Molecular and Cellular Mediators of the Inflammatory Response

2015 ◽  
Author(s):  
Amy T. Makley ◽  
Michael D. Goodman ◽  
Timothy A. Pritts
Keyword(s):  
Inflammatory Response ◽  
Activated Protein C ◽  
Inflammatory Cells ◽  
Cellular Responses ◽  
Sepsis Syndrome ◽  
Reactive Oxygen Metabolites ◽  
Therapeutic Implications ◽  
Susceptibility To Infection ◽  
Cellular Mediators ◽  
Definition Of

Inflammation is a highly complex process involving vascular, neurogenic, humoral, and cellular responses. Although the descriptive features of acute inflammation have long been known (i.e., heat, redness, pain, swelling), a single satisfactory definition of this phenomenon is still lacking. Successful therapy for inflammation rests not only on investigating the type of injury, but also on the timing of the intervention. This review focuses on humoral and cellular responses to injury, defining essential and interrelated inflammatory pathways. Systemic inflammatory response system (SIRS), in relation to sepsis syndrome, is defined by the global proinflammatory physiologic response to a stimulus. In contrast, compensatory antiinflammatory response (CARS) results from a predominant antiinflammatory response to an insult, also causing immunosuppression and increased susceptibility to infection. Also discussed are the roles of cytokines, adhesion molecules, inflammatory cells such as neutrophils, mast cells, and lymphocytes, extracellular vesicles, sphingolipids, reactive oxygen metabolites, nitric oxide, the complement cascade, and eicosanoids. Therapeutic implications and trials are examined in relation to cytokines in SIRS and CARS, activated protein C, and inflammatory bowel disease. This review contains 11 figures, 4 tables, and 79 references.

Molecular and Cellular Mediators of the Inflammatory Response

2015 ◽  
Author(s):  
Amy T. Makley ◽  
Michael D. Goodman ◽  
Timothy A Pritts
Keyword(s):  
Inflammatory Response ◽  
Activated Protein C ◽  
Inflammatory Cells ◽  
Cellular Responses ◽  
Sepsis Syndrome ◽  
Reactive Oxygen Metabolites ◽  
Therapeutic Implications ◽  
Susceptibility To Infection ◽  
Cellular Mediators ◽  
Definition Of

Inflammation is a highly complex process involving vascular, neurogenic, humoral, and cellular responses. Although the descriptive features of acute inflammation have long been known (i.e., heat, redness, pain, swelling), a single satisfactory definition of this phenomenon is still lacking. Successful therapy for inflammation rests not only on investigating the type of injury, but also on the timing of the intervention. This review focuses on humoral and cellular responses to injury, defining essential and interrelated inflammatory pathways. Systemic inflammatory response system (SIRS), in relation to sepsis syndrome, is defined by the global proinflammatory physiologic response to a stimulus. In contrast, compensatory antiinflammatory response (CARS) results from a predominant antiinflammatory response to an insult, also causing immunosuppression and increased susceptibility to infection. Also discussed are the roles of cytokines, adhesion molecules, inflammatory cells such as neutrophils, mast cells, and lymphocytes, extracellular vesicles, sphingolipids, reactive oxygen metabolites, nitric oxide, the complement cascade, and eicosanoids. Therapeutic implications and trials are examined in relation to cytokines in SIRS and CARS, activated protein C, and inflammatory bowel disease. This review contains 11 figures, 4 tables, and 79 references.

scholarly journals Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Shi ◽  
Zhirong Zhang ◽  
Danli Cai ◽  
Jing Kuang ◽  
Shuifang Jin ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Animal Model ◽  
Inflammatory Response ◽  
Inflammatory Cell ◽  
Pulmonary Thromboembolism ◽  
Thrombus Formation ◽  
Inflammatory Cells ◽  
Hemodynamic Instability ◽  
Synergistic Action ◽  
Determining Factor

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

Use of Vicryl (Polyglactin 910) Mesh to Limit Epidural Scar Formation after Laminectomy

Neurosurgery ◽  
1990 ◽  
Vol 26 (4) ◽  
pp. 649-654 ◽  
Author(s):  
Charles E. Nussbaum ◽  
Joseph V. McDonald ◽  
Raymond B. Baggs
Keyword(s):  
Inflammatory Response ◽  
Subcutaneous Fat ◽  
Inflammatory Cells ◽  
Scar Formation ◽  
Good Survival ◽  
Polyglactin 910 ◽  
Chronic Inflammatory Response ◽  
Fat Grafts ◽  
Free Grafts ◽  
Vicryl Mesh

