of NFIB suppressed EMT and attenuated the severity of bleomycin-induced lung fibrosis in mice. Mechanistically, we identified post-translational regulation of NFIB by miR-326, a miRNA with anti-fibrotic effects that is diminished in IPF. Specifically, we showed that miR-326 stabilized and increased the expression of NFIB through its 3'UTR target sites for Human antigen R (HuR). Moreover, treatment of mice with either NFIB plasmid or miR-326 reversed airway collagen deposition and fibrosis. In conclusion, our study emphasizes the critical role of NFIB in lung development and maturation, and its reduction in IPF leading to EMT and loss of alveolar structures. Our study highlights the potential of miR-326 as a therapeutic intervention for IPF. The schema shows the role of NFIB in maintaining the normal epithelial cell characteristics in the lungs and how its reduction leads to a shift towards mesenchymal cell-like features and pulmonary fibrosis. A In normal lungs, NFIB is expressed abundantly in the epithelial cells, which helps in maintaining their shape, cell polarity and adhesion molecules. However, when the lungs are exposed to factors that induce pulmonary fibrosis, such as bleomycin, or TGF-β, the epithelial cells undergo epithelial to mesenchymal transition (EMT), which leads to a decrease in NFIB. B The mesenchymal cells that arise from EMT appear as spindle-shaped with loss of cell junctions, increased cell migration, loss of polarity and expression of markers associated with mesenchymal cells/fibroblasts. C We designed a therapeutic approach that involves exogenous administration of NFIB in the form of overexpression plasmid or microRNA-326. This therapeutic approach decreases the mesenchymal cell phenotype and restores the epithelial cell phenotype, thus preventing the development or progression of pulmonary fibrosis.
MeSH term(s)	Humans ; Mice ; Animals ; Epithelial-Mesenchymal Transition ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; NFI Transcription Factors/metabolism ; NFI Transcription Factors/pharmacology ; Lung/metabolism ; Idiopathic Pulmonary Fibrosis/chemically induced ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/metabolism ; MicroRNAs/metabolism ; Epithelial Cells/metabolism ; Bleomycin/toxicity
Chemical Substances	Transforming Growth Factor beta ; NFI Transcription Factors ; MicroRNAs ; Bleomycin (11056-06-7) ; NFIB protein, human ; MIRN326 microRNA, human
Language	English
Publishing date	2023-11-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-05005-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 195: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Oral Feeding of Cow Milk Containing A1 Variant of β Casein Induces Pulmonary Inflammation in Male Balb/c Mice.

Yadav, Shikha / Yadav, Nakul Dev S / Gheware, Atish / Kulshreshtha, Ankur / Sharma, Pankaj / Singh, V P

Scientific reports

2020 Volume 10, Issue 1, Page(s) 8053

Abstract: Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in several ... ...

Abstract	Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in several pathologies, but direct effect on lungs has not been studied. The objective of the present study was to evaluate the A1and A2 β casein variants of cow milk as factors causing allergic airway disease in murine model. Mice fed with A1A1 milk exhibited increased airway hyperresponsiveness with increasing concentration of bronchoconstrictor (methacholine), which was not observed in mice fed with A2A2 milk. Significantly elevated levels of IL-4 and IL-5 were found in bronchoalveolar lavage and serum of A1A1 variant fed mice. Increased IgE and IgG levels along with increased infiltration of lymphocytes and eosinophils, leading to peribronchial inflammation was also observed in A1A1 variant fed mice, although, no goblet cell hyperplasia or airway remodeling was observed. In contrast, A2A2 milk fed mice presented phenotype matching the control group, while A1A2 milk fed group presented an intermediate phenotype. In summary, our results show that A1 form of cow milk has a proinflammatory effect on the lung resulting in phenotype closely matching with the typical allergic asthma phenotype.
MeSH term(s)	Animal Feed/adverse effects ; Animals ; Biomarkers ; Caseins/adverse effects ; Caseins/genetics ; Cattle ; Cytokines/metabolism ; Disease Susceptibility ; Eosinophils/immunology ; Eosinophils/metabolism ; Genetic Variation ; Genotype ; Immunoglobulin E/immunology ; Immunoglobulin G/immunology ; Inflammation Mediators/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Milk/adverse effects ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; Th2 Cells/immunology ; Th2 Cells/metabolism
Chemical Substances	Biomarkers ; Caseins ; Cytokines ; Immunoglobulin G ; Inflammation Mediators ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2020-05-15
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-64997-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: STAT1 Employs Myeloid Cell-Extrinsic Mechanisms to Regulate the Neutrophil Response and Provide Protection against Invasive Klebsiella pneumoniae Lung Infection.

