scholarly journals A Cumulative Effect of Food and Viruses to Trigger Celiac Disease (CD): A Commentary on the Recent Literature

2021 ◽  
Vol 22 (4) ◽  
pp. 2027
Author(s):  
Maria Vittoria Barone ◽  
Salvatore Auricchio
Keyword(s):  
Celiac Disease ◽  
Protective Effect ◽  
Inflammatory Diseases ◽  
Cumulative Effect ◽  
Chronic Inflammatory Diseases ◽  
Clinical Observations ◽  
Effect Of Food ◽  
Gliadin Protein

Celiac disease (CD) is a type of inflammatory chronic disease caused by nutrients such as gliadin that induce a TC (T cell)-mediated response in a partially known genetical background in an environment predisposed to inflammation, including viruses and food. Various experimental and clinical observations suggest that multiple agents such as viruses and bacteria have some common, inflammatory pathways predisposing individuals to chronic inflammatory diseases including celiac disease (CD). More recently, a Western diet and lifestyle have been linked to tissue inflammation and increase in chronic inflammatory diseases. In CD, the gliadin protein itself has been shown to be able to induce inflammation. A cooperation between viruses and gliadin is present in vitro and in vivo with common mechanisms to induce inflammation. Nutrients could have also a protective effect on CD, and in fact the anti-inflammatory Mediterranean diet has a protective effect on the development of CD in children. The possible impact of these observations on clinical practice is discussed.

Exploiting Anti-Inflammation Effects of Flavonoids in Chronic Inflammatory Diseases

2020 ◽  
Vol 26 (22) ◽  
pp. 2610-2619 ◽  
Author(s):  
Tarique Hussain ◽  
Ghulam Murtaza ◽  
Huansheng Yang ◽  
Muhammad S. Kalhoro ◽  
Dildar H. Kalhoro
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Diseases ◽  
Therapeutic Option ◽  
Cellular Level ◽  
Antiinflammatory Drugs ◽  
Suitable Alternative ◽  
Chronic Inflammatory Diseases

Background: Inflammation is a complex response of the host defense system to different internal and external stimuli. It is believed that persistent inflammation may lead to chronic inflammatory diseases such as, inflammatory bowel disease, neurological and cardiovascular diseases. Oxidative stress is the main factor responsible for the augmentation of inflammation via various molecular pathways. Therefore, alleviating oxidative stress is effective a therapeutic option against chronic inflammatory diseases. Methods: This review article extends the knowledge of the regulatory mechanisms of flavonoids targeting inflammatory pathways in chronic diseases, which would be the best approach for the development of suitable therapeutic agents against chronic diseases. Results: Since the inflammatory response is initiated by numerous signaling molecules like NF-κB, MAPK, and Arachidonic acid pathways, their encountering function can be evaluated with the activation of Nrf2 pathway, a promising approach to inhibit/prevent chronic inflammatory diseases by flavonoids. Over the last few decades, flavonoids drew much attention as a potent alternative therapeutic agent. Recent clinical evidence has shown significant impacts of flavonoids on chronic diseases in different in-vivo and in-vitro models. Conclusion: Flavonoid compounds can interact with chronic inflammatory diseases at the cellular level and modulate the response of protein pathways. A promising approach is needed to overlook suitable alternative compounds providing more therapeutic efficacy and exerting fewer side effects than commercially available antiinflammatory drugs.

scholarly journals The Involvement of Phospholipases A2in Asthma and Chronic Obstructive Pulmonary Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Ewa Pniewska ◽  
Rafal Pawliczak
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Animal Models ◽  
Pulmonary Disease ◽  
Cell Cultures ◽  
Inflammatory Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Diseases

The increased morbidity, mortality, and ineffective treatment associated with the pathogenesis of chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD) have generated much research interest. The key role is played by phospholipases from the A2superfamily: enzymes which are involved in inflammation through participation in pro- and anti-inflammatory mediators production and have an impact on many immunocompetent cells. The 30 members of the A2superfamily are divided into 7 groups. Their role in asthma and COPD has been studiedin vitroandin vivo(animal models, cell cultures, and patients). This paper contains complete and updated information about the involvement of particular enzymes in the etiology and course of asthma and COPD.

