BROWN FAT LESIONS AND REGENERATION IN EXPERIMENTAL COXSACKIE B-l VIRUS INFECTION, AND AFTER LOCALIZED FREEZING

1963 ◽  
Vol 9 (6) ◽  
pp. 891-897 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster
Keyword(s):  
Virus Infection ◽  
Inflammatory Response ◽  
Experimental Infection ◽  
Central Zone ◽  
Cell Lysis ◽  
Regenerative Process ◽  
Brown Fat ◽  
Fat Tissue ◽  
Coxsackie B ◽  
Localized Damage

Prompt regeneration of brown fat tissue in the albino mouse is observed following experimental infection with Coxsackie B-l virus. The sequence of changes is recorded in detail.The inflammatory response and regenerative process differ in the central and peripheral zones of the brown fat lobules. Cell lysis is predominant in the central zone while a necrotic process often accompanied by the formation of lipogran-ulomas is seen in the peripheral zones.Similar inflammatory and regenerative changes are observed following localized damage of the brown fat tissue inflicted by freezing.

THE AGE FACTOR IN EXPERIMENTAL COXSACKIE B-3 INFECTION

1959 ◽  
Vol 5 (6) ◽  
pp. 595-604 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster
Keyword(s):  
White Mouse ◽  
Brown Fat ◽  
Fat Tissue ◽  
Standard Strain ◽  
Adult Mice ◽  
Age Factor ◽  
Large Groups ◽  
Heart Lesions ◽  
The Brain ◽  
Coxsackie B

A detailed study of the influence of the age factor upon the susceptibility of the white mouse to experimental infection with a standard strain of Coxsackie B-3 virus has been undertaken. A fairly accurate assessment of the susceptibility of the brain, heart, and brown fat tissues has been achieved by examining sufficiently large groups of animals inoculated at ages varying from 4 days to 182 days by histological and virological procedures.The contrasting patterns of changing susceptibility in the brain and heart were quite remarkable. Brain lesions were not found in mice inoculated after 12 days of age but heart lesions were severest in animals inoculated between 12 and 23 days of age. In both heart and brown fat tissue lesions could be found in adult animals infected with Coxsackie B-3 virus. Attention is drawn to the fact that the pathological response in the brown fat tissue is different in sucklings, weanlings, and adult mice.

Anti-obesity effect of taurine through inhibition of adipogenesis in white fat tissue but not in brown fat tissue in a high-fat diet-induced obese mouse model

Amino Acids ◽  
2018 ◽  
Vol 51 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Kyoung Soo Kim ◽  
Min Ju Jang ◽  
Sungsoon Fang ◽  
Seul Gi Yoon ◽  
Il Yong Kim ◽  
...  
Keyword(s):  
Mouse Model ◽  
High Fat Diet ◽  
Brown Fat ◽  
Obese Mouse ◽  
Fat Tissue ◽  
High Fat ◽  
White Fat

scholarly journals The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection

2015 ◽  
Vol 59 (10) ◽  
pp. 6317-6327 ◽  
Author(s):  
Hussein Traboulsi ◽  
Alexandre Cloutier ◽  
Kumaraswamy Boyapelly ◽  
Marc-André Bonin ◽  
Éric Marsault ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Inflammatory Cell ◽  
Influenza Virus Infection ◽  
Cytokine Gene Expression ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment ◽  
Anti Inflammatory