Gonzalez-Ferrer, Shekina / Peñaloza, Hernán F / van der Geest, Rick / Xiong, Zeyu / Gheware, Atish / Tabary, Mohammadreza / Kochin, Megan / Dalton, Kathryn / Zou, Henry / Lou, Dequan / Lockwood, Karina / Zhang, Yingze / Bain, William G / Mallampalli, Rama K / Ray, Anuradha / Ray, Prabir / Van Tyne, Daria / Chen, Kong / Lee, Janet S

ImmunoHorizons

2024 Volume 8, Issue 1, Page(s) 122–135

Abstract: Klebsiella pneumoniae (KP) is an extracellular Gram-negative bacterium that causes infections in the lower respiratory and urinary tracts and the bloodstream. STAT1 is a master transcription factor that acts to maintain T cell quiescence under ... ...

Abstract	Klebsiella pneumoniae (KP) is an extracellular Gram-negative bacterium that causes infections in the lower respiratory and urinary tracts and the bloodstream. STAT1 is a master transcription factor that acts to maintain T cell quiescence under homeostatic conditions. Although STAT1 helps defend against systemic spread of acute KP intrapulmonary infection, whether STAT1 regulation of T cell homeostasis impacts pulmonary host defense during acute bacterial infection and injury is less clear. Using a clinical KP respiratory isolate and a pneumonia mouse model, we found that STAT1 deficiency led to an early neutrophil-dominant transcriptional profile and neutrophil recruitment in the lung preceding widespread bacterial dissemination and lung injury development. Yet, myeloid cell STAT1 was dispensable for control of KP proliferation and dissemination, because myeloid cell-specific STAT1-deficient (LysMCre/WT;Stat1fl/fl) mice showed bacterial burden in the lung, liver, and kidney similar to that of their wild-type littermates. Surprisingly, IL-17-producing CD4+ T cells infiltrated Stat1-/- murine lungs early during KP infection. The increase in Th17 cells in the lung was not due to preexisting immunity against KP and was consistent with circulating rather than tissue-resident CD4+ T cells. However, blocking global IL-17 signaling with anti-IL-17RC administration led to increased proliferation and dissemination of KP, suggesting that IL-17 provided by other innate immune cells is essential in defense against KP. Contrastingly, depletion of CD4+ T cells reduced Stat1-/- murine lung bacterial burden, indicating that early CD4+ T cell activation in the setting of global STAT1 deficiency is pathogenic. Altogether, our findings suggest that STAT1 employs myeloid cell-extrinsic mechanisms to regulate neutrophil responses and provides protection against invasive KP by restricting nonspecific CD4+ T cell activation and immunopathology in the lung.
MeSH term(s)	Animals ; Mice ; Interleukin-17 ; Klebsiella pneumoniae ; Lung/microbiology ; Myeloid Cells ; Neutrophils/immunology ; STAT1 Transcription Factor/metabolism ; Klebsiella Infections/immunology
Chemical Substances	Interleukin-17 ; Stat1 protein, mouse ; STAT1 Transcription Factor
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Journal Article
ISSN	2573-7732
ISSN (online)	2573-7732
DOI	10.4049/immunohorizons.2300104
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Adhatoda vasica

Gheware, Atish / Panda, Lipsa / Khanna, Kritika / Bhatraju, Naveen Kumar / Jain, Vaibhav / Sagar, Shakti / Kumar, Manish / Singh, Vijay Pal / Kannan, Sadasivam / Subramanian, Venkatesan / Mukerji, Mitali / Agrawal, Anurag / Prasher, Bhavana

American journal of physiology. Lung cellular and molecular physiology

2021 Volume 320, Issue 5, Page(s) L757–L769

Abstract: Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, ... ...

Abstract	Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, we elucidate the therapeutic effects and mechanistic basis of
MeSH term(s)	Animals ; Asthma/drug therapy ; Asthma/etiology ; Asthma/metabolism ; Asthma/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Hypoxia/complications ; Justicia/chemistry ; Male ; Mice ; Mice, Inbred BALB C ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Phytochemicals/pharmacology ; Plant Extracts/pharmacology ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; Pneumonia/prevention & control
Chemical Substances	Phytochemicals ; Plant Extracts
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00511.2020
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Molecular signature of postmortem lung tissue from COVID-19 patients suggests distinct trajectories driving mortality.

Budhraja, Anshul / Basu, Anubhav / Gheware, Atish / Abhilash, Dasari / Rajagopala, Seesandra / Pakala, Suman / Sumit, Madhuresh / Ray, Animesh / Subramaniam, Arulselvi / Mathur, Purva / Nambirajan, Aruna / Kumar, Sachin / Gupta, Ritu / Wig, Naveet / Trikha, Anjan / Guleria, Randeep / Sarkar, Chitra / Gupta, Ishaan / Jain, Deepali

Disease models & mechanisms

2022 Volume 15, Issue 5

Abstract: To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ...

Abstract	To elucidate the molecular mechanisms that manifest lung abnormalities during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, we performed whole-transcriptome sequencing of lung autopsies from 31 patients with severe COVID-19 and ten uninfected controls. Using metatranscriptomics, we identified the existence of two distinct molecular signatures of lethal COVID-19. The dominant 'classical' signature (n=23) showed upregulation of the unfolded protein response, steroid biosynthesis and complement activation, supported by massive metabolic reprogramming leading to characteristic lung damage. The rarer signature (n=8) that potentially represents 'cytokine release syndrome' (CRS) showed upregulation of cytokines such as IL1 and CCL19, but absence of complement activation. We found that a majority of patients cleared SARS-CoV-2 infection, but they suffered from acute dysbiosis with characteristic enrichment of opportunistic pathogens such as Staphylococcus cohnii in 'classical' patients and Pasteurella multocida in CRS patients. Our results suggest two distinct models of lung pathology in severe COVID-19 patients, which can be identified through complement activation, presence of specific cytokines and characteristic microbiome. These findings can be used to design personalized therapy using in silico identified drug molecules or in mitigating specific secondary infections.
MeSH term(s)	Autopsy ; COVID-19 ; Cytokines ; Humans ; Lung/pathology ; SARS-CoV-2
Chemical Substances	Cytokines
Language	English
Publishing date	2022-06-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.049572
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Oral Feeding of Cow Milk Containing A1 Variant of β Casein Induces Pulmonary Inflammation in Male Balb/c Mice

Shikha Yadav / Nakul Dev S. Yadav / Atish Gheware / Ankur Kulshreshtha / Pankaj Sharma / V. P. Singh

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 8

Abstract: Abstract Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in ...

Abstract	Abstract Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in several pathologies, but direct effect on lungs has not been studied. The objective of the present study was to evaluate the A1and A2 β casein variants of cow milk as factors causing allergic airway disease in murine model. Mice fed with A1A1 milk exhibited increased airway hyperresponsiveness with increasing concentration of bronchoconstrictor (methacholine), which was not observed in mice fed with A2A2 milk. Significantly elevated levels of IL-4 and IL-5 were found in bronchoalveolar lavage and serum of A1A1 variant fed mice. Increased IgE and IgG levels along with increased infiltration of lymphocytes and eosinophils, leading to peribronchial inflammation was also observed in A1A1 variant fed mice, although, no goblet cell hyperplasia or airway remodeling was observed. In contrast, A2A2 milk fed mice presented phenotype matching the control group, while A1A2 milk fed group presented an intermediate phenotype. In summary, our results show that A1 form of cow milk has a proinflammatory effect on the lung resulting in phenotype closely matching with the typical allergic asthma phenotype.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Transcriptome analysis and connectivity mapping of Cissampelos pareira L. provides molecular links of ESR1 modulation to viral inhibition.

Haider, Madiha / Dholakia, Dhwani / Panwar, Aleksha / Garg, Parth / Gheware, Atish / Singh, Dayanidhi / Singhal, Khushboo / Burse, Shaunak A / Kumari, Surekha / Sharma, Anmol / Ray, Arjun / Medigeshi, Guruprasad R / Sharma, Upendra / Prasher, Bhavana / Mukerji, Mitali

Scientific reports

2021 Volume 11, Issue 1, Page(s) 20095

Abstract: Bioactive fractions obtained from medicinal plants which have been used for the treatment of multiple diseases could exert their effects by targeting common pathways. Prior knowledge of their usage could allow us to identify novel molecular links. In ... ...

Abstract	Bioactive fractions obtained from medicinal plants which have been used for the treatment of multiple diseases could exert their effects by targeting common pathways. Prior knowledge of their usage could allow us to identify novel molecular links. In this study, we explored the molecular basis of action of one such herbal formulation Cissampelos pareira L. (Cipa), used for the treatment of female hormone disorders and fever. Transcriptomic studies on MCF7 cell lines treated with Cipa extract carried out using Affymetrix arrays revealed a downregulation of signatures of estrogen response potentially modulated through estrogen receptor α (ERα). Molecular docking analysis identified 38 Cipa constituents that potentially bind (ΔG < - 7.5) with ERα at the same site as estrogen. The expression signatures in the connectivity map ( https://clue.io/; ) revealed high positive scores with translation inhibitors such as emetine (score: 99.61) and knockdown signatures of genes linked to the antiviral response such as ribosomal protein RPL7 (score: 99.92), which is a reported ERα coactivator. Further, gene knockdown experiments revealed that Cipa exhibits antiviral activity in dengue infected MCF7 cells potentially modulated through estrogen receptor 1. This approach reveals a novel pathway involving the ESR1-RPL7 axis which could be a potential target in dengue viral infection.
MeSH term(s)	Antiviral Agents/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Breast Neoplasms/virology ; Cissampelos/chemistry ; Dengue/drug therapy ; Dengue/metabolism ; Dengue/pathology ; Dengue/virology ; Dengue Virus ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Humans ; MCF-7 Cells ; Plant Extracts/pharmacology ; Transcriptome/drug effects
Chemical Substances	Antiviral Agents ; ESR1 protein, human ; Estrogen Receptor alpha ; Plant Extracts
Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-99444-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito