scholarly journals Hepatic Mitochondrial Dysfunction and Immune Response in a Murine Model of Peanut Allergy

Nutrients ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 744 ◽  
Author(s):  
Giovanna Trinchese ◽  
Lorella Paparo ◽  
Rosita Aitoro ◽  
Carmela Fierro ◽  
Michela Varchetta ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masahiro Kitabatake ◽  
Yoko Matsumura ◽  
Noriko Ouji-Sageshima ◽  
Tatsuki Nishioka ◽  
Atsushi Hara ◽  
...  

AbstractUlcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) induced by dysregulation of the immune response in the intestinal mucosa. Although the underlying mechanisms of UC development are not fully understood, disruption of gut microbiota, “dysbiosis”, is thought to lead to the development of IBD. Persimmon (Ebenaceae Diospyros kaki Thunb.)-derived tannin, which is a condensed polymeric tannin consisting of catechin groups, has antioxidant, anti-inflammatory, and antimicrobial activities. In this study, we assessed the effect of persimmon-derived tannin on a murine model of UC established by dextran sulfate sodium-induced colitis in female mice. Dietary supplementation of tannin significantly decreased disease activity and colon inflammation. A hydrolysate of tannin directly suppressed expression of inflammatory genes in macrophages in vitro. In faecal microbiota, the relative abundance of Bacteroides was increased significantly by tannin supplementation. Alpha-diversity indices in colitis-induced mice were significantly higher in the tannin diet group compared with the control diet group. Additionally, expansion of Enterobacteriaceae and Enterococcus, which is associated with disease progression of IBD, was remarkably suppressed in the tannin diet group. These results suggest that persimmon-derived tannin ameliorates colon inflammation in UC through alteration of the microbiota composition and immune response, which may be a promising candidate for IBD therapy.


2020 ◽  
Vol 24 ◽  
pp. 102137 ◽  
Author(s):  
Leticia Santos Pimentel ◽  
Carolina Alvarenga Turini ◽  
Paula Souza Santos ◽  
Mariana Abilio de Morais ◽  
Aline Gomes Souza ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-2
Author(s):  
Jorday Hernández-Aguas ◽  
José Luis Montiel-Hernández ◽  
Myriam A. De La Garza-Ramos ◽  
Rosa Velia Ruiz-Ramos ◽  
Erandi Escamilla García ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
pp. 11-16
Author(s):  
AR Awan ◽  
OL Tulp ◽  
HJ Field

Equine herpes virus (EHV-1) causes respiratory infections in equine, and results in abortion, paresis, neonatal death, and retinopathy and the virus may become latent following initial infection. Virus entry is via the respiratory route, and the virus replicates in the host in ciliated and non-ciliated epithelial cells of the respiratory tract and in Type 1 and Type 2 pneumocytes in the lung parenchyma. After viral replication in the respiratory system, the virus can become disseminated to other parts of body via viraemic cells. The virus also can cross the placenta which leads to abortion of live or dead fetuses without premonitory signs. Infected horses show transient immunity after natural or experimental infection and immune responses to EHV-1, but the immunoprotective status begins to decline after a few months of active infection. Due to the transient immune response, recovered horses are not immunoprotected and thus are prone to subsequent re-infection. Immunity is not long lived after experimental or natural infection, and as a result the development of an effective vaccine has remained a challenge. In this study viraemic cells were studied in a murine EHV-1 infection model. Mice were infected intranasally and viraemic cells were studied on days three and five which occurs during the peak of the infection. The results of this study may help to identify the nature of viraemic cells and their role in the transient immune response to infection. Buffy coat cells and lungs were removed and stained with a fluorescent antibody test for EHV-1 antigen, and lung specimens were subjected to transmission electron microscopy. Both techniques confirmed the presence of viraemic cells in lung tissues. These viraemic cells were further stained for EHV-1 antigen, and for CD4 or CD8 biomarkers and results are discussed re: pathogenesis of EHV-1 infection, identification of viraemic cells in a murine model and possible link of viraemia to transient immune responses in EHV-1 infection, which demonstrate the validity of this murine model for the investigation of the cytopathologic mechanism and sequelae of EHV manifestation in this model.


