Inflammatory Compounds: Neuropeptide Substance Pand Cytokines

2009 ◽  
Vol 7 (2) ◽  
pp. 63-69 ◽  
Author(s):  
M.L. Castellani ◽  
P. Felaco ◽  
F. Pandolfp ◽  
V. Salini ◽  
D. De Amicis ◽  
...  
Keyword(s):  
Substance P ◽  
Tissue Injury ◽  
Inflammatory Diseases ◽  
Potential Therapeutic Target ◽  
Complement Components ◽  
Neuroimmune Interactions ◽  
Inflammatory Processes ◽  
Membrane Bound ◽  
Nf Kappab ◽  
Inflammatory Molecules

Inflammatory diseases represent one of the major causes of morbidity and mortality throughout the world and they affect the functions of several tissues. The pathophysiology of these diseases involves release of many pro-inflammatory mediators such as cytokines/chemokines, histamine, C3a, C5a (complement components), bradykinin, leukotrienes (LTC4, LTD4, LTE4), PAF, and substance P, in addition to anti-inflammatory molecules. Recently, it has been demonstrated that neuroimmune interactions are important in the initiation and progress of inflammatory processes. Substance P is an 11-amino acid neuropeptide that is released from nerve endings in many tissues. It acts via membrane-bound NK1 receptors (NK1R). Inflammatory and neuropeptides such as substance P stimulate the release of chemokines, in particular IL-8, a potent neutrophil chemoattractant. Expression of IL-8 is regulated mainly by the transcription factors NF-kappaB, activating protein-1. Substance P plays an important role in immunological and inflammatory states, and it is a mediator of tissue injury, asthma, arthritis, allergy and autoimmune diseases. In this article, our studies revisited the interrelationship between these two powerful inflammatory compounds: substance P and cytokines. These observations suggest that these inflammatory molecules may represent a potential therapeutic target to treat several inflammatory states.

Biologics in Microangiopathic Wounds

2018 ◽  
Vol 17 (4) ◽  
pp. 205-213
Author(s):  
Massimo Papi ◽  
Claudia Papi
Keyword(s):  
Inflammatory Diseases ◽  
Platelet Rich Plasma ◽  
Connective Tissue Diseases ◽  
Local Therapy ◽  
Biologic Agents ◽  
Biologic Drugs ◽  
New Class ◽  
Skin Ulcers ◽  
Inflammatory Processes ◽  
Inflammatory Molecules

In the last decades the possibility to diagnose a skin ulcer has greatly improved. We learnt that a consistent percentage of nonhealing ulcers may be caused by a microangiopathic disorder that has not been properly investigated and cured. Pathogenetically, we can distinguish 2 main groups: (1) ulcers due to inflammatory microangiopathy, mainly including cutaneous small and medium vessel vasculitis, pyoderma gangrenosum, and connective tissue diseases, and (2) ulcers due to occlusive microangiopathy. The group of microangiopathic occlusive ulcers is more heterogeneous and includes different disorders ranging from livedo vasculopathy to calciphylaxis, hydroxyurea-induced ulcers, antiphospholipid antibodies ulcers, and various other types. These conditions can induce thromboses or anatomo-functional occlusion of cutaneous microvessels. Despite different physiopathologic mechanisms, the ulcer resulting from a primitive microangiopathy may receive basic treatments that are in the complex similar to other pathogenetically different wounds, including MOIST-based local therapy and elastic compression when it is not contraindicated. Persistent inflammatory processes are increasingly demonstrated as responsible for the chronicity of many skin ulcers. New data concerning the biological phases of wound healing and the molecules that play crucial roles in this process suggested the use of new specific therapies. Some of them such as growth factors and platelet-rich plasma are prevalently used as topical biologic agents with variable benefits. In recent years, a new class of systemic anti-inflammatory molecules, better known as biologic drugs, have been introduced in the cure of chronic inflammatory diseases that can induce microangiopathic injuries and ulcerative complication. They enlarged the therapeutic options in case of nonresponder microangiopathic ulcers and could represent a future model of “pathogenetically based” therapy of skin ulcers.

Crosstalk between the CX3CL1/CX3CR1 Axis and Inflammatory Signaling Pathways in Tissue Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 844-854 ◽  
Author(s):  
Quan Zhuang ◽  
Jiarui Ou ◽  
Sheng Zhang ◽  
Yingzi Ming
Keyword(s):  
Signaling Pathways ◽  
Tissue Injury ◽  
Signaling Networks ◽  
Toll Like Receptor ◽  
Inflammatory Signaling ◽  
Inflammatory Cascade ◽  
Inflammatory Processes ◽  
Membrane Bound ◽  
G Protein Coupled ◽  
Receptor Cx3cr1

During inflammation, chemokines play a central role by mediating the activation of inflammatory cascade responses in tissue injury. Among more than 200 chemokines, CX3CL1 is a special chemotactic factor existing in both membrane-bound and soluble forms. Its only receptor, CX3CR1, is a member of the G protein-coupled receptor superfamily. The CX3CL1/CX3CR1 axis can affect many inflammatory processes by communicating with different inflammatory signaling pathways, such as JAK-STAT, Toll-like receptor, MAPK, AKT, NF-κB, Wnt/β-catenin, as well as others. These inflammatory networks are involved in much pathology. Determining the crosstalk between the CX3CL1/CX3CR1 axis and these inflammatory signaling pathways could contribute to solving problems in tissue injury, and the CX3CL1/CX3CR1 axis may be a better therapeutic target than inflammatory signaling pathways for preventing tissue injury due to the complexity of inflammatory signaling networks.

