Immune memory is a defining feature of the acquired immune system, but activation of the innate immune system can also result in enhanced responsiveness to subsequent triggers. This process has been termed 'trained immunity', a de facto innate immune memory. Research in the past decade has pointed to the broad benefits of trained immunity for host defence but has also suggested potentially detrimental outcomes in immune-mediated and chronic inflammatory diseases. Here we define 'trained immunity' as a biological process and discuss the innate stimuli and the epigenetic and metabolic reprogramming events that shape the induction of trained immunity.

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Defining trained immunity and its role in health and disease

BCG Vaccination Protects against Experimental Viral Infection in Humans through the Induction of Cytokines Associated with Trained Immunity

Countless times each day, the acute inflammatory response protects us from invading microbes, injuries, and insults from within, as in surgery-induced tissue injury. These challenges go unnoticed because they are self-limited and naturally resolve without progressing to chronic inflammation. Peripheral blood markers of inflammation are present in many common diseases, including inflammatory bowel disease, cardiovascular disease, neurodegenerative disease, and cancer. While acute inflammation is protective, excessive swarming of neutrophils amplifies collateral tissue damage and inflammation. Hence, understanding the mechanisms that control the resolution of acute inflammation provides insight into preventing and treating inflammatory diseases in multiple organs. This Review focuses on the resolution phase of inflammation with identification of specialized pro-resolving mediators (SPMs) that involve three separate biosynthetic and potent mediator families, which are defined using the first quantitative resolution indices to score this vital process. These are the resolvins, protectins, and maresins: bioactive metabolomes that each stimulate self-limited innate responses, enhance innate microbial killing and clearance, and are organ-protective. We briefly address biosynthesis of SPMs and their activation of endogenous resolution programs as terrain for new therapeutic approaches that are not, by definition, immunosuppressive, but rather new immunoresolvent therapies.

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Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators.

The outbreak of coronavirus disease (COVID-19) in late December 2019 in China, which later developed into a pandemic, has forced different countries to implement strict sanitary regimes and social distancing measures. Globally, at least four billion people were under lockdown, working remotely, homeschooling children, and facing challenges coping with quarantine and the stressful events. The present cross-sectional online survey of adult Poles (n = 1097), conducted during a nationwide quarantine, aimed to assess whether nutritional and consumer habits have been affected under these conditions. Over 43.0% and nearly 52% reported eating and snacking more, respectively, and these tendencies were more frequent in overweight and obese individuals. Almost 30% and over 18% experienced weight gain (mean ± SD 3.0 ± 1.6 kg) and loss (−2.9 ± 1.5 kg), respectively. Overweight, obese, and older subjects (aged 36–45 and >45) tended to gain weight more frequently, whereas those with underweight tended to lose it further. Increased BMI was associated with less frequent consumption of vegetables, fruit, and legumes during quarantine, and higher adherence to meat, dairy, and fast-foods. An increase in alcohol consumption was seen in 14.6%, with a higher tendency to drink more found among alcohol addicts. Over 45% of smokers experienced a rise in smoking frequency during the quarantine. The study highlights that lockdown imposed to contain an infectious agent may affect eating behaviors and dietary habits, and advocates for organized nutritional support during future epidemic-related quarantines, particularly for the most vulnerable groups, including overweight and obese subjects.

Dietary Choices and Habits during COVID-19 Lockdown: Experience from Poland.

Emerging evidence has spurred a considerable evolution of concepts relating to atherosclerosis, and has called into question many previous notions. Here I review this evidence, and discuss its implications for understanding of atherosclerosis. The risk of developing atherosclerosis is no longer concentrated in Western countries, and it is instead involved in the majority of deaths worldwide. Atherosclerosis now affects younger people, and more women and individuals from a diverse range of ethnic backgrounds, than was formerly the case. The risk factor profile has shifted as levels of low-density lipoprotein (LDL) cholesterol, blood pressure and smoking have decreased. Recent research has challenged the protective effects of high-density lipoprotein, and now focuses on triglyceride-rich lipoproteins in addition to low-density lipoprotein as causal in atherosclerosis. Non-traditional drivers of atherosclerosis—such as disturbed sleep, physical inactivity, the microbiome, air pollution and environmental stress—have also gained attention. Inflammatory pathways and leukocytes link traditional and emerging risk factors alike to the altered behaviour of arterial wall cells. Probing the pathogenesis of atherosclerosis has highlighted the role of the bone marrow: somatic mutations in stem cells can cause clonal haematopoiesis, which represents a previously unrecognized but common and potent age-related contributor to the risk of developing cardiovascular disease. Characterizations of the mechanisms that underpin thrombotic complications of atherosclerosis have evolved beyond the ‘vulnerable plaque’ concept. These advances in our understanding of the biology of atherosclerosis have opened avenues to therapeutic interventions that promise to improve the prevention and treatment of now-ubiquitous atherosclerotic diseases. This Review discusses recent research that has transformed our understanding of the biology of atherosclerosis, and examines its implications for the treatment of atherosclerotic cardiovascular disease.

Debjani Biswas

Papers

Western Diet Triggers NLRP3-Dependent Innate Immune Reprogramming