Abstract 415: Resolvin D1 Limits 5-lipoxygenase Nuclear Localization and Leukotriene B4 Synthesis by Inhibiting a Calcium-activated Kinase Pathway

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Gabrielle Fredman
Keyword(s):  
Nuclear Localization ◽  
Inflammatory Diseases ◽  
Intracellular Localization ◽  
Cytosolic Calcium ◽  
Leukotriene B4 ◽  
Resolvin D1 ◽  
Chronic Inflammatory Diseases ◽  
And Shifts

Introduction: Imbalances between pro-inflammatory and pro-resolving mediators can lead to chronic inflammatory diseases, such as atherosclerosis. Hypothesis: The balance of arachidonic acid (AA)-derived mediators in leukocytes is thought to be achieved through intracellular localization of 5-lipoxygenase (5-LOX): nuclear 5-LOX favors the biosynthesis of pro-inflammatory leukotriene B 4 (LTB 4 ), while, in theory, cytoplasmic 5-LOX could favor the biosynthesis of pro-resolving lipoxin A 4 (LXA 4 ). This balance is shifted in favor of LXA 4 by resolvin D1 (RvD1), a specialized pro-resolving mediator (SPM) derived from docosahexaenoic acid (DHA), but the mechanism is not known. Hence we hypothesized that RvD1 regulates 5-LOX localization in macrophages. Methods/Results: Here we report a new pathway through which RvD1 promotes nuclear exclusion of 5-LOX and thereby suppresses LTB 4 and enhances LXA 4 in macrophages. RvD1, by activating its receptor FPR2/ALX, suppresses cytosolic calcium and decreases activation of the calcium-sensitive kinase CaMKII. CaMKII inhibition suppresses activation P38 and MAPKAPK2 kinases, which reduces Ser271 phosphorylation of 5-LOX and shifts 5-LOX from the nucleus to the cytoplasm. As such, RvD1’s ability to decrease nuclear 5-LOX and the LTB 4 :LXA 4 ratio in vitro and in vivo was mimicked by macrophages lacking CaMKII or expressing S271A-5-LOX. Importantly, nuclear localization of 5-LOX has been reported in unstable advanced human atherosclerotic lesions, hence strategies to reverse this process are of interest. In this regard, RvD1 treatment of Ldlr -/- mice reduced macrophage 5-LOX localization and stabilized advanced plaques. Conclusions: Knowledge of this mechanism may provide new strategies for promoting inflammation resolution in chronic inflammatory diseases, like atherosclerosis.

scholarly journals Chrysanthemum indicum Attenuates Cisplatin-induced Nephrotoxicity both in vivo and in vitro

2015 ◽  
Vol 10 (3) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Tae-Won Kim ◽  
Young-Jung Kim ◽  
So-Ra Park ◽  
Chang-Seob Seo ◽  
Hyekyung Ha ◽  
...  
Keyword(s):  
Protective Effect ◽  
Inflammatory Diseases ◽  
In Vitro Study ◽  
Ethanol Extract ◽  
Sprague Dawley ◽  
Pk15 Cell ◽  
P53 Expression ◽  
Chrysanthemum Indicum

Chrysanthemum indicum Linné has been used in traditional medicine to treat various inflammatory diseases in East Asia. The aim of the present study was to investigate the protective effect of C. indicum ethanol extract (CILE) against cisplatin-induced nephrotoxicity. An HPLC-photodiode array method was used for fingerprint analysis of the CILE and ten major constituents were quantitatively analyzed. The protective effect of CILE on cisplatin-induced nephrotoxicity was assessed using both in vitro (porcine kidney cell; PK15 cell) and in vivo (Sprague Dawley rat) experiments. In the in vitro study, CILE enhanced PK15 cell viability after cisplatin treatment with recovered antioxidant status. Moreover, the increased p53 expression after cisplatin treatment was decreased in the CILE pretreated cells. In the in vivo study, SD rats were treated for 28 consecutive days with CILE (0, 100, 300 and 500 mg/kg). On day 23, a single dose of cisplatin (5 mg/kg) was injected to induce nephrotoxicity. The CILE pretreated group showed recovered serum renal function index with ameliorated oxidative stress. Histopathological alterations and apoptosis in the kidney were also decreased in CILE pretreated rats. Taken together, CILE could attenuate cisplatin-induced nephrotoxicity and might be a beneficial agent for acute renal failure management.

