resolvin-d1 has been researched along with Chronic-Disease* in 6 studies
6 other study(ies) available for resolvin-d1 and Chronic-Disease
Article | Year |
---|---|
Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a murine model of early chronic Chagas disease.
Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America and is widely distributed worldwide because of migration. In 30% of cases, after years of infection and in the absence of treatment, the disease progresses from an acute asymptomatic phase to a chronic inflammatory cardiomyopathy, leading to heart failure and death. An inadequate balance in the inflammatory response is involved in the progression of chronic Chagas cardiomyopathy. Current therapeutic strategies cannot prevent or reverse the heart damage caused by the parasite. Aspirin-triggered resolvin D1 (AT-RvD1) is a pro-resolving mediator of inflammation that acts through N-formyl peptide receptor 2 (FPR2). AT-RvD1 participates in the modification of cytokine production, inhibition of leukocyte recruitment and efferocytosis, macrophage switching to a nonphlogistic phenotype, and the promotion of healing, thus restoring organ function. In the present study, AT-RvD1 is proposed as a potential therapeutic agent to regulate the pro-inflammatory state during the early chronic phase of Chagas disease.. C57BL/6 wild-type and FPR2 knock-out mice chronically infected with T. cruzi were treated for 20 days with 5 μg/kg/day AT-RvD1, 30 mg/kg/day benznidazole, or the combination of 5 μg/kg/day AT-RvD1 and 5 mg/kg/day benznidazole. At the end of treatment, changes in immune response, cardiac tissue damage, and parasite load were evaluated. The administration of AT-RvD1 in the early chronic phase of T. cruzi infection regulated the inflammatory response both at the systemic level and in the cardiac tissue, and it reduced cellular infiltrates, cardiomyocyte hypertrophy, fibrosis, and the parasite load in the heart tissue.. AT-RvD1 was shown to be an attractive therapeutic due to its regulatory effect on the inflammatory response at the cardiac level and its ability to reduce the parasite load during early chronic T. cruzi infection, thereby preventing the chronic cardiac damage induced by the parasite. Topics: Animals; Chagas Cardiomyopathy; Chronic Disease; Disease Models, Animal; Docosahexaenoic Acids; Female; Heart; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium; Nitroimidazoles; Parasite Load; Receptors, Formyl Peptide; Trypanosoma cruzi | 2021 |
Resolvin D1 treatment on goblet cell mucin and immune responses in the chronic allergic eye disease (AED) model.
Severe, chronic eye allergy is an understudied, vision-threatening condition. Treatments remain limited. We used a mouse model of severe allergic eye disease (AED) to determine whether topical application of the pro-resolution mediator Resolvin D1 (RvD1) terminates the response. AED was induced by injection of ovalbumin (OVA) followed by topical challenge of OVA daily. RvD1 was applied topically prior to OVA. Clinical symptoms were scored. Eye washes were assayed for MUC5AC. After 7 days, eyes were removed and the number of goblet cells, T helper cell responses and presence of immune cells in draining lymph nodes and conjunctiva determined. Topical RvD1 treatment significantly reduced symptoms of AED. RvD1 did not alter the systemic type 2 immune response in the lymph nodes. AED increased the total amount of goblet cell mucin secretion, but not the number of goblet cells. RvD1 prevented this increase, but did not alter goblet cell number. Absolute numbers of CD4 + T cells, total CD11b + myeloid cells, eosinophils, neutrophils, and monocytes, but not macrophages increased in AED versus RvD1-treated mice. We conclude that topical application of RvD1 reduced the ocular allergic response by local actions in conjunctival immune response and a decrease in goblet cell mucin secretion. Topics: Allergens; Animals; Cells, Cultured; Chronic Disease; Disease Models, Animal; Docosahexaenoic Acids; Eye Diseases; Goblet Cells; Humans; Hypersensitivity; Immunity, Cellular; Mice; Mice, Inbred C57BL; Mucin 5AC; Ovalbumin | 2019 |
Resolvin D1 enhances the resolution of lung inflammation caused by long-term Pseudomonas aeruginosa infection.
Pseudomonas aeruginosa lung infection is a main cause of disability and mortality worldwide. Acute inflammation and its timely resolution are crucial for ensuring bacterial clearance and limiting tissue damage. Here, we investigated protective actions of resolvin (Rv) D1 in lung infection induced by the RP73 clinical strain of P. aeruginosa. RvD1 significantly diminished bacterial growth and neutrophil infiltration during acute pneumonia caused by RP73. Inoculum of RP73, immobilized in agar beads, resulted in persistent lung infection up to 21 days, leading to a non resolving inflammation reminiscent of human pathology. RvD1 significantly reduced bacterial titer, leukocyte infiltration, and lung tissue damage. In murine lung macrophages sorted during P. aeruginosa chronic infection, RvD1 regulated the expression of Toll-like receptors, downstream genes, and microRNA (miR)-21 and 155, resulting in reduced inflammatory signaling. In vitro, RvD1 enhanced phagocytosis of P. aeruginosa by neutrophils and macrophages, recapitulating its in vivo actions. These results unveil protective functions and mechanisms of action of RvD1 in acute and chronic P. aeruginosa pneumonia, providing evidence for its potent pro-resolution and tissue protective properties on airway mucosal tissue during infection. Topics: Acute Disease; Animals; Bacterial Load; Cells, Cultured; Chronic Disease; Docosahexaenoic Acids; Female; Humans; Macrophages, Alveolar; Male; Mice; Mice, Inbred C57BL; MicroRNAs; Neutrophil Infiltration; Pneumonia; Pseudomonas aeruginosa; Pseudomonas Infections | 2018 |
Rapid and sustained antidepressant effects of resolvin D1 and D2 in a chronic unpredictable stress model.
Resolvin D1 (RvD1) and D2 (RvD2) are lipid mediators that are derived from docosahexaenoic acid. We recently demonstrated that intracerebroventricular (i.c.v.) infusions of RvD1 or RvD2 attenuate lipopolysaccharide-induced depression-like behaviors via mammalian target of rapamycin complex 1 signaling. However, the antidepressant effects of RvD1 and RvD2 have not been fully investigated. Here, we examined the antidepressant effects of RvD1 and RvD2 using the tail suspension test (TST) and forced swim test (FST) in murine chronic unpredictable stress (CUS) model. Male BALB/c mice (7 weeks) were subjected to 5 weeks of CUS and then received with a single i.c.v. infusion of RvD1 (10ng), RvD2 (10ng), or vehicle. In vehicle-infused mice, CUS significantly increased immobility in the TST both 2 and 24h after i.c.v. infusion, these depression-like behaviors were significantly ameliorated by RvD1 or RvD2. Similar results were obtained from the FST. Intracerebroventricular infusion of RvD1 or RvD2 did not affect locomotor activity. These results demonstrate that RvD1 and RvD2 produce rapid and sustained antidepressant effects in the CUS model. Topics: Analysis of Variance; Animals; Antidepressive Agents; Catheters, Indwelling; Chronic Disease; Depressive Disorder; Disease Models, Animal; Docosahexaenoic Acids; Male; Mice, Inbred BALB C; Motor Activity; Stress, Psychological; Time Factors; Uncertainty | 2017 |
Resolvin D1 Reduces Emphysema and Chronic Inflammation.
Chronic obstructive pulmonary disease is characterized, in part, by chronic inflammation that persists even after smoking cessation, suggesting that a failure to resolve inflammation plays an important role in the pathogenesis of the disease. It is widely recognized that the resolution of inflammation is an active process, governed by specialized proresolving lipid mediators, including lipoxins, resolvins, maresins, and protectins. Here, we report that proresolving signaling and metabolic pathways are disrupted in lung tissue from patients with chronic obstructive pulmonary disease, suggesting that supplementation with proresolving lipid mediators might reduce the development of emphysema by controlling chronic inflammation. Groups of mice were exposed long-term to cigarette smoke and treated with the proresolving mediator resolvin D1. Resolvin D1 was associated with a reduced development of cigarette smoke-induced emphysema and airspace enlargement, with concurrent reductions in inflammation, oxidative stress, and cell death. Interestingly, resolvin D1 did not promote the differentiation of M2 macrophages and did not promote tissue fibrosis. Taken together, our results suggest that cigarette smoking disrupts endogenous proresolving pathways and that supplementation with specialized proresolving lipid mediators is an important therapeutic strategy in chronic lung disease, especially if endogenous specialized proresolving lipid mediator signaling is impaired. Topics: Adult; Aged; Aged, 80 and over; Animals; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Chronic Disease; Docosahexaenoic Acids; Drug Evaluation, Preclinical; Female; Humans; Macrophages, Alveolar; Male; Mice, Inbred C57BL; Middle Aged; Oxidative Stress; Pneumonia; Pulmonary Disease, Chronic Obstructive; Pulmonary Emphysema; Signal Transduction; Smoking | 2015 |
The precursor of resolvin D series and aspirin-triggered resolvin D1 display anti-hyperalgesic properties in adjuvant-induced arthritis in rats.
Resolution of inflammation is mediated by endogenous molecules with anti-inflammatory and pro-resolving activities and they have generated new possibilities for the treatment of inflammatory diseases. Here, we have investigated the possible anti-hyperalgesic effects of two lipids, aspirin-triggered resolvin D1 (AT-RvD1) and its precursor, 17(R)-hydroxy-4Z,7Z,10Z,13Z,15E,17R,19Z-docosahexaenoic acid (17(R)HDoHE).. The anti-hyperalgesic effects of both lipid mediators were evaluated, using mechanical and thermal stimuli, at different time-points in adjuvant-induced arthritis in rats. Cytokine levels were measured, and immunohistochemistry and real-time PCR for pro-inflammatory mediators were also performed.. The precursor of resolvin D series, 17(R)HDoHE, given systemically, inhibited the development and the maintenance of mechanical hyperalgesia in acute inflammation. Such effects were likely to be associated with modulation of both NF-κB and COX-2 in dorsal root ganglia and spinal cord. 17(R)HDoHE was also effective against sub-chronic pain. Unexpectedly, repeated treatment with 17(R)HDoHE did not modify paw and joint oedema in the sub-chronic model, while joint stiffness was prevented. Notably, AT-RvD1 exhibited marked anti-hyperalgesic effects in acute inflammation when given systemically. The efficacy of long-term treatment with either 17(R)HDoHE or AT-RvD1 was partly related to decreased production of TNF-α and IL-1β in rat hind paw.. Our findings provide fresh evidence for the anti-hyperalgesic properties of 17(R)HDoHE and its pro-resolution metabolite AT-RvD1. Such lipid mediators might be useful for treating pain associated with acute or chronic inflammation. LINKED ARTICLE This article is commented on by Xu and Ji, pp. 274-277 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476-5381.2011.01348.x. Topics: Animals; Arthritis; Chronic Disease; Docosahexaenoic Acids; Dose-Response Relationship, Drug; Freund's Adjuvant; Hot Temperature; Inflammation; Male; Pain; Rats | 2011 |