Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339197 | ENA |
REPOSITORIES: ENA
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Project description:Inhalation and low-dose aspiration elicit highly similar pulmonary inflammation which was confirmed by activation of essentially similar biological pathways and even the same genes. Present results provide evidence that oropharyngeal aspiration is valid approach for hazard assessment of nanomaterials and proper alternative method for inhalation exposure.
2017-05-01 | GSE85711 | GEO
Project description:Exposure to rod-shaped carbon nanotubes reveals novel innate immunity mediated asthma-like inflammation in mice. Inhalation of rCNT elicited a drastic infiltration of eosinophils into the lungs but only minor infiltration of neutrophils and lymphocytes. Transcriptomic study revealed remarkable effects of rCNT exposure, affecting almost exclusively pathways essential for innate immunity.
2014-10-01 | GSE50176 | GEO
Project description:Exposure to rod-shaped carbon nanotubes reveals novel innate immunity mediated asthma-like inflammation in mice. Inhalation of rCNT elicited a drastic infiltration of eosinophils into the lungs but only minor infiltration of neutrophils and lymphocytes. Transcriptomic study revealed remarkable effects of rCNT exposure, affecting almost exclusively pathways essential for innate immunity. Mice were exposed to rCNT or tCNT for 4 h and sacrificed immediately or 24 h after the exposure. The total RNA was extracted from lung samples, hybridized to Agilent microarray and analyzed with BioConductor package Limma. Untreated mice were used as control.
2014-10-01 | E-GEOD-50176 | biostudies-arrayexpress
Project description:Inhalation of rod-like carbon nanotubes causes unconventional asthma
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Project description:Ozone, the major component of air pollution, is an oxidant gas. Inhalation of high ambient levels of ozone causes oxidative stress and airway inflammation. To assess the biological responses of airway inflammatory cells to ozone-induced oxidative stress, we examined the gene expression of airway inflammatory cells in response to inhalation of ozone.
2015-06-15 | GSE58682 | GEO
Project description:Mice were aspirated with multiwalled carbon nanotubes in four doses ranging from 10 µg to 80 µg, plus control, and sacrificed after 1, 7, 28, and 56 days. RNA was extracted from the lungs and expression profilling by microarray was performed. This is a reference design two-color experiment. Each array was hybridized with RNA extracted from mouse lung labeled with Cy3, and universal reference RNA labeled with Cy5. Five different doses (0, 10ug, 20ug, 40ug, and 80ug) of multiwalled carbon nanotube aspiration were used and mice were sacrificed after 1, 7, 28, and 56 days. Eight replicates were used at each time/dose condition for a total of 160 arrays.
2012-06-25 | E-GEOD-29042 | biostudies-arrayexpress
Project description:Multipotent stromal cells (MSCs) are currently in clinical trials for a number of inflammatory diseases. Recent studies have demonstrated the ability of MSCs to attenuate inflammation in rodent models of acute lung injury (ALI) suggesting that MSCs may also be beneficial in treating ALI. To better understand how human MSCs (hMSCs) may act in ALI, the lungs of immunocompetent mice were exposed to lipopolysaccharide (LPS) and 4 hr later bone marrow derived hMSCS were delivered by oropharyngeal aspiration (OA). Administration of hMSCs significantly reduced the expression of pro-inflammatory cytokines, neutrophil counts and total protein in bronchoalveolar lavage. There was a concomitant reduction in pulmonary edema as indicated by a decrease in lung wet/dry weight ratio. The anti-inflammatory effects of hMSCs were not dependent on localization to the lung, as intraperitoneal administration of hMSCs also attenuated LPS-induced inflammation in the lung. Microarray analysis revealed significant induction of TNF-α-induced protein 6 (TSG-6) expression by hMSCs 12 hr after OA delivery to LPS-exposed lungs. Knockdown of TSG-6 expression in hMSCs by RNA interference abrogated most of their anti-inflammatory effects. In addition, intra-pulmonary delivery of recombinant human TSG-6 reduced LPS-induced inflammation in the lung. These results show that hMSCs recapitulate the observed beneficial effects of rodent MSCs in animal models of ALI and suggest that the anti-inflammatory properties of hMSCs in the lung are explained, at least in part, by activation of hMSCs to secrete TSG-6. Eight- to 10-week-old female BALB/C mice were treated with either 1 mg/kg lipopolysaccharide (LPS) in 100 μl PBS or an equal volume of PBS, as vehicle control, by oropharyngeal aspiration (OA). Four hours after LPS exposure, 250,000 human multipotent stromal cells in 100 μl of PBS were given by OA and 30 min later a second dose of equal concentration was administered, for a total of 500,000 hMSC. As a control, 200 μl PBS was delivered as described above. After 12 h, total RNA was isolated from (A) lungs of LPS-exposed mice treated with either hMSCs (LPS+MSC) or PBS (LPS+PBS), and (B) lungs of PBS-exposed mice treated with hMSCs (PBS+MSC). To obtain additional controls, hMSCs were mixed in vitro with either LPS- (LPS+MSC in vitro mix) or PBS-exposed (PBS+MSC in vitro mix) mouse lungs just before RNA isolation. RNA samples containing mouse and human RNA were first analyzed for amount of human RNA based on human GAPDH signal from real-time RT PCR. Samples with similar human RNA content were used for both mouse and human microarrays
2011-01-13 | E-GEOD-26567 | biostudies-arrayexpress
Project description:Aeroallergen sensing by airway epithelial cells can trigger pathogenic immune responses leading to chronic type 2 inflammation, the hallmark of airway diseases such as asthma. Airway tuft cells are specialized chemosensory epithelial cells and the dominant source of the epithelial cytokine IL-25 in the trachea and of cysteinyl leukotrienes (CysLTs) in the naïve murine nasal mucosa. How IL-25 and CysLTs might cooperatively promote type 2 inflammation in the airways has not been clarified. Here, we showed that inhalation of LTC4 in combination with a subthreshold dose of IL-25 led to dramatic synergistic induction of type 2 inflammation throughout the lungs, causing rapid eosinophilia, inflammatory type 2 innate lymphoid cell (ILC2) proliferation and type 2 cytokine production, dendritic cell (DC) and CD4+ T cell recruitment and goblet cell hyperplasia. While lung eosinophilia was dominantly mediated through the classical CysLT receptor CysLT1R, type 2 cytokines and activation of innate immune cells required signaling through both CysLT1R and CysLT2R. Tuft cell-specific deletion of Ltc4s, the terminal enzyme required for CysLT production, reduced lung inflammation and the systemic immune response after inhalation of the mold aeroallergen Alternaria; this effect was further enhanced by concomitant blockade of IL-25. Our findings identified a potent synergy of CysLTs and IL-25 downstream of aeroallergen-trigged activation of airway tuft cells leading to a highly polarized type 2 immune response and further implicate airway tuft cells as powerful modulators of type 2 immunity in the lungs.
2021-12-25 | GSE188820 | GEO
Project description:C57BL/6 mice were exposed by oropharyngeal aspiration to 28 nanomaterials including different surface functionalizations on 4 concecutive days with the dose of 10ug/day. Total RNA was collected from the mice lung biopsies after sacrificing.
2021-05-26 | GSE157266 | GEO
Project description:To evaluate the biological effects at the transcriptional level of manufactured nanomaterials, whole genome microarray analysis of rat lungs intratracheally instilled with cellulose nanofibrils (CNFs) with different physicochemical properties or multi-walled carbon nanotubes (MWCNTs) were performed.
2020-07-09 | GSE154013 | GEO