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Aims: Inflammageing, the age-related systemic increase of proinflammatory factors, has been linked to the development of cardiovascular disease, chronic kidney disease and cancer in the elderly. Chronic inflammation is believed to be a causative factor in the development of diabetic complications. However, exactly how type 2 diabetes impacts the inflammatory state of the immune system is incompletely characterised., Methods: Blood collection and anthropometric measurements were performed in patients with type 2 diabetes (n = 49) and control subjects (n = 30). The phenotype, proliferation capacity and cytokine production by cytotoxic lymphocytes were analysed using multiparametric flow cytometry., Results: Type 2 diabetes did not impact the phenotype or proliferation of the investigated cells. However, we observed a significantly increased production of tumour necrosis factor-α by CD8 + T cells and Granzyme B by natural killer cells and γδ T cells compared to controls. Hyperresponsiveness of cytotoxic blood lymphocytes did not correlate with glycaemia or body mass index, but instead was associated with older age and longer diabetes duration., Conclusions: Type 2 diabetes is associated with an increased pro-inflammatory potential of cytotoxic blood lymphocytes correlating with age and diabetes duration. Further research is necessary to explore potential benefits of diabetes medications in reverting this effect., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Peripheral arterial disease (PAD) reduces functional capacity and raises cardiovascular risks, but underdiagnosis is common, resulting in less comprehensive care than other cardiovascular conditions. While diabetes has long been viewed as a key risk factor for PAD, recent studