Subcutaneous injection of Mycobacterium ulcerans causes necrosis, chronic inflammatory response and fibrosis in skeletal muscle

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.

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Systemic administration of fractions from Nyctanthes arbor-tristis attenuates chronic inflammatory response in Freund′s-complete-adjuvant-induced arthritis in rats

International Journal of Green Pharmacy ◽

10.4103/0973-8258.140168 ◽

2014 ◽

Vol 8 (3) ◽

pp. 147

Author(s):

Swapnil Goyal ◽

NavinR Sheth ◽

DN Srivastava

Keyword(s):

Inflammatory Response ◽

Systemic Administration ◽

Chronic Inflammatory Response ◽

Adjuvant Induced Arthritis

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9: LYMPHEDEMA IS A FIBROPROLIFERATIVE CONDITION ASSOCIATED WITH A PRO-FIBROTIC CHRONIC INFLAMMATORY RESPONSE

Plastic & Reconstructive Surgery ◽

10.1097/01.prs.0000371745.47053.10 ◽

2010 ◽

Vol 125 (Supplement) ◽

pp. 14

Author(s):

T Avraham ◽

SV Daluvoy ◽

JC Zampell ◽

A Yan ◽

E Kueberuwa

Keyword(s):

Inflammatory Response ◽

Chronic Inflammatory Response

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Low Dose of IL-2 Normalizes Hypertension and Mitochondrial Function in the RUPP Rat Model of Placental Ischemia

Cells ◽

10.3390/cells10102797 ◽

2021 ◽

Vol 10 (10) ◽

pp. 2797

Author(s):

Evangeline Deer ◽

Lorena M. Amaral ◽

Nathan Campbell ◽

Sarah Fitzgerald ◽

Owen Herrock ◽

...

Keyword(s):

Inflammatory Response ◽

Rat Model ◽

Low Dose ◽

Perfusion Pressure ◽

Chronic Inflammatory Response ◽

Respiration Rates ◽

Inflammatory Conditions ◽

Uterine Perfusion ◽

Placental Ischemia ◽

New Onset

IL-2 is a cytokine released from CD4+T cells with dual actions and can either potentiate the inflammatory response or quell a chronic inflammatory response depending on its circulating concentration. IL-2 is elevated in many chronic inflammatory conditions and is increased during preeclampsia (PE). PE is characterized by new-onset hypertension during pregnancy and organ dysfunction and increasing evidence indicates that proinflammatory cytokines cause hypertension and mitochondrial (mt) dysfunction during pregnancy. The reduced uterine perfusion pressure (RUPP) model of placental ischemia is a rat model of PE that we commonly use in our laboratory and we have previously shown that low doses of recombinant IL-2 can decrease blood pressure in RUPP rats. The objective of this study was to determine the effects of a low dose of recombinant IL-2 on multi-organ mt dysfunction in the RUPP rat model of PE. We tested our hypothesis by infusing recombinant IL-2 (0.05 ng/mL) into RUPP rats on GD14 and examined mean arterial pressure (MAP), renal, placental and endothelial cell mt function compared to control RUPP. MAP was elevated in RUPP rats (n = 6) compared to controls (n = 5) (122 ± 5 vs. 102 ± 3 mmHg, p < 0.05), but was reduced by administration of LD recombinant IL-2 (107 ± 1 vs. 122 ± 5 mmHg, n = 9, p < 0.05). Renal, placental and endothelial mt ROS were significantly increased in RUPP rats compared to RUPP+ IL-2 and controls. Placental and renal respiration rates were reduced in RUPP rats compared to control rats but were normalized with IL-2 administration to RUPPs. These data indicate that low-dose IL-2 normalized multi-organ mt function and hypertension in response to placental ischemia.