scholarly journals Obstructive Sleep Apnea and Inflammation: Proof of Concept Based on Two Illustrative Cytokines

2019 ◽  
Vol 20 (3) ◽  
pp. 459 ◽  
Author(s):  
Leila Kheirandish-Gozal ◽  
David Gozal
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Inflammatory Diseases ◽  
Sleep Apnea Syndrome ◽  
Special Focus ◽  
Normal Body Mass Index ◽  
Low Grade ◽  
Obstructive Sleep ◽  
Inflammatory Processes ◽  
Factor Α

Obstructive sleep apnea syndrome (OSAS) is a markedly prevalent condition across the lifespan, particularly in overweight and obese individuals, which has been associated with an independent risk for neurocognitive, behavioral, and mood problems as well as cardiovascular and metabolic morbidities, ultimately fostering increases in overall mortality rates. In adult patients, excessive daytime sleepiness (EDS) is the most frequent symptom leading to clinical referral for evaluation and treatment, but classic EDS features are less likely to be reported in children, particularly among those with normal body-mass index. The cumulative evidence collected over the last two decades supports a conceptual framework, whereby sleep-disordered breathing in general and more particularly OSAS should be viewed as low-grade chronic inflammatory diseases. Accordingly, it is assumed that a proportion of the morbid phenotypic signature in OSAS is causally explained by underlying inflammatory processes inducing end-organ dysfunction. Here, the published links between OSAS and systemic inflammation will be critically reviewed, with special focus on the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), since these constitute classical prototypes of the large spectrum of inflammatory molecules that have been explored in OSAS patients.

scholarly journals Mutant glucocorticoid receptor binding elements on the interleukin-6 promoter regulate dexamethasone effects

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wen-Teng Chang ◽  
Ming-Yuan Hong ◽  
Chien-Liang Chen ◽  
Chi-Yuan Hwang ◽  
Cheng-Chieh Tsai ◽  
...  
Keyword(s):  
Binding Sites ◽  
Inflammatory Diseases ◽  
Inducible Promoter ◽  
Transcriptional Factor ◽  
Factor Binding ◽  
Inflammatory Processes ◽  
Nuclear Receptor Family ◽  
Specificity Protein ◽  
Receptor Family ◽  
Pro Inflammatory Cytokines

Abstract Background Glucocorticoids (GCs) have been extensively used as essential modulators in clinical infectious and inflammatory diseases. The GC receptor (GR) is a transcription factor belonging to the nuclear receptor family that regulates anti-inflammatory processes and releases pro-inflammatory cytokines, such as interleukin (IL)-6. Results Five putative GR binding sites and other transcriptional factor binding sites were identified on theIL-6 promoter, and dexamethasone (DEX) was noted to reduce the lipopolysaccharide (LPS)-induced IL-6 production. Among mutant transcriptional factor binding sites, nuclear factor-kappa B (NF-κB), activator protein (AP)-1, and specificity protein (Sp)1–2 sites reduced basal and LPS-induced IL-6 promoter activities through various responses. The second GR binding site (GR2) was noted to play a crucial role in both basal and inducible promoter activities in LPS-induced inflammation. Conclusions We concluded that selective GR2 modulator might exert agonistic and antagonistic effects and could activate crucial signaling pathways during the LPS-stimulated inflammatory process.

scholarly journals Apoptosis and inflammation

1995 ◽  
Vol 4 (1) ◽  
pp. 5-15 ◽  
Author(s):  
C. Haanen ◽  
I. Vermes
Keyword(s):  
Cell Death ◽  
Inflammatory Reaction ◽  
Inflammatory Diseases ◽  
Apoptotic Cell ◽  
Cell Damage ◽  
Target Cells ◽  
Apoptotic Bodies ◽  
Accidental Injury ◽  
Inflammatory Reactions ◽  
Inflammatory Processes

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.

Toxic effects of cell-free hemoglobin on the microvascular endothelium: implications for pulmonary and non-pulmonary organ dysfunction

2021 ◽  
Author(s):  
Jamie E Meegan ◽  
Julie A. Bastarache ◽  
Lorraine B. Ware
Keyword(s):  
Organ Dysfunction ◽  
Tissue Injury ◽  
Inflammatory Diseases ◽  
Severity Of Illness ◽  
Therapeutic Strategies ◽  
Free Hemoglobin ◽  
Microvascular Endothelium ◽  
Endothelial Inflammation ◽  
Signaling Mechanisms ◽  
Novel Therapeutic Strategies

Levels of circulating cell-free hemoglobin are elevated during hemolytic and inflammatory diseases and contribute to organ dysfunction and severity of illness. Though several studies have investigated the contribution of hemoglobin to tissue injury, the precise signaling mechanisms of hemoglobin-mediated endothelial dysfunction in the lung and other organs are not yet completely understood. The purpose of this review is to highlight the knowledge gained thus far and the need for further investigation regarding hemoglobin-mediated endothelial inflammation and injury in order to develop novel therapeutic strategies targeting the damaging effects of cell-free hemoglobin.

The importance of antivirus in surgery

1938 ◽  
Vol 34 (1) ◽  
pp. 108-108
Author(s):  
B. Ivanov
Keyword(s):  
Inflammatory Diseases ◽  
Abdominal Cavity ◽  
Infected Wounds ◽  
Mucous Membranes ◽  
Inflammatory Processes

Antivirus is used in surgery, firstly, to treat infected wounds and inflammatory processes of the skin and mucous membranes, and, secondly, to prevent and treat inflammatory diseases of the peritoneum and abdominal cavity.

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