scholarly journals Caloric restriction attenuates C57BL/6J mouse lung injury and extra-pulmonary toxicity induced by real ambient particulate matter exposure

2020 ◽  
Author(s):  
Daochuan Li ◽  
Shen Chen ◽  
Qiong Li ◽  
Liping Chen ◽  
Haiyan Zhang ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Caloric Restriction ◽  
Pulmonary Toxicity ◽  
Cell Activation ◽  
Dietary Intervention ◽  
Xenobiotic Metabolism ◽  
Mouse Lung ◽  
Human Beings ◽  
Exposure System ◽  
Extra Pulmonary

Abstract Background: Caloric restriction (CR) is known to improve health and extend lifespan in human beings. The effects of CR on adverse health outcomes in response to particulate matter (PM) exposure and the underlying mechanisms have yet to be defined.Results: Male C57BL/6J mice were fed with a CR diet or ad libitum (AL) and exposed to PM for 4 weeks in a real-ambient PM exposure system located at Shijiazhuang, China, with a daily mean concentration (95.77 μg/m³) of PM2.5. Compared to AL-fed mice, CR-fed mice showed attenuated PM-induced pulmonary injury and extra-pulmonary toxicity characterized by reduction in oxidative stress, DNA damage and inflammation. RNA sequence analysis revealed that several pulmonary pathways that were involved in production of reactive oxygen species (ROS), cytokine production, and inflammatory cell activation were inactivated, while those mediating antioxidant generation and DNA repair were activated in CR-fed mice upon PM exposure. In addition, transcriptome analysis of murine livers revealed that CR led to induction of xenobiotic metabolism and detoxification pathways, corroborated by increased levels of urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and decreased cytotoxicity measured in an ex vivo assay.Conclusion: These novel results demonstrate, for the first time, that CR in mice confers resistance against pulmonary injuries and extra-pulmonary toxicity induced by PM exposure. CR led to activation of xenobiotic metabolism and enhanced detoxification of PM-bound chemicals. These findings provide evidence that dietary intervention may afford therapeutic means to reduce the health risk associated with PM exposure.

Caloric restriction attenuates C57BL/6J mouse lung injury and systemic toxicity induced by real ambient particulate matter exposure

2020 ◽  
Author(s):  
Daochuan Li ◽  
Shen Chen ◽  
Qiong Li ◽  
Liping Chen ◽  
Haiyan Zhang ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Rna Sequencing ◽  
Caloric Restriction ◽  
Dietary Intervention ◽  
Xenobiotic Metabolism ◽  
Systemic Toxicity ◽  
Mouse Lung ◽  
Pulmonary Injury ◽  
Human Beings ◽  
Exposure System

Abstract Background: Caloric restriction (CR) is known to improve health and extend life span in human beings. The effects of CR on adverse health outcomes in response to particulate matter (PM) exposure and the underlying mechanisms have yet to be defined. Results: Male C57BL/6J mice were fed with CR diet or ad libitum (AL) and exposed to PM for 4 weeks in a real-ambient PM exposure system located at Shijiazhuang, China, with a daily mean concentration (95.77 μg/m³) of PM 2.5. Compared to AL-fed mice, CR-fed mice attenuated PM-induced pulmonary injury and systemic toxicity characterized by reduction in oxidative stress, DNA damage and inflammation. Analysis of RNA sequencing revealed that several pulmonary pathways involved in production of ROS, cytokine production, and inflammatory cell activation were inactivated, while those mediating antioxidant generation and DNA repair were activated in CR-fed mice upon PM exposure. In addition, transcriptome analysis of murine livers revealed that CR led to induction of xenobiotic metabolism and detoxification pathways, corroborated by increased levels of urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and decreased cytotoxicity measured in an ex vivo assay. Conclusion: These novel results demonstrate, for the first time, that CR in mice confers resistance against pulmonary injuries and systemic toxicity induced by PM exposure. CR led to activation of xenobiotic metabolism and enhanced detoxification of PM-bound chemicals. These findings provide evidence that dietary intervention may afford therapeutic means to reduce the health risk associated with PM exposure. Keywords: Caloric restriction, particulate matter, pulmonary injury, systemic effects, RNA sequencing, xenobiotic metabolism.

scholarly journals Effects of Late-Life Caloric Restriction on Age-Related Alterations in the Rat Cortex and Hippocampus

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 232
Author(s):  
Claudia Tonini ◽  
Marco Segatto ◽  
Francesca Martino ◽  
Luisa Cigliano ◽  
Martina Nazzaro ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Dietary Intervention ◽  
Cholesterol Metabolism ◽  
Late Life ◽  
Experimental Models ◽  
Human Beings ◽  
Dietary Regimen ◽  
Age Related ◽  
Energetic Balance ◽  
The Brain

Background: A major problem of aging is the disruption of metabolic homeostasis. This is particularly relevant in the brain where it provokes neurodegeneration. Caloric restriction is a physiologic intervention known to delay the deleterious consequences of aging in several species ranging from yeast to mammals. To date, most studies on experimental models have started this dietary intervention from weaning, which is very difficult to be translated to human beings. Here, we study the effects of a more realistic dietary regimen in rats, starting at an advanced age and lasting for six months. Methods: we analyzed in the cortex and hippocampus, the proteins involved in the energetic balance of the cells, cholesterol metabolism, oxidative stress response, inflammation, synaptic impairment, and brain trophism. Results: our results suggest that caloric restriction in late life can revert only some age-related changes studied here.

Application of a real-ambient fine particulate matter exposure system on different animal models

2021 ◽  
Vol 105 ◽  
pp. 64-70
Author(s):  
Yuanyuan Song ◽  
Lifang Zhao ◽  
Zenghua Qi ◽  
Yanhao Zhang ◽  
Guodong Cao ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Animal Models ◽  
Fine Particulate Matter ◽  
Exposure System ◽  
Fine Particulate ◽  
Particulate Matter Exposure

scholarly journals In Vivo Role of Dendritic Cells in a Murine Model of Pulmonary Cryptococcosis

2006 ◽  
Vol 74 (7) ◽  
pp. 3817-3824 ◽  
Author(s):  
Karen L. Wozniak ◽  
Jatin M. Vyas ◽  
Stuart M. Levitz
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Ex Vivo ◽  
Interleukin 2 ◽  
Mouse Lung

ABSTRACT Dendritic cells (DC) have been shown to phagocytose and kill Cryptococcus neoformans in vitro and are believed to be important for inducing protective immunity against this organism. Exposure to C. neoformans occurs mainly by inhalation, and in this study we examined the in vivo interactions of C. neoformans with DC in the lung. Fluorescently labeled live C. neoformans and heat-killed C. neoformans were administered intranasally to C57BL/6 mice. At specific times postinoculation, mice were sacrificed, and lungs were removed. Single-cell suspensions of lung cells were prepared, stained, and analyzed by microscopy and flow cytometry. Within 2 h postinoculation, fluorescently labeled C. neoformans had been internalized by DC, macrophages, and neutrophils in the mouse lung. Additionally, lung DC from mice infected for 7 days showed increased expression of the maturation markers CD80, CD86, and major histocompatibility complex class II. Finally, ex vivo incubation of lung DC from infected mice with Cryptococcus-specific T cells resulted in increased interleukin-2 production compared to the production by DC from naïve mice, suggesting that there was antigen-specific T-cell activation. This study demonstrated that DC in the lung are capable of phagocytosing Cryptococcus in vivo and presenting antigen to C. neoformans-specific T cells ex vivo, suggesting that these cells have roles in innate and adaptive pulmonary defenses against cryptococcosis.

scholarly journals T-cell activation-inhibitory assay: a proposed novel method for screening caloric restriction mimetics

2019 ◽  
Vol 40 (6) ◽  
pp. 235-241
Author(s):  
Shu IURA ◽  
Yuusei OJIMA ◽  
Yoshiaki AMAKURA ◽  
Morio YOSHIMURA ◽  
Atsushi SAWAMOTO ◽  
...  
Keyword(s):  
T Cell ◽  
Caloric Restriction ◽  
T Cell Activation ◽  
Cell Activation ◽  
Novel Method

scholarly journals Resveratrol inhibits IL-33–mediated mast cell activation by targeting the MK2/3–PI3K/Akt axis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shotaro Nakajima ◽  
Kayoko Ishimaru ◽  
Anna Kobayashi ◽  
Guannan Yu ◽  
Yuki Nakamura ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cytokine Production ◽  
Allergic Diseases ◽  
Mast Cell Activation ◽  
Akt Pathway ◽  
Mouse Lung ◽  
Mouse Bone Marrow ◽  
Interleukin 33

AbstractInterleukin-33 (IL-33)/ST2–mediated mast cell activation plays important roles in the pathophysiology of allergic diseases. Hence, pharmacologically targeting the IL-33/ST2 pathway in mast cells could help to treat such diseases. We found that resveratrol inhibits IL-33/ST2–mediated mast cell activation. Resveratrol suppressed IL-33–induced IL-6, IL-13, and TNF-α production in mouse bone marrow–derived mast cells (BMMCs), mouse fetal skin–derived mast cells, and human basophils. Resveratrol also attenuated cytokine expression induced by intranasal administration of IL-33 in mouse lung. IL-33–mediated cytokine production in mast cells requires activation of the NF-κB and MAPK p38–MAPK-activated protein kinase-2/3 (MK2/3)–PI3K/Akt pathway, and resveratrol clearly inhibited IL-33–induced activation of the MK2/3–PI3K/Akt pathway, but not the NF-κB pathway, without affecting p38 in BMMCs. Importantly, resveratrol inhibited the kinase activity of MK2, and an MK2/3 inhibitor recapitulated the suppressive effects of resveratrol. Resveratrol and an MK2/3 inhibitor also inhibited IgE-dependent degranulation and cytokine production in BMMCs, concomitant with suppression of the MK2/3–PI3K/Akt pathway. These findings indicate that resveratrol inhibits both IL-33/ST2–mediated and IgE-dependent mast cell activation principally by targeting the MK2/3–PI3K/Akt axis downstream of p38. Thus, resveratrol may have potential for the prevention and treatment of broad ranges of allergic diseases.

scholarly journals The Role of Fucoidans Isolated from the Sporophylls of Undaria pinnatifida against Particulate-Matter-Induced Allergic Airway Inflammation: Evidence of the Attenuation of Oxidative Stress and Inflammatory Responses

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2869 ◽  
Author(s):  
Kalahe Hewage Iresha Nadeeka Madushani Herath ◽  
Hyo Jin Kim ◽  
Areum Kim ◽  
Chung Eui Sook ◽  
Boo-Yong Lee ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Inflammatory Response ◽  
Airway Inflammation ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Undaria Pinnatifida ◽  
Mast Cell Activation ◽  
Cell Hyperplasia ◽  
Mucus Hypersecretion ◽  
Asthma Symptoms

Ambient particulate matter (PM) is a critical environment pollutant that promotes the onset and aggravation of respiratory diseases such as asthma through airway inflammation and hypersecretion of mucus. In this study, we aimed to identify the effects of fucoidans isolated from sporophylls of Undaria pinnatifida on asthma symptoms such as the inflammatory response and mucus secretion using a mouse model. Balb/c mice, intraperitoneally sensitized with ovalbumin (OVA, 10 μg) dissolved in 200 µL saline and 2 mg Al(OH)3, were exposed to PM (5 mg/m3) for 7 consecutive days. In parallel, along with PM exposure, we orally administrated fucoidans (100, 400 mg/Kg) or prednisone (5 mg/Kg), an anti-inflammatory drug. We found that oral administration of fucoidans significantly attenuated PM-induced lipid peroxidation and infiltration of inflammatory cells like F4/80+ macrophages, Gr-1+ granulocytes, and CD4+ T lymphocytes. Fucoidans also attenuated the level of PM-exacerbated IL-4, a primitive cytokine released in Th2 mediated eosinophilic asthma. This further suppressed mast cell activation, degranulation and IgE synthesis of PM exposed mice. Interestingly, fucoidans attenuated PM-exacerbated mucus hypersecretion and goblet cell hyperplasia. Therefore, our results suggest that fucoidans are effective at alleviating PM-exacerbated allergic asthma symptoms by attenuating the airway inflammatory response and mucus hypersecretion.

Extra Pulmonary Toxicity Assessment of Gold and Silver Nanorods Following Intra Tracheal Instillation in Rats

Drug Research ◽  
2017 ◽  
Vol 67 (10) ◽  
pp. 606-612
Author(s):  
Harikiran Lingabathula ◽  
Narsimhareddy Yellu
Keyword(s):  
Serum Creatinine ◽  
Pulmonary Toxicity ◽  
Biochemical Analysis ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Lymphocytic Infiltration ◽  
Central Vein ◽  
Silver Nanorods ◽  
Serum Biochemical ◽  
Extra Pulmonary

AbstractThe gold nanorods (GNRs) and silver nanorods (SNRs) are utilized in various types of industrial and commercial applications. But, there is limited availability of extra pulmonary toxicity data regarding these nanorods. The present investigation evaluated the extra pulmonary toxicity induced by 10 and 25 nm GNRs and SNRs in rats following intra tracheal instillation. The serum biochemical analysis results have shown elevated levels of serum alanine transaminase (ALT) and serum creatinine following 1 day and 1 week post instillation. GNRs have shown greatly increased serum ALT levels at 1 day, 1 week and 1 month post exposure periods compared to SNRs and quartz (QTZ) treated rats. In case of serum creatinine levels, both GNRs and SNRs have shown similar elevated levels. Histopathology studies of rat liver tissues following exposure of GNRs and SNRs displayed that congestion of central vein, shrinkage and ballooning of hepatocytes and lymphocytic infiltration leading to degeneration after 1 week and 1 month post instillation periods. The histopathology of rat kidney tissue was showed tubular dilation, degeneration and necrosis with 10 nm SNRs and 10 nm GNRs after 1 month post instillation period. The 10 nm GNRs and SNRs have shown great changes in serum biochemical analysis and histopathological studies compared to 25 nm test nanorods. These observations suggest the size and dose dependent translocation and extra pulmonary toxicity of both GNRs and SNRs.

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