scholarly journals Effect of Tea Tree Oil on the Expression of Genes Involved in the Innate Immune System in Goat Rumen Epithelial Cells

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2460
Author(s):  
Zixuan Hu ◽  
Miao Lin ◽  
Xiaoyu Ma ◽  
Guoqi Zhao ◽  
Kang Zhan
Keyword(s):  
Epithelial Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Tea Tree Oil ◽  
Tea Tree ◽  
Rumen Epithelium ◽  
Expression Of Genes ◽  
Tnf Α ◽  
Rumen Epithelial Cells ◽  
Goat Rumen

In subacute rumen acidosis (SARA), the rumen epithelium is frequently attacked by endotoxin (LPS), which is caused by the lysis of dead Gram-negative bacteria. However, the rumen epithelium innate immune system can actively respond to the infection. Previous studies have demonstrated that tea tree oil (TTO) has good bactericidal and anti-inflammatory effects. Therefore, the aim of this study was to investigate the effect of TTO on the expression of genes involved in the inflammatory cytokines in goat rumen epithelial cells (GRECs) triggered by LPS. Our study shows that rumen epithelial cells isolated from goat rumen tissue can be cultured in vitro in 0.25% trypsin for a long time. These cells were identified as epithelial cells by the expression of cytokeratin 18, monocarboxylate transporter 4 (MCT4), Na[+]/H[+] hydrogen exchanger 1 (NHE1), putative anion transporter 1 (PAT1), vH+ ATPase B subunit (vH+ ATPase), and anion exchanger 2 (AE2). The mRNA expression of IL-1β, IL-6, TNF-α, TLR-2, NF-κB, CXCL6 and CXCL8 genes was significantly increased when LPS was used compared to untreated controls. In addition, mRNA expression of IL-1β, IL-6, TNF-α, TLR-2, NF-κB, CXCL8, CXCL6 and interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) genes was also significantly higher in the LPS group compared to the 0.05% TTO group. However, the expression of IL-1β, IL-6, TNF-α, TLR-2, CXCL6 and IFIT3 genes was significantly lower in the LPS and 0.05% TTO group compared to the 1 μg/mL LPS group. These results suggest that TTO can inhibit LPS-induced inflammatory cytokines expression in GRECs.

Tea tree oil prevents mastitis-associated inflammation in lipopolysaccharide-stimulated bovine mammary epithelial cells

2020 ◽  
Author(s):  
Zhi Chen ◽  
Yi Zhang ◽  
Jingpeng Zhou ◽  
Yu Tian ◽  
Qiaoni Zhou ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Differentially Expressed ◽  
Quantitative Detection ◽  
Tea Tree Oil ◽  
Tea Tree ◽  
Bovine Mammary Epithelial Cells ◽  
Tnf Α ◽  
Prevention And Treatment

Abstract Background Effective prevention and treatment of cow mastitis can provide a good guarantee for the healthy growth of cows and the qualified production of dairy products. The main purpose of this study was to explore the effect of tea tree oil on lipopolysaccharide (LPS) -induced mastitis in dairy cows, and the key gene in LPS -stimulated bovine mammary epithelial cells (BMECs) was identified. Results In this study, a model of mastitis induced by LPS was constructed, to which tea tree oil and LPS were added. The protective effects of tea tree oil on LPS-induced mastitis in BMECs were verified by the CCK-8 method, flow cytometry, real-time fluorescence quantitative detection, ELISA and other methods. The results showed that LPS at a concentration of 200 μg/ml could reduce the proliferative activity of the cells, induce a high proportion of apoptosis, and promote the expression of TNF-α, IL-6 and STAT1. Upon addition of tea tree oil, the proportion of apoptosis was reduced, and the expression of NF-κB, MAPK and caspase-3 was inhibited. Mammary epithelial cells were compared under control and LPS-treatment conditions and analyzed by second-generation sequencing. A total of 1270 mRNAs were identified as differentially expressed, of which 787 genes were upregulated and 483 were downregulated. These differentially expressed genes include TNF - α, IL6, STAT1, mapk4, etc. H&E staining and immunohistochemistry were used to verify the function of candidate genes. TNF-α and IL6 were observed to play important roles in mediating the preventive effect of tea tree oil on mastitis in LPS-stimulated bovine mammary epithelial cells. Conclusions The results showed that tea tree oil had a protective effect against LPS-induced mastitis. TNF - α and IL6 may be the marker genes of LPS-induced mastitis which provided a theoretical basis and experimental support for further research to determine new strategies for the prevention and treatment of mastitis and improvement of milk quality.

