scholarly journals Inflammation in Focus: The Beginning and the End

2022 ◽  
Vol 27 ◽  
Author(s):  
Anna L. Kiss
Keyword(s):  
Chronic Inflammation ◽  
Inflammatory Cytokines ◽  
Bacterial Infections ◽  
Acute Inflammation ◽  
Tissue Injury ◽  
Biological Response ◽  
Signaling Cascade ◽  
Target Cells ◽  
Oxygen Species ◽  
Early Endosomes

The inflammation is an important biological response induced by various harmful stimuli, like viruses, bacterial infections, toxins, toxic compounds, tissue injury. During inflammation inflammatory cytokines and reactive oxygen species are produced. Inflammatory cytokines act on various receptors present on the plasma membrane of target cells. To initiate signaling cascade, and activate transcription factors, receptors should be internalized and enter the early endosomes, where the members of the signaling cascade can meet. The further cytoplasmic fate of the receptor plays crucial role in the progression and the course of inflammation. Usually acute inflammation removes injurious stimuli and helps to regain the normal healthy status of the organism. In contrast to this the uncontrolled chronic inflammation—stimulating other than immune cells, inducing transdifferentiation—can provide base of various serious diseases. This paper draws the attention of the long-lasting consequence of chronic inflammation, pointing out that one of the most important step in medication is to identify in time the factors initiating and maintaining inflammation.

scholarly journals Upregulation of TLR1, TLR2, TLR4, and IRAK-2 Expression During ML-1 Cell Differentiation to Macrophages: Role in the Potentiation of Cellular Responses to LPS and LTA

ISRN Oncology ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Kassim Traore ◽  
Barry Zirkin ◽  
Rajesh K. Thimmulappa ◽  
Shyam Biswal ◽  
Michael A. Trush
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Differentiation ◽  
Inflammatory Cytokines ◽  
Cellular Responses ◽  
Signaling Cascade ◽  
Oxygen Species ◽  
Induced Differentiation ◽  
Protein Levels

12-O-tetradecanoylphorbol 13-acetate (TPA) induces the differentiation of human myeloid ML-1 cells to macrophages. In the current study, the expression, responsiveness, and regulation of toll-like receptors (TLRs) in TPA-induced ML-1-derived macrophages were investigated. We have found that TPA-induced differentiation of ML-1 cells was accompanied by the upregulation of TLR1, TLR2, TLR4, and CD14 expression at both the mRNA and protein levels. Interestingly, TLR1 and TLR4 protein expression on ML-1 cells could be blocked by pretreatment with U0126, suggesting the role of an Erk1/2-induced differentiation signal in this process. In addition, the expression of IRAK-2, a key member of the TLR/IRAK-2/NF-κB-dependent signaling cascade was also induced in response to TPA. Accordingly, we demonstrated an increased cellular release of inflammatory cytokines (TNF-α and various interleukins) upon stimulation with LPS and LTA ligands for TLR4 and TLR2, respectively. Furthermore, using luminol-dependent chemiluminescence, addition of LPS and LTA induces a sustained DPI-inhibitable generation of reactive oxygen species (ROS) by the differentiated ML-1 cells. Together, these data suggest that the increase in the responsiveness of TPA-treated ML-1 cells to LPS and LTA occurs in response to the upregulation of their respective receptors as well as an induction of the IRAK-2 gene expression.

Association of Human Papillomavirus Infection and Inflammation in Cervical Cancer

2019 ◽  
Author(s):  
Nima Hemmat ◽  
Hossein Bannazadeh Baghi
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Chronic Inflammation ◽  
Inflammatory Cytokines ◽  
Tissue Injury ◽  
Hpv Infection ◽  
Papillomavirus Infection ◽  
E6 And E7 ◽  
Pg E2 ◽  
Pro Inflammatory Cytokines