Acne, the microbiome and innate immunity

2016 ◽  
Vol 19 (5) ◽  
pp. 279-282
Author(s):  
Marius-Anton A Ionescu ◽  
M. Feuiolley ◽  
J. Enault ◽  
P. Wolkenstein ◽  
G. Robert ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Inflammatory Process ◽  
Ex Vivo ◽  
Inflammatory Diseases ◽  
Seborrheic Dermatitis ◽  
In Vivo Studies ◽  
Chronic Inflammatory Diseases ◽  
Acne Rosacea

In the laste years several articles focalized on human microbioma - the microorganisms from skin, mucosae, bowel - and on its role in chronic inflammatory diseases of the skin as acne, rosacea, atopic dermatitis, seborrheic dermatitis. In this article the authors present an update on particular acne skin’s microbioma, on innate immunity in acne and new physiopathology mecanisms described in inflammatory process in acne, and at the end we present in vitro, ex vivo and in vivo studies on the microbioma modulation and microbiofilm of pathogenic ribotypes of P. acnes leading to a significant improvement of acne in a series of 74 acne patients.

scholarly journals Phytochemicals as Anti-Inflammatory Agents in Animal Models of Prevalent Inflammatory Diseases

Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 5932
Author(s):  
Seong Ah Shin ◽  
Byeong Jun Joo ◽  
Jun Seob Lee ◽  
Gyoungah Ryu ◽  
Minjoo Han ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Defense Mechanism ◽  
Inflammatory Diseases ◽  
Disease Model ◽  
Model Systems ◽  
Molecular Signaling ◽  
Chronic Inflammatory Diseases ◽  
Anti Inflammatory

Phytochemicals are known to have anti-inflammatory effects in vitro and in vivo, such as in inflammatory disease model systems. Inflammation is an essential immune response to exogenous stimuli such as infection and injury. Although inflammation is a necessary host-defense mechanism, chronic inflammation is associated with the continuous local or systemic release of inflammatory mediators, non-cytokine mediators, such as ROS and NO, and inflammatory cytokines are strongly implicated in the pathogenesis of various inflammatory disorders. Phytochemicals that exhibit anti-inflammatory mechanisms that reduce sustained inflammation could be therapeutic candidates for various inflammatory diseases. These phytochemicals act by modulating several main inflammatory signaling pathways, including NF-κB, MAPKs, STAT, and Nrf-2 signaling. Here, we discuss the characteristics of phytochemicals that possess anti-inflammatory activities in various chronic inflammatory diseases and review the molecular signaling pathways altered by these anti-inflammatory phytochemicals, with a focus on transcription factor pathways. Furthermore, to evaluate the phytochemicals as drug candidates, we translate the effective doses of phytochemicals in mice or rat disease models into the human-relevant equivalent and compare the human-relevant equivalent doses of several phytochemicals with current anti-inflammatory drugs doses used in different types of chronic inflammatory diseases.

scholarly journals Cyclosporine A Promotes Bone Remodeling in LPS-Related Inflammation via Inhibiting ROS/ERK Signaling: Studies In Vivo and In Vitro

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Yuwei Zhao ◽  
Jing Gao ◽  
Yarong Zhang ◽  
Xueqi Gan ◽  
Haiyang Yu
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Bone Remodeling ◽  
Cyclosporine A ◽  
Alveolar Bone ◽  
Inflammatory Diseases ◽  
Bone Destruction ◽  
Erk Signaling

In some inflammatory diseases of bone, osteogenesis and osteoclasis are uncoupled and the balance is usually tipped resulting in bone destruction. The underlying mechanism of osteogenic dysfunction in inflammation still needs further study. This study is aimed at investigating the effects of cyclosporine A (CsA) on bone remodeling in lipopolysaccharide- (LPS-) related inflammation. In vivo, an alveolar bone defect model was established using 10-week-old C57BL/6J mice. The mice were divided into phosphate-buffered saline (PBS), LPS, and LPS+CsA groups. After 3 weeks, micro-CT analysis and histomorphometric evaluation were conducted. In vitro, murine osteoblasts were treated with vehicle medium, LPS, LPS+CsA, LPS+extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor (LPS+PD98059), and LPS+antioxidant (LPS+EUK134). Cell proliferation, osteogenic behaviors, oxidative stress, and ERK signaling were determined. By these approaches, LPS inhibited bone remodeling and promoted oxidative stress accumulation in alveolar bone defects. When animals were treated with CsA, all LPS-induced biochemical changes ameliorated with a marked protective effect. In vitro, the reactive oxygen species (ROS) levels in mitochondria increased in LPS-treated osteoblasts, with decreased expression of osteogenic differentiation genes. The CsA, PD98059, and EUK134 presented remarkable protective effects against LPS treatment. CsA effectively enhanced bone remodeling and attenuated oxidative stress caused by LPS via inhibiting ROS/ERK signaling. Taken together, the protective effect of CsA and the inhibitory effect of ERK signaling on the maintenance of mitochondrial function and reduction of ROS levels hold promise as a potential novel therapeutic strategy for inflammatory diseases in bones.

scholarly journals Inflammation induces pro-NETotic neutrophils via TNFR2 signaling

2021 ◽  
Author(s):  
Friederike Neuenfeldt ◽  
Jan Christoph Schumacher ◽  
Ricardo Grieshaber-Bouyer ◽  
Jüri Habicht ◽  
Jutta Schröder-Braunstein ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Diseases ◽  
Diagnostic Value ◽  
Polymorphonuclear Neutrophils ◽  
Oxygen Species ◽  
Chronic Inflammatory Diseases ◽  
Cytokine Treatment ◽  
Inflamed Tissue

Cytokines released during chronic inflammatory diseases induce pro-inflammatory properties in polymorphonuclear neutrophils (PMN). Here we show that in vitro cytokine treatment leads to the development of a subgroup of human PMN expressing CCR5, termed CCR5+ cytokine-induced PMN (CCR5+ cPMN). Auto/paracrine TNF signaling increases intracellular neutrophil elastase (ELANE) abundance and induces NETosis in CCR5+ cPMN. Triggering of CCR5 amplifies NETosis. Membranous TNF (mTNF) outside-in signaling induces the formation of reactive oxygen species, a known activator of NETosis. In vivo, we find an increased number of CCR5+ cPMN in the peripheral blood and inflamed lamina propria of patients with ulcerative colitis (UC) but not Crohn's disease (CD). Notably, failure of anti-TNF therapy is associated with higher frequencies of CCR5+ cPMN. In conclusion, we identify a phenotype of pro-NETotic, CCR5 positive PMN present in inflamed tissue in vivo and inducible in vitro. These cells may reflect an important component of tissue damage during chronic inflammation and could be of diagnostic value.

Protective Effect of Boswellic Resin Against Memory Loss and Alzheimer’s Induced by Aluminum Tetrachloride and D-Galactose (Experimental study in Mice)

2020 ◽  
Author(s):  
K. Zerrouki ◽  
N. Djebli ◽  
L. Gadouche ◽  
I. Erdogan Orhan ◽  
F. SezerSenol Deniz ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Protective Effect ◽  
Cell Damage ◽  
Memory Loss ◽  
Control Group ◽  
Total Extract ◽  
Swiss Mice ◽  
Octyl Acetate

Nowadays, because of the industrialization, a lot of contaminant were available ; the consequences of this availability are apparition of diseases including neurodegeneration. Neurodegenerative diseases of the human brain comprise a variety of disorders that affect an increasing percentage of the population. This study is based on the effect of the Boswellic resin, which is from a medicinal plant and known for its antioxidant effects on nerve cell damage. The objective of this work was to evaluate the in vitro and in vivo effects of the Boswellic resin on anticholinesterase activity and Alzheimer’s disease (AD) induced by D-galactose and aluminum tetrachloride in Swiss mice. Chemical composition of the resin essential oil was identified by the CG-MS analysis. The antioxidant activity was also assessed by the DMPD and metal chelation methods. In order to understand the mechanism of memory improvement, the acetylcholinesterase, AChE, and butyrylcholinesterase, BChE, inhibitory assays were performed. In vivo part of the study was achieved on Swiss mice divided into four groups: control, AD model, treated AD, and treated control group. The identification of chemical composition by CG-MS reach the 89.67% of the total extract compounds presented some very important molecules (p-Cymene, n-Octyl acetate, α-Pinene…). The present study proves that Boswellic resin improves memory and learning in treated Alzheimer’s group, modulates the oxidative stress and be involved in the protective effect against amyloid deposition and neurodegeneration, and stimulates the immune system in mice’s brain.

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