scholarly journals Bacillus anthracis Spores Stimulate Cytokine and Chemokine Innate Immune Responses in Human Alveolar Macrophages through Multiple Mitogen-Activated Protein Kinase Pathways

2006 ◽  
Vol 74 (8) ◽  
pp. 4430-4438 ◽  
Author(s):  
Kaushik Chakrabarty ◽  
Wenxin Wu ◽  
J. Leland Booth ◽  
Elizabeth S. Duggan ◽  
K. Mark Coggeshall ◽  
...  
Keyword(s):  
Immune System ◽  
Bacillus Anthracis ◽  
Alveolar Macrophages ◽  
Innate Immune System ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Tnf Α ◽  
Human Alveolar Macrophages ◽  
Mitogen Activated Protein ◽  
Multiple Signaling

ABSTRACT Contact with the human alveolar macrophage plays a key role in the innate immune response to Bacillus anthracis spores. Because there is a significant delay between the initial contact of the spore with the host and clinical evidence of disease, there appears to be temporary containment of the pathogen by the innate immune system. Therefore, the early macrophage response to Bacillus anthracis exposure is important in understanding the pathogenesis of this disease. In this paper, we studied the initial events after exposure to spores, beginning with the rapid internalization of spores by the macrophages. Spore exposure rapidly activated the mitogen-activated protein kinase signaling pathways extracellular signal-regulated kinase, c-Jun-NH2-terminal kinase, and p38. This was followed by the transcriptional activation of cytokine and primarily monocyte chemokine genes as determined by RNase protection assays. Transcriptional induction is reflected at the translational level, as interleukin-1α (IL-1α), IL-1β, IL-6, and tumor necrosis factor alpha (TNF-α) cytokine protein levels were markedly elevated as determined by enzyme-linked immunosorbent assay. Induction of IL-6 and TNF-α, and, to a lesser extent, IL-1α and IL-1β, was partially inhibited by the blockade of individual mitogen-activated protein kinases, while the complete inhibition of cytokine induction was achieved when multiple signaling pathway inhibitors were used. Taken together, these data clearly show activation of the innate immune system in human alveolar macrophages by Bacillus anthracis spores. The data also show that multiple signaling pathways are involved in this cytokine response. This report is the first comprehensive examination of this process in primary human alveolar macrophages.

scholarly journals Differential Activation of Innate Immune Responses by Adenovirus and Adeno-Associated Virus Vectors

2002 ◽  
Vol 76 (9) ◽  
pp. 4580-4590 ◽  
Author(s):  
Anne-Kathrin Zaiss ◽  
Qiang Liu ◽  
Gloria P. Bowen ◽  
Norman C. W. Wong ◽  
Jeffrey S. Bartlett ◽  
...  
Keyword(s):  
Immune System ◽  
Intravenous Administration ◽  
Innate Immune System ◽  
Innate Immune ◽  
Target Cells ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Adeno Associated Virus ◽  
Tnf Α ◽  
Adenovirus Vectors

ABSTRACT Adenovirus vectors induce acute inflammation of infected tissues due to activation of the innate immune system and expression of numerous chemokines and cytokines in transduced target cells. In contrast, adeno-associated virus (AAV) vectors are not associated with significant inflammation experimentally or clinically. We tested the ability of AAV vectors to induce the expression of chemokines in vitro and to activate the innate immune system in vivo. In human HeLa cells and murine renal epithelium-derived cells (REC cells) the adenovirus vector AdlacZ induced the expression of multiple inflammatory chemokines including RANTES, interferon-inducible protein 10 (IP-10), interleukin-8 (IL-8), MIP-1β, and MIP-2 in a dose-dependent manner. The use of AAVlacZ did not induce the expression of these chemokines above baseline levels despite 40-fold-greater titers than AdlacZ and greater amounts of intracellular AAVlacZ genomes according to Southern and slot blot analysis. This finding confirmed that the lack of AAVlacZ induction of chemokine was not due to reduced transduction. In DBA/2 mice, the intravenous administration of 2.5 × 1011 particles of AAVlacZ resulted in the rapid induction of liver tumor necrosis factor alpha (TNF-α), RANTES, IP-10, MIP-1β, MCP-1, and MIP-2 mRNAs. However, 6 h following injection, chemokine mRNA levels returned to baseline. As expected, administration of 10-fold less AdlacZ caused an induction of liver TNF-α and chemokine mRNAs that persisted for more than 24 h posttransduction. Whereas intravenous administration of 2.5 × 1011 particles of AAVlacZ triggered a transient infiltration of neutrophils and CD11b+ cells into liver, this response stood in contrast to widespread inflammation and toxicity induced by AdlacZ. Kupffer cell depletion abolished AAVlacZ but not AdlacZ-induced chemokine expression and neutrophil infiltration. In summary, these results show that AAV vectors activate the innate immune system to a lesser extent than do adenovirus vectors and offer a possible explanation for the reduced inflammatory properties of AAV compared to adenovirus vectors.