Abstract Human papillomavirus (HPV) associated cancers, and in particular cervical cancer, are considered to be directly stimulated by HPV oncogenes. Alternatively, these types of cancers could also be indirectly stimulated by HPV-induced chronic inflammations, which in turn are also caused by HPV oncogenes activity. Chronic inflammation is associated with repeated tissue injury and development of mutations in the vital tumor suppressor genes. Thus, it is important to understand that the persistent HPV infection and its associated chronic inflammation is responsible for the progression of HPV-induced cancers. HPV E5, E6, and E7 could upregulate the expression of cyclooxygenase (COX)-2 and prostaglandin (PG) E2 followed by the activation of the COX-PG pathway. This pathway is assumed to be the main cause of HPV-induced inflammation. Additionally, HPV oncogenes could have an impact on the upregulation of pro-inflammatory cytokines in HPV-positive patients. The upregulation of such cytokines accelerates the incidence of inflammation following HPV infection. Other factors such as microRNAs, which are involved in the inflammation pathways and aging, give rise to the increased level of pro-inflammatory cytokines and could also be responsible for the acceleration of HPV-induced inflammation and consequent cervical cancer. In this review, the exact roles of HPV oncogenes in the occurrence of inflammation in cervical tissue, and the effects of other factors in this event are evaluated.

Acute inflammation and oxidative stress induced by lipopolysaccharide and the ameliorative effect of stingless bee honey

2020 ◽  
Vol 23 ◽  
Author(s):  
Yazan Ranneh ◽  
Ayman M. Mahmoud ◽  
Abdulmannan Fadel ◽  
Mohammed Albujja ◽  
Abdah Md Akim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Inflammatory Cytokines ◽  
Oxidative Dna Damage ◽  
Acute Inflammation ◽  
Tissue Injury ◽  
Multiple Organ ◽  
Stingless Bee ◽  
Ameliorative Effect ◽  
Pro Inflammatory Cytokines

Background: Systemic acute inflammation is the hallmark of sepsis and associated with multiple organ dysfunction. Objective: This study investigated the potential of stingless bee honey (SBH) to suppress lipopolysaccharide (LPS)-induced systemic acute inflammation in rats and to reveal the probable mechanism of action. Methods: Rats received 4.6 and 9.2 g/kg SBH for 7 days followed by a single injection of LPS and samples were collected after 6 h. Results: LPS induced liver, kidney, heart and lung injury manifested by increased serum transaminases, alkaline phosphatase, creatine kinase, creatinine and urea, along with multiple histological alterations, particularly, leukocyte infiltrations. Pro-inflammatory cytokines were elevated in serum, and NF-κB p65, p38 MAPK and HMGB-1 were significantly increased in different tissues of LPS-challenged rats. SBH prevented tissue injury, ameliorated pro-inflammatory cytokines, and suppressed NF-κB p65, p38 MAPK and HMGB-1 in rats received LPS. In addition, SBH diminished reactive oxygen species (ROS) production, lipid peroxidation and oxidative DNA damage, and enhanced glutathione and Nrf2 in LPS-induced rats. Conclusion: SBH prevents systemic acute inflammation by suppressing NF-κB, p38 MAPK, HMGB-1, oxidative stress and tissue injury in rats. Thus, SBH may represent an effective anti-inflammatory nutraceutical, pending further mechanistic studies.

Effect of Nectaroscordum koelzi Methanolic Extract on Acute and Chronic Inflammation in Male Mice

2020 ◽  
Vol 20 ◽  
Author(s):  
Karam Hossein Hasanvand ◽  
Mojtaba Khaksarian ◽  
Maryam Alipour ◽  
Hormoz Mahmoudvand ◽  
Massumeh Naizi ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Chronic Inflammation ◽  
Acute Inflammation ◽  
Methanol Extract ◽  
Significant Activity ◽  
Paw Edema ◽  
Ear Edema ◽  
Edema Volume ◽  
Cotton Pellet ◽  
Acute And Chronic Inflammation

Introduction: The present study deals with the effect of Nectaroscordum koelzi fruit extract on acute and chronic inflammation. Methods: Totally, 84 NMRI mice were used in this study. The extract effect on acute inflammation was analyzed by increasing vascular permeability via acetic acid and xylene induced ear edema among mice. The extract was evaluated in terms of effects on chronic inflammation by means of the cotton pellet test among mice. For the assessment of inflammation degree, the mice paw edema volume was measured by the plethysmometric test. Results: The findings showed that the extract was effective on acute inflammation induced by acetic acid in mice. In the xylene ear edema, N. koelzi extract indicated the significant activity in mice. In the cotton pellet method, the methanol extract produced a significant reduction in comparison with the control and dexamethasone. Mice paw edema volume decreased with the extract. Conclusion: In general, the data from the experiments indicated that the methanol extract of N. koelzi has an anti-inflammatory effect on acute and chronic inflammation. However, the exact contributing mechanisms have not been investigated for the pharmacological effects.

scholarly journals NKG2D Natural Killer Cell Receptor—A Short Description and Potential Clinical Applications

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1420
Author(s):  
Jagoda Siemaszko ◽  
Aleksandra Marzec-Przyszlak ◽  
Katarzyna Bogunia-Kubik
Keyword(s):  
Nk Cells ◽  
Natural Killer ◽  
Bacterial Infections ◽  
Killer Cell ◽  
Cell Receptor ◽  
Target Cells ◽  
Effector Cells ◽  
Stressed Cells ◽  
The Right ◽  
Nkg2d Receptor

Natural Killer (NK) cells are natural cytotoxic, effector cells of the innate immune system. They can recognize transformed or infected cells. NK cells are armed with a set of activating and inhibitory receptors which are able to bind to their ligands on target cells. The right balance between expression and activation of those receptors is fundamental for the proper functionality of NK cells. One of the best known activating receptors is NKG2D, a member of the CD94/NKG2 family. Due to a specific NKG2D binding with its eight different ligands, which are overexpressed in transformed, infected and stressed cells, NK cells are able to recognize and attack their targets. The NKG2D receptor has an enormous significance in various, autoimmune diseases, viral and bacterial infections as well as for transplantation outcomes and complications. This review focuses on the NKG2D receptor, the mechanism of its action, clinical relevance of its gene polymorphisms and a potential application in various clinical settings.

scholarly journals Oxidative Stress and Inflammation in Renal and Cardiovascular Complications of Diabetes

Biology ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 18
Author(s):  
Amelia Charlton ◽  
Jessica Garzarella ◽  
Karin A. M. Jandeleit-Dahm ◽  
Jay C. Jha
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Tissue Injury ◽  
Cardiovascular Complications ◽  
Therapeutic Strategies ◽  
Cellular Damage ◽  
Antioxidant Defenses ◽  
Pathological State ◽  
Oxygen Species ◽  
Emerging Therapies

Oxidative stress and inflammation are considered major drivers in the pathogenesis of diabetic complications, including renal and cardiovascular disease. A symbiotic relationship also appears to exist between oxidative stress and inflammation. Several emerging therapies target these crucial pathways, to alleviate the burden of the aforementioned diseases. Oxidative stress refers to an imbalance between reactive oxygen species (ROS) and antioxidant defenses, a pathological state which not only leads to direct cellular damage but also an inflammatory cascade that further perpetuates tissue injury. Emerging therapeutic strategies tackle these pathways in a variety of ways, from increasing antioxidant defenses (antioxidants and Nrf2 activators) to reducing ROS production (NADPH oxidase inhibitors and XO inhibitors) or inhibiting the associated inflammatory pathways (NLRP3 inflammasome inhibitors, lipoxins, GLP-1 receptor agonists, and AT-1 receptor antagonists). This review summarizes the mechanisms by which oxidative stress and inflammation contribute to and perpetuate diabetes associated renal and cardiovascular disease along with the therapeutic strategies which target these pathways to provide reno and cardiovascular protection in the setting of diabetes.

scholarly journals Cromoglycate and nedocromil enhanced the reactive oxygen species-dependent suppressions with, but not without, dexamethasone in ischaemic and histamine paw oedema of mice

1997 ◽  
Vol 6 (5-6) ◽  
pp. 369-374
Author(s):  
Y. Oyanagui
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Glucocorticoid Receptor ◽  
Low Dose ◽  
Natural Antioxidant ◽  
Target Cells ◽  
Oxygen Species ◽  
Paw Oedema ◽  
Β Carotene