2015 ◽  
Vol 135 (2) ◽  
pp. AB235 ◽  
Author(s):  
Kamal D. Srivastava ◽  
Alyssa Siefert ◽  
Tarek Fahmy ◽  
Michael J. Caplan ◽  
Xiu-Min Li ◽  
...  

2010 ◽  
Vol 78 (11) ◽  
pp. 4839-4849 ◽  
Author(s):  
Alexandra Correia ◽  
Ulrich Lermann ◽  
Luzia Teixeira ◽  
Filipe Cerca ◽  
Sofia Botelho ◽  
...  

ABSTRACTCandida albicanssecreted aspartyl proteinases (Saps) are considered virulence-associated factors. Several members of the Sap family were claimed to play a significant role in the progression of candidiasis established by the hematogenous route. This assumption was based on the observed attenuated virulence ofsap-null mutant strains. However, the exclusive contribution ofSAPgenes to their attenuated phenotype was not unequivocally confirmed, as the Ura status of these mutant strains could also have contributed to the attenuation. In this study, we have reassessed the importance ofSAP1toSAP6in a murine model of hematogenously disseminated candidiasis usingsap-null mutant strains not affected in theirURA3gene expression and compared their virulence phenotypes with those of Ura-blastersapmutants. The median survival time of BALB/c mice intravenously infected with a mutant strain lackingSAP1toSAP3was equivalent to that of mice infected with wild-type strain SC5314, while those infected with mutant strains lackingSAP5showed slightly extended survival times. Nevertheless, no differences could be observed between the wild type and a Δsap456mutant in their abilities to invade mouse kidneys. Likewise, a deficiency inSAP4toSAP6had no noticeable impact on the immune response elicited in the spleens and kidneys ofC. albicans-infected mice. These results contrast with the behavior of equivalent Ura-blaster mutants, which presented a significant reduction in virulence. Our results suggest that Sap1 to Sap6 do not play a significant role inC. albicansvirulence in a murine model of hematogenously disseminated candidiasis and that, in this model, Sap1 to Sap3 are not necessary for successfulC. albicansinfection.


2018 ◽  
Vol 36 (3) ◽  
pp. 381-410 ◽  
Author(s):  
Angela M Jarrett ◽  
Meghan J Bloom ◽  
Wesley Godfrey ◽  
Anum K Syed ◽  
David A Ekrut ◽  
...  

Abstract The goal of this study is to develop an integrated, mathematical–experimental approach for understanding the interactions between the immune system and the effects of trastuzumab on breast cancer that overexpresses the human epidermal growth factor receptor 2 (HER2+). A system of coupled, ordinary differential equations was constructed to describe the temporal changes in tumour growth, along with intratumoural changes in the immune response, vascularity, necrosis and hypoxia. The mathematical model is calibrated with serially acquired experimental data of tumour volume, vascularity, necrosis and hypoxia obtained from either imaging or histology from a murine model of HER2+ breast cancer. Sensitivity analysis shows that model components are sensitive for 12 of 13 parameters, but accounting for uncertainty in the parameter values, model simulations still agree with the experimental data. Given theinitial conditions, the mathematical model predicts an increase in the immune infiltrates over time in the treated animals. Immunofluorescent staining results are presented that validate this prediction by showing an increased co-staining of CD11c and F4/80 (proteins expressed by dendritic cells and/or macrophages) in the total tissue for the treated tumours compared to the controls ($p < 0.03$). We posit that the proposed mathematical–experimental approach can be used to elucidate driving interactions between the trastuzumab-induced responses in the tumour and the immune system that drive the stabilization of vasculature while simultaneously decreasing tumour growth—conclusions revealed by the mathematical model that were not deducible from the experimental data alone.


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