scholarly journals INHIBITORY EFFECTS ON TUMOR NECROSIS FACTOR ALPHA AND INTERLEUKIN 12 USING CLOBETASOL PROPIONATE LOADED TEA TREE OIL NANOEMULSION GEL ON ANIMAL MODEL

2018 ◽  
Vol 11 (6) ◽  
pp. 182
Author(s):  
Md Sarfaraz Alam ◽  
Mohamammad Daud Ali ◽  
Md Salahuddin Ansari ◽  
Pankaj Sharma
Keyword(s):  
Clobetasol Propionate ◽  
Interleukin 12 ◽  
Tea Tree Oil ◽  
Necrosis Factor Alpha ◽  
Tea Tree ◽  
Tnf Α ◽  
Nanoemulsion Gel ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Objective: The main objective of our study is to explore anti-inflammatory activity at its molecular level like tumor necrosis factor alpha (TNF-α), interleukin 12 (IL-12) expression, and histopathological study.Methods: As per solubility/miscibility of clobetasol propionate (CP) with tea tree oil (TTO), surfactant and cosurfactant (Smix), and water in a ratio of oil:Smix:water (15:35:50) taken in milliliter for the preparation of nanoemulsion. Induced allergic contact dermatitis (ACD) with dinitrofluorobenzene (DNFB) was used for the study. TNF-α and interleukin 12 (IL-12) were estimated with rabbit antimouse TNF-α and rat antimouse IL-12 antibodies in 1% of bovine serum albumin in phosphate buffer.Results: Topical application of CP loaded nanoemulsion gel inhibits ear inflammation and erythema in DNFB-induced ACD in mice and significantly reduces the intracellular edema and infiltration with inflammatory mediator cells involving of mononuclear cells and neutrophils. CP loaded nanoemulsion gel reduces expression of protein level of TNF-α and IL-12.Conclusion: CP loaded nanoemulsion gel confirmed that anti-inflammatory effects showed more rapidly than the placebo and marketed gel preparation. However, the animals treated with placebo nanoemulsion gel showed a somehow comparable reduction of their inflammation during treatment compared with the marketed gel. This effect may be due to anti-inflammatory effect of TTO. This result suggested that anti-inflammatory activity of placebo nanoemulsion gel may be due to TTO present in nanoemulsion as vehicle.

scholarly journals Case Report: Innate Immune System Challenge Unleashes Paraneoplastic Neurological Autoimmunity

2020 ◽  
Vol 11 ◽  
Author(s):  
Mingqin Zhu ◽  
Yuetao Ma ◽  
Anastasia Zekeridou ◽  
Vanda A. Lennon
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Protein Complexes ◽  
Innate Immune ◽  
Neurological Symptoms ◽  
Autoimmune Response ◽  
Tnf Α ◽  
Bladder Instillation ◽  
Molecular Patterns ◽  
Symptoms And Signs

Paraneoplastic autoimmune neurological disorders reflect tumor-initiated immune responses against onconeural antigens. Symptoms and signs can affect the central and/or peripheral nervous systems, neuromuscular junction or muscle, and typically evolve subacutely before an underlying neoplasm is discovered. We describe four patients whose neurological symptoms were precipitated by potent innate immune system challenges: bladder instillation of BCG, tick bite and an “alternative cancer therapy” with bacterial extracts and TNF-α. We hypothesize that a tumor-initiated autoimmune response (evidenced by autoantibody profiles), pre-dating the immune system challenge, was unmasked or amplified in these patients by cytokines released systemically from innate immune cells activated by microbial pathogen-associated molecular patterns (PAMPs). The resultant upregulation of cognate onconeural peptides as MHC1 protein complexes on neural cell surfaces would render those cells susceptible to killing by CD8+ T cells, thus precipitating the patient's neurological symptoms.

