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AimsExercise-induced cellular stress and sterile inflammation are of increasing interest. ASC specks are a component of the intracellular NLRP3-inflammasome and can be released into the blood. For example, serum ASC specks are increased after marathon running. We therefore tested whether ASC specks are potentially associated with the individual response to physical training and cardiopulmonary capacity.MethodsWe performed a prospective study in 45 healthy athletes. Blood samples were taken before and after cardiopulmonary exercise testing (CPET). ASC speck concentrations were quantitated using flow cytometry.ResultsBaseline ASC speck levels correlated with clinical parameters of body composition (height, weight, BMI) and parameters of cardiopulmonary performance (peak VO2, peak oxygen pulse, heart rate after exercise). Athletes with lowest baseline ASC speck concentrations have a significantly lower BMI (22.0 ± 1.8 vs. 24.9 ± 1.6 kg/m2), higher heart rate at rest (72 ± 10 vs. 58 ± 10 beats/min), lower peak VO2 (2692 ± 629 vs. 3404 ± 747 mL/min) and lower peak oxygen pulse (15.6 ± 3.4 vs. 20.7 ± 3.5 mL/heart rate). Overall, ASC speck concentrations showed no significant change after CPET (7.0 ± 4.5 vs. 8.0 ± 5.4 ASC specks/µL, p = 0.3). However, subgroup analysis revealed a significant increase in circulating ASC specks in athletes with the lowest baseline values (2.37 ± 0.84 vs. 8.43 ± 7.52 ASC specks/µL, p < 0.05). Athletes with an increase in ASC speck concentrations in response to CPET had a lower peak oxygen pulse compared to those with a decrease (17.1 ± 4.2 vs. 19.8 ± 4.1, p < 0.05).ConclusionLow ASC speck baseline values as well as an increase in response to exercise are associated with lower peak oxygen pulse in healthy athletes.

The use of synthetic drugs has increased in recent years; however, herbal medicine is yet more trusted among a huge population worldwide; This could be due to minimal side effects, affordable prices, and traditional beliefs. Lemongrass ( Melissa officinalis ) has been widely used for reducing stress and anxiety, increasing appetite and sleep, reducing pain, healing wounds, and treating poisonous insect bites and bee stings for a long time. Today, research has shown that this plant can also fight viruses including Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), Herpes Simplex Virus (HSV), and Human Immunodeficiency Virus (HIV) through various mechanisms such as inhibiting HSV-1 from binding to host cell, inhibiting HSV-1 replication during the post-adsorption or inhibiting main protease and spike protein of SARS-CoV-2, furthermore, be effective in treating related diseases. This Review investigated the antiviral properties of Melissa officinalis and its effect on viral diseases. More in vitro and in vivo studies are needed to determine Melissa officinaliss underlying mechanism, and more randomized controlled trials should be done to identify its effect in humans. Also, due to the usefulness and lack of side effects, it can be used more as a complementary medicine.

Abstract Inflammation driven by intracellular activation of the NLRP3 inflammasome is involved in the pathogenesis of a variety of diseases including vascular pathologies. Inflammasome specks are released into the extracellular compartment from disrupting pyroptotic cells. The potential uptake and function of extracellular NLRP3 inflammasomes in human coronary artery smooth muscle cells (HCASMC) are unknown. Fluorescently labeled NLRP3 inflammasome particles were isolated from a mutant NLRP3-YFP cell line and used to treat primary HCASMC for 4 and 24 h. Fluorescent and expressional analyses showed that extracellular NLRP3-YFP particles are internalized into HCASMC, where they remain active and stimulate intracellular caspase-1 (1.9-fold) and IL-1β (1.5-fold) activation without inducing pyroptotic cell death. Transcriptomic analysis revealed increased expression level of pro-inflammatory adhesion molecules (ICAM1, CADM1), NLRP3 and genes involved in cytoskleleton organization. The NLRP3-YFP particle-induced gene expression was not dependent on NLRP3 and caspase-1 activation. Instead, the effects were partly abrogated by blocking NFκB activation. Genes, upregulated by extracellular NLRP3 were validated in human carotid artery atheromatous plaques. Extracellular NLRP3-YFP inflammasome particles promoted the secretion of pro-atherogenic and inflammatory cytokines such as CCL2/MCP1, CXCL1 and IL-17E, and increased HCASMC migration (1.8-fold) and extracellular matrix production, such as fibronectin (5.8-fold) which was dependent on NFκB and NLRP3 activation. Extracellular NLRP3 inflammasome particles are internalized into human coronary artery smooth muscle cells where they induce pro-inflammatory and pro-atherogenic effects representing a novel mechanism of cell-cell communication and perpetuation of inflammation in atherosclerosis. Therefore, extracellular NLRP3 inflammasomes may be useful to improve the diagnosis of inflammatory diseases and the development of novel anti-inflammatory therapeutic strategies.