Low-Dose Therapy for the Treatment of Low-Grade Chronic Inflammation

2017 ◽  
pp. 27-38 ◽  
Author(s):  
Massimo Fioranelli ◽  
Marco Del Prete ◽  
Jahaira Carolina Aracena ◽  
Maria Grazia Roccia ◽  
Carlo Dal Lin ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Low Dose ◽  
Low Grade ◽  
Dose Therapy

scholarly journals Regulation of Inflammatory Reaction in Health and Disease

2021 ◽  
Vol 22 (10) ◽  
pp. 5277
Author(s):  
Massimo Fioranelli ◽  
Maria Grazia Roccia ◽  
Dana Flavin ◽  
Linda Cota
Keyword(s):  
Inflammatory Response ◽  
Chronic Inflammation ◽  
Inflammatory Reaction ◽  
Low Dose ◽  
Low Grade ◽  
Systems Medicine ◽  
Therapeutic Approaches ◽  
Inflammatory Conditions ◽  
Multistep Process ◽  
Health And Disease

Inflammation is a key mechanism for the clearance of infective agents and other inflammatory triggers and is pivotal for the repairing processes of the affected tissues. Inflammation is a multistep process driven by a great number of mediators which regulate specific aspects of the inflammatory response, in agreement with a well-defined chronobiological program. A great number of inflammation-related diseases show a deeply altered immune chronobiology (e.g., COVID-19-related cytokines storm). This aspect highlights the need for a deeper understanding of the inflammatory phenomenon. It is fundamental to study inflammation as a multilevel phenomenon. Of particular interest is the low-grade chronic inflammation, which is an etiological factor of many chronic diseases. Nowadays, the therapeutic approach to low grade chronic inflammation is one of the great challenges of traditional pharmacology. Currently, no drugs specifically designed for the treatment of chronic inflammatory forms are available. Today, bioregulatory systems medicine (BrSM) and low dose medicine (LDM), two pharmacological paradigms grounded in systems medicine, potentially represent new tools for the treatment of inflammation-related diseases. Scientific research has assessed the effectiveness and safety of both these therapeutic approaches, in particular for the management of chronic inflammatory conditions and chronic immunological dysregulations.

scholarly journals NLRP3 Inflammasome: A Possible Link Between Obesity-Associated Low-Grade Chronic Inflammation and Colorectal Cancer Development

2018 ◽  
Vol 9 ◽  
Author(s):  
Patricia Ahechu ◽  
Gabriel Zozaya ◽  
Pablo Martí ◽  
José Luis Hernández-Lizoáin ◽  
Jorge Baixauli ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Nlrp3 Inflammasome ◽  
Cancer Development ◽  
Low Grade

γδ T cells for immune therapy of patients with lymphoid malignancies

Blood ◽  
2003 ◽  
Vol 102 (1) ◽  
pp. 200-206 ◽  
Author(s):  
Martin Wilhelm ◽  
Volker Kunzmann ◽  
Susanne Eckstein ◽  
Peter Reimer ◽  
Florian Weissinger ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Antitumor Activity ◽  
Low Dose ◽  
Γδ T Cells ◽  
Low Grade ◽  
Treatment Schedule ◽  
Γδ T Cell

Abstract There is increasing evidence that γδ T cells have potent innate antitumor activity. We described previously that synthetic aminobisphosphonates are potent γδ T cell stimulatory compounds that induce cytokine secretion (ie, interferon γ [IFN-γ]) and cell-mediated cytotoxicity against lymphoma and myeloma cell lines in vitro. To evaluate the antitumor activity of γδ T cells in vivo, we initiated a pilot study of low-dose interleukin 2 (IL-2) in combination with pamidronate in 19 patients with relapsed/refractory low-grade non-Hodgkin lymphoma (NHL) or multiple myeloma (MM). The objectives of this trial were to determine toxicity, the most effective dose for in vivo activation/proliferation of γδ T cells, and antilymphoma efficacy of the combination of pamidronate and IL-2. The first 10 patients (cohort A) who entered the study received 90 mg pamidronate intravenously on day 1 followed by increasing dose levels of continuous 24-hour intravenous (IV) infusions of IL-2 (0.25 to 3 × 106 IU/m2) from day 3 to day 8. Even at the highest IL-2 dose level in vivo, γδ T-cell activation/proliferation and response to treatment were disappointing with only 1 patient achieving stable disease. Therefore, the next 9 patients were selected by positive in vitro proliferation of γδ T cells in response to pamidronate/IL-2 and received a modified treatment schedule (6-hour bolus IV IL-2 infusions from day 1-6). In this patient group (cohort B), significant in vivo activation/proliferation of γδ T cells was observed in 5 patients (55%), and objective responses (PR) were achieved in 3 patients (33%). Only patients with significant in vivo proliferation of γδ T cells responded to treatment, indicating that γδ T cells might contribute to this antilymphoma effect. Overall, administration of pamidronate and low-dose IL-2 was well tolerated. In conclusion, this clinical trial demonstrates, for the first time, that γδ T-cell–mediated immunotherapy is feasible and can induce objective tumor responses. (Blood. 2003;102:200-206)

Corrections: levodopa for parkinson’s disease (9 July, page 56)

1990 ◽  
Vol 28 (21) ◽  
pp. 84-84
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Low Dose ◽  
Dose Therapy

The table incorrectly described Sinemet LS and Sinemet Plus, which are both capsules, and Madopar 125 and 62.5, which are both tablets. Reference 14 refers to the study by Lees and Stern described in the paragraph ‘Low Dose Therapy’, and should have been cited there, not later.

scholarly journals DUSP1 Is a Potential Marker of Chronic Inflammation in Arabs with Cardiovascular Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Abdelkrim Khadir ◽  
Sina Kavalakatt ◽  
Mohammed Dehbi ◽  
Monira Alarouj ◽  
Abdullah Bennakhi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Inflammation ◽  
Plasma Levels ◽  
Recurrent Events ◽  
Multivariate Logistic Regression Analysis ◽  
Least Square ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Grade ◽  
Potential Marker ◽  
Diabetes Status

Background. Cardiovascular disease (CVD) risks persist in patients despite the use of conventional treatments. This might be due to chronic inflammation as reflected in epidemiological studies associating circulating low-grade inflammatory markers with CVD recurrent events. Here, we explored this potential link by assessing plasma dual-specificity phosphatase 1 (DUSP1) levels and comparing them to high-sensitivity CRP (hsCRP) and oxidized low-density lipoprotein (oxLDL) levels and their associations to conventional CVD risk factors in confirmed CVD patients. Methods. Human adults with reported CVD (n=207) and controls (n=70) living in Kuwait were used in this study. Anthropometric and classical biochemical parameters were determined. Plasma levels of DUSP1, oxLDL, and hsCRP were measured using human enzyme-linked immunosorbent assay kits. Results. DUSP1 and hsCRP plasma levels and their least square means were higher in CVD cases, while oxLDL plasma levels were lower (p<0.05). Multivariate logistic regression analysis showed that DUSP1 and hsCRP are independently associated with CVD in the studied population, as reflected by 2-fold and 1.5-fold increased risks with increased levels of DUSP1 and hsCRP, respectively. In our study, DUSP1 levels were found to be associated with CVD despite statin treatment and diabetes status (p<0.05), whereas hsCRP mainly correlated with obesity markers. Conclusions. Circulating DUSP1 might be a predictor of chronic subclinical inflammation and residual risk in CVD patients, whereas our data suggest that the association between hsCRP and CVD is largely accounted for adiposity risk factors.

scholarly journals Systemic, but not local, low-grade endotoxinemia increases plasma sCD163 independently of the cortisol response

2019 ◽  
Vol 8 (2) ◽  
pp. 95-99
Author(s):  
Ermina Bach ◽  
Niels Møller ◽  
Jens Otto L Jørgensen ◽  
Mads Buhl ◽  
Holger Jon Møller
Keyword(s):  
Metabolic Syndrome ◽  
Low Dose ◽  
Human Subjects ◽  
Femoral Vein ◽  
Independent Effect ◽  
Low Grade ◽  
Similar Response ◽  
Dependent Manner ◽  
The Metabolic Syndrome ◽  
And Gender

Aims/hypothesis The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low-grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as a result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aim of this study was to investigate if low-grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner. Methods We studied eight male hypopituitary patients and eight age- and gender-matched healthy controls during intravenous low-dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360-min infusion with saline and low-dose LPS in each leg respectively. Results: Systemic low-grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65 ± 0.51 mg/L (placebo) to 1.92 ± 0.46 mg/L (LPS) at 220 min, P = 0.005 and from 1.66 ± 0.42 mg/L (placebo) to 2.19 ± 0.56 mg/L (LPS) at 340 min, P = 0.006. A very similar response was observed in hypopituitary patients: from 1.59 ± 0.53 mg/L (placebo) to 1.83 ± 0.45 mg/L (LPS) at 220 min, P = 0.021 and from 1.52 ± 0.53 mg/L (placebo) to 2.03 ± 0.44 mg/L (LPS) at 340 min, P < 0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163. Conclusion: Systemic low-grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.

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