scholarly journals Adenoviruses Use Lactoferrin as a Bridge for CAR-Independent Binding to and Infection of Epithelial Cells

2006 ◽  
Vol 81 (2) ◽  
pp. 954-963 ◽  
Author(s):  
Cecilia Johansson ◽  
Mari Jonsson ◽  
Marko Marttila ◽  
David Persson ◽  
Xiao-Long Fan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Host Cells ◽  
Tear Fluid ◽  
Adenovirus Infection ◽  
Dependent Manner ◽  
Polarized Cells ◽  
Adenovirus Receptor ◽  
Dose Dependent

ABSTRACT Most adenoviruses bind to the coxsackie- and adenovirus receptor (CAR). Surprisingly, CAR is not expressed apically on polarized cells and is thus not easily available to viruses. Consequently, alternative mechanisms for entry of coxsackievirus and adenovirus into cells have been suggested. We have found that tear fluid promotes adenovirus infection, and we have identified human lactoferrin (HLf) as the tear fluid component responsible for this effect. HLf alone was found to promote binding of adenovirus to epithelial cells in a dose-dependent manner and also infection of epithelial cells by adenovirus. HLf was also found to promote gene delivery from an adenovirus-based vector. The mechanism takes place at the binding stage and functions independently of CAR. Thus, we have identified a novel binding mechanism whereby adenovirus hijacks HLf, a component of the innate immune system, and uses it as a bridge for attachment to host cells.

scholarly journals Mycobacterium avium Biofilm Attenuates Mononuclear Phagocyte Function by Triggering Hyperstimulation and Apoptosis during Early Infection

2013 ◽  
Vol 82 (1) ◽  
pp. 405-412 ◽  
Author(s):  
Sasha J. Rose ◽  
Luiz E. Bermudez
Keyword(s):  
Immune System ◽  
Mycobacterium Avium ◽  
Innate Immune System ◽  
Innate Immune ◽  
Mononuclear Phagocytes ◽  
Bacterial Killing ◽  
Content Type ◽  
Tnf Α

ABSTRACTMycobacterium aviumsubsp.hominissuisis an opportunistic human pathogen that has been shown to form biofilmin vitroandin vivo. Biofilm formationin vivoappears to be associated with infections in the respiratory tract of the host. The reasoning behind howM. aviumsubsp.hominissuisbiofilm is allowed to establish and persist without being cleared by the innate immune system is currently unknown. To identify the mechanism responsible for this, we developed anin vitromodel using THP-1 human mononuclear phagocytes cocultured with establishedM. aviumsubsp.hominissuisbiofilm and surveyed various aspects of the interaction, including phagocyte stimulation and response, bacterial killing, and apoptosis.M. aviumsubsp.hominissuisbiofilm triggered robust tumor necrosis factor alpha (TNF-α) release from THP-1 cells as well as superoxide and nitric oxide production. Surprisingly, the hyperstimulated phagocytes did not effectively eliminate the cells of the biofilm, even when prestimulated with gamma interferon (IFN-γ) or TNF-α or cocultured with natural killer cells (which have been shown to induce anti-M. aviumsubsp.hominissuisactivity when added to THP-1 cells infected with planktonicM. aviumsubsp.hominissuis). Time-lapse microscopy and the TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay determined that contact with theM. aviumsubsp.hominissuisbiofilm led to early, widespread onset of apoptosis, which is not seen until much later in planktonicM. aviumsubsp.hominissuisinfection. Blocking TNF-α or TNF-R1 during interaction with the biofilm significantly reduced THP-1 apoptosis but did not lead to elimination ofM. aviumsubsp.hominissuis. Our data collectively indicate thatM. aviumsubsp.hominissuisbiofilm induces TNF-α-driven hyperstimulation and apoptosis of surveilling phagocytes, which prevents clearance of the biofilm by cells of the innate immune system and allows the biofilm-associated infection to persist.

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