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High-dose pyruvate treatment alters skeletal muscle differentiation and expression of inflammation-related genes

10.1101/2020.09.21.305847 ◽

2020 ◽

Author(s):

Kazuya Hasegawa ◽

Yuya Yamaguchi ◽

Yutthana Pengjam

Keyword(s):

Gene Expression ◽

Skeletal Muscle ◽

Inflammatory Response ◽

Muscle Contraction ◽

Signaling Pathway ◽

Receptor Interaction ◽

High Dose ◽

Ppi Network ◽

Acid Therapy ◽

High Doses

ABSTRACTPyruvic acid therapy is used for various diseases, but the therapeutic effect decreases at high doses. The molecular mechanism of high-dose pyruvate is not well understood. The purpose of this study was to identify the effects of high dose pyruvate addition on skeletal muscle using C2C12. The gene expression profile for the GSE5497 dataset was taken from the Gene Expression Omnibus database. GEO2R was used to identify specifically expressed genes (DEGs). Functional analysis and pathway enrichment analysis of DEG were performed using the DAVID database. The protein-protein interaction (PPI) network was built in the STRING database and visualized using Cytoscape. GO analysis showed that up-regulated DEG was primarily involved in angiogenesis, cell adhesion, and inflammatory response. We also showed that down-regulated DEG is involved in the regulation of muscle contraction, skeletal muscle fiber development. In addition, the upregulated KEGG pathway of DEG included Rheumatoid arthritis, Chemokine signaling pathway, and Cytokine-cytokine receptor interaction. Downregulated DEG included Calcium signaling pathway, hypertrophic cardiomyopathy (HCM), Dilated cardiomyopathy, Neuroactive ligand-receptor interaction, and Cardiac muscle contraction. Further, analysis of two modules selected from the PPI network showed that high-dose pyruvate exposure to C2C12 was primarily associated with muscle contraction, muscle organ morphogenesis, leukocyte chemotaxis, and chemokine activity. In conclusion, High-dose pyruvate treatment of C2C12 was found to be associated with an increased inflammatory response and decreased skeletal muscle formation. However, further studies are still needed to verify the function of these molecules at high doses of pyruvate.

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Implications of the Acute and Chronic Inflammatory Response and the Foreign Body Reaction to the Immune Response of Implanted Biomaterials

The Immune Response to Implanted Materials and Devices ◽

10.1007/978-3-319-45433-7_2 ◽

2016 ◽

pp. 15-36 ◽

Cited By ~ 6

Author(s):

James M. Anderson ◽

Sirui Jiang

Keyword(s):

Immune Response ◽

Foreign Body ◽

Inflammatory Response ◽

Foreign Body Reaction ◽

Chronic Inflammatory Response

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The resolution of inflammation through omega-3 fatty acids in atherosclerosis, intimal hyperplasia, and vascular calcification

Seminars in Immunopathology ◽

10.1007/s00281-019-00767-y ◽

2019 ◽

Vol 41 (6) ◽

pp. 757-766 ◽

Cited By ~ 7

Author(s):

Miguel Carracedo ◽

Gonzalo Artiach ◽

Hildur Arnardottir ◽

Magnus Bäck

Keyword(s):

Fatty Acids ◽

Inflammatory Response ◽

Cardiovascular Prevention ◽

Vascular Wall ◽

Lipid Mediator ◽

Omega 3 Fatty Acids ◽

Omega 3 ◽

Resolution Of Inflammation ◽

Chronic Inflammatory Response ◽

Omega 3 Fatty Acid

Abstract Omega-3 fatty acids serve as the substrate for the formation of a group of lipid mediators that mediate the resolution of inflammation. The cardiovascular inflammatory response in atherosclerosis and vascular injury is characterized by a failure in the resolution of inflammation, resulting in a chronic inflammatory response. The proresolving lipid mediator resolvin E1 (RvE1) is formed by enzymatic conversion of the omega-3 fatty acid eicosapentaenoic acid (EPA), and signals resolution of inflammation through its receptor ChemR23. Importantly, the resolution of cardiovascular inflammation is an active, multifactorial process that involves modulation of the immune response, direct actions on the vascular wall, as well as close interactions between macrophages and vascular smooth muscle cells. Promoting anti-atherogenic signalling through the stimulation of endogenous resolution of inflammation pathways may provide a novel therapeutic strategy in cardiovascular prevention.

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