Abstract A variety of substances have been used at laminectomy sites to prevent postoperative epidural scarring. Free grafts of autologous subcutaneous fat are commonly used both clinically and experimentally. The free fat grafts usually survive, but decrease in size by about 50%. Postoperatively, subcutaneous seroma has been observed with the use of fat grafts, as well as recurrent symptoms of neural compression by the graft that required additional operations. When compared to the use of free fat grafts after laminectomy in dogs, Vicryl mesh produced slightly more scarring, but consistently less than that observed in control animals. The Vicryl mesh was resorbed by a minimal chronic inflammatory response over about 45 days. Seven of 11 fat-grafted zones showed signs of necrosis, at times with a greater collection of inflammatory cells than that associated with the Vicryl mesh. Of the 4 fat-grafted zones that showed good survival. 2 had gross evidence of neural compression. No surgical zone treated with Vicryl mesh exhibited evidence of neural compression. In view of these results, the use of Vicryl mesh at laminectomy sites may be a safer method of limiting postoperative epidural scar formation.

Proteases from Inflammatory Cells: Regulation of Inflammatory Response

2011 ◽  
pp. 73-100 ◽  
Author(s):  
Magali Pederzoli-Ribeil ◽  
Julie Gabillet ◽  
Véronique Witko-Sarsat
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cells

scholarly journals New Definition of Sepsis

2013 ◽  
Vol 2 (1) ◽  
pp. 37
Author(s):  
Fuzhou Wang
Keyword(s):  
Septic Shock ◽  
Intensive Care ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Organ Dysfunction ◽  
Medical Science ◽  
Accurate Diagnosis ◽  
Causes Of Mortality ◽  
New Challenges ◽  
Definition Of

Sepsis or septic shock is one of the major causes of mortality in intensive care medicine. How to define and how to make an accurate diagnosis possess critical implications for patients and intensive caregivers. With the development of modern medical science, new challenges rose for how to re-define sepsis and also revision is needed. Should we add organ dysfunction to the diagnostic criteria of systemic inflammatory response syndrome, and whether are there early symptoms or signs of organ dysfunction need to be considered critically. May be the new definition of sepsis can save more lives.

scholarly journals Il6/Sil6R Regulates Tnfα-Inflammatory Response In Synovial Fibroblasts Through Modulation of Transcriptional and Post-Transcriptional Mechanisms

2020 ◽  
Author(s):  
Alvaro Valin ◽  
Manuel J. Del Rey ◽  
Cristina Municio ◽  
Alicia Usategui ◽  
Marina Romero ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mononuclear Cells ◽  
De Novo ◽  
Inflammatory Cells ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteases ◽  
P Value ◽  
Polymorphonuclear Cells ◽  
Expression Of Genes

Abstract Introduction: The clinical efficacy of specific interleukin-6 inhibitors has confirmed the central role of IL6 in rheumatoid arthritis (RA). However the local role of IL6, in particular in synovial fibroblasts (SF) as a direct cellular target to IL6/sIL6R signal is not well characterized. The purpose of the study was to characterize the crosstalk between TNFα and IL6/sIL6R signaling to the effector pro-inflammatory response of SF. Methods SF lines were stimulated with either TNFα or IL6 and sIL6R for the time and dose indicated for each experiment, and where indicated, cells were treated with inhibitors actinomycin D, adalimumab, ruxolitinib and cicloheximide. mRNA expression of cytokines, chemokines and matrix metalloproteases (MMPs) were analyzed by quantitative RT-PCR. Level of IL8 and CCL8 in culture supernatants was measured by ELISA. Mononuclear and polymorphonuclear cells migration assays were assesed by transwell using conditioned medium from SF cultures. Statistical analyses were performed as indicated in the corresponding figure legends and a p-value < 0.05 was considered statistically significant. Results IL6/sIL6R stimulation of TNFα treated SF cooperatively promotes the expression of mono- and lymphocytic chemokines such as IL6, CCL8 and CCL2, as well as matrix degrading enzymes such as MMP1, while inhibiting the induction of central neutrophil chemokines such as IL8. These changes in the pattern of chemokines expression resulted in reduced polymorphonuclear (PMN) and increased mononuclear cells (MNC) chemoattraction by SF. Mechanistic analyses of the temporal expression of genes demonstrated that the cooperative regulation mediated by these two factors is mostly induced through de novo transcriptional mechanisms activated by IL6/sIL6R. Furthermore, we also demonstrate that TNFα and IL6/sIL6R cooperation is partially mediated by the expression of secondary factors signaling through JAK/STAT pathways. Conclusions These results point out to a highly orchestrated response to IL6 in TNFα-induced SF and provide additional insights into the role of IL6/sIL6R in the context of RA, highlighting the contribution of IL6/sIL6R to the interplay of SF with other inflammatory cells.

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