ABSTRACTThe host response to influenza virus infection is characterized by an acute lung inflammatory response in which intense inflammatory cell recruitment, hypercytokinemia, and a high level of oxidative stress are present. The sum of these events contributes to the virus-induced lung damage that leads to high a level of morbidity and mortality in susceptible infected patients. In this context, we identified compounds that can simultaneously reduce the excessive inflammatory response and the viral replication as a strategy to treat influenza virus infection. We investigated the anti-inflammatory and antiviral potential activities of isoliquiritigenin (ILG). Interestingly, we demonstrated that ILG is a potent inhibitor of influenza virus replication in human bronchial epithelial cells (50% effective concentration [EC50] = 24.7 μM). In addition, our results showed that this molecule inhibits the expression of inflammatory cytokines induced after the infection of cells with influenza virus. We demonstrated that the anti-inflammatory activity of ILG in the context of influenza virus infection is dependent on the activation of the peroxisome proliferator-activated receptor gamma pathway. Interestingly, ILG phosphate (ILG-p)-treated mice displayed decreased lung inflammation as depicted by reduced cytokine gene expression and inflammatory cell recruitment. We also demonstrated that influenza virus-specific CD8+effector T cell recruitment was reduced up to 60% in the lungs of mice treated with ILG-p (10 mg/kg) compared to that in saline-treated mice. Finally, we showed that administration of ILG-p reduced lung viral titers and morbidity of mice infected with the PR8/H1N1 virus.

scholarly journals Proinflammatory responses in SARS-CoV-2 infected and soluble spike glycoprotein S1 subunit activated human macrophages

2021 ◽  
Author(s):  
Kim Chiok ◽  
Kevin Hutchison ◽  
Lindsay Grace Miller ◽  
Santanu Bose ◽  
Tanya A Miura
Keyword(s):  
Virus Infection ◽  
Inflammatory Response ◽  
Virus Replication ◽  
Inflammatory Mediators ◽  
Inflammatory Responses ◽  
Activated Macrophages ◽  
Human Macrophages ◽  
Tnf Α ◽  
Proinflammatory Responses

Critically ill COVID-19 patients infected with SARS-CoV-2 display signs of generalized hyperinflammation. Macrophages trigger inflammation to eliminate pathogens and repair tissue, but this process can also lead to hyperinflammation and resulting exaggerated disease. The role of macrophages in dysregulated inflammation during SARS-CoV-2 infection is poorly understood. We used SARS-CoV-2 infected and glycosylated soluble SARS-CoV-2 Spike S1 subunit (S1) treated THP-1 human-derived macrophage-like cell line to clarify the role of macrophages in pro-inflammatory responses. Soluble S1 upregulated TNF-α and CXCL10 mRNAs, and induced secretion of TNF-α from THP-1 macrophages. While THP-1 macrophages did not support productive SARS-CoV-2 replication, virus infection resulted in upregulation of both TNF-α and CXCL10 genes. Our study shows that S1 is a key viral component inducing inflammatory response in macrophages, independently of virus replication. Thus, virus-infected or soluble S1-activated macrophages may become sources of pro-inflammatory mediators contributing to hyperinflammation in COVID-19 patients.

Immunological Response of the Newborn Infant to Coxsackie B-4 Infection

PEDIATRICS ◽  
1967 ◽  
Vol 40 (3) ◽  
pp. 444-446
Author(s):  
OTTO F. SIEBER ◽  
ANDREW H. KILGUS ◽  
VINCENT A. FULGINITI ◽  
DAVID PEARLMAN
Keyword(s):  
Virus Infection ◽  
Newborn Infant ◽  
Antibody Formation ◽  
Immunological Response ◽  
Neutralizing Antibody ◽  
Neutralizing Activity ◽  
Coxsackie B

The sequence of antibody formation was followed from birth to 3 months of age in an infant who developed a mild neonatal Coxsackie B-4 virus infection. The infant produced specific 19-S Coxsackie B-4 neutralizing antibody by 14 days of age, with persistence of neutralizing activity in a 2 ME resistant fraction of immunoglobulin by 3 months of age.

Cytoplasmic p16 Is Expressed in Normal Brown Fat and Hibernomas

2020 ◽  
Vol 28 (5) ◽  
pp. 496-501
Author(s):  
Georgia Karpathiou ◽  
Jean Marc Dumollard ◽  
Zoe Evangelou ◽  
Anna Batistatou ◽  
Michel Peoc’h ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Brown Fat ◽  
Fat Tissue ◽  
P16 Expression ◽  
Tissue Browning

White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.

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