Anti-inflammatory actions of two anti-allergic drugs, alone or with dexamethasone (Dex) were examined in two models, because inflammation is claimed to be important for allergic events, especially for asthma. Cromoglycate and nedocromil were tested in ischaemic- and histamineinduced paw oedema models of mice. These antiallergic drugs (1–100 mg/kg, i.p.) failed to suppress these oedemata, but enhanced the suppressions by a low dose of dexamethasone (0.1 mg/kg, s.c.) at 3–8 h after Dex injection. The mode of effects by anti-allergic drugs resembled that of a natural antioxidant (α-tocopherol, β-carotene etc.), and was different from that of an immunosuppressant like FK506. The enhancing potencies of the two anti-allergic drugs were similar at 6 h after Dex in both oedemata, and were diminished by superoxide dismutase (SOD) or catalase (i.p.). Cycloheximide completely abolished suppressions. Nedocromil, but not cromoglycate, inhibits inflammatory events. Therefore, there are common unknown actions by which the two anti-allergics enhance suppression by Dex. A possible mechanism of this action was supposed to enhance the superoxide and/or hydrogen peroxide-dependent glucocorticoid receptor (GR) signalling in the target cells.

Hyperglycemia Induces Generation of Reactive Oxygen Species and Accelerates Apoptotic Cell Death in Salivary Gland Cells

Pathobiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Naoyuki Matsumoto ◽  
Daisuke Omagari ◽  
Ryoko Ushikoshi-Nakayama ◽  
Tomoe Yamazaki ◽  
Hiroko Inoue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salivary Gland ◽  
Tissue Injury ◽  
Ros Production ◽  
Oxygen Species ◽  
Saliva Secretion ◽  
Salivary Gland Tissue ◽  
Gland Tissue

<b><i>Introduction:</i></b> Type-2 diabetes mellitus (T2DM) is associated with several systemic vascular symptoms and xerostomia. It is considered that hyperglycemia-induced polyuria and dehydration cause decreased body-water volume, leading to decreased saliva secretion and, ultimately, xerostomia. In T2DM, increased production of reactive oxygen species (ROS) causes tissue damage to vascular endothelial cells as well as epithelial tissue, including pancreas and cornea. Hence, a similar phenomenon may occur in other tissues and glands in a hyperglycemic environment. <b><i>Methods:</i></b> Salivary gland tissue injury was examined, using T2DM model mouse (db/db). Transferase‐mediated dUTP nick‐end labeling (TUNEL) was conducted to evaluate tissue injury. The levels of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine, Bax/Bcl-2 ratio were measured as indicator of oxidative stress. Moreover, in vitro ROS production and cell injury was evaluated by mouse salivary gland-derived normal cells under high-glucose condition culture. <b><i>Results:</i></b> In vivo and in vitro analysis showed a higher percentage of TUNEL-positive cells and higher levels of MDA and 8-hydroxy-2′-deoxyguanosine in salivary gland tissue of db/db mice. This suggests damage of saliva secretion-associated lipids and DNA by hyperglycemic-induced oxidative stress. To analyze the mechanism by which hyperglycemia promotes ROS production, mouse salivary gland-derived cells were isolated. The cell culture with high-glucose medium enhanced ROS production and promotes apoptotic and necrotic cell death. <b><i>Conclusion:</i></b> These findings suggest a novel mechanism whereby hyperglycemic-induced ROS production promotes salivary gland injury, resulting in hyposalivation.

Neuropeptides and skin aging

2013 ◽  
Vol 16 (1) ◽  
Author(s):  
Rana Elewa ◽  
Evgenia Makrantonaki ◽  
Christos C. Zouboulis
Keyword(s):  
Human Skin ◽  
Inflammatory Cytokines ◽  
Vasoactive Intestinal Polypeptide ◽  
Skin Aging ◽  
Target Cells ◽  
Hormone Metabolism ◽  
Skin Cells ◽  
Calcitonin Gene ◽  
Aged Skin ◽  
Human Skin Cells

AbstractNeuropeptides (NP) are peptides that are released as chemical messengers from nerve cells. They act either in an endocrine manner, where they reach their target cells via the bloodstream or a paracrine manner, as co-transmitters modulating the function of neurotransmitters. To date approximately 100 different NP have been described in the literature. In recent years, several studies have documented that human skin expresses several functional receptors for NP, such as corticotropin-releasing hormone, melanocortins, β-endorphin, vasoactive intestinal polypeptide, neuropeptide Y and calcitonin gene-related peptide. These receptors modulate the production of inflammatory cytokines, proliferation, differentiation, lipogenesis and hormone metabolism in human skin cells. In addition, several NP are directly produced by human skin cells, indicating the complexity of understanding the real functions of NPs in human skin. In this review we address the possible effects of neuropeptides on the pathogenesis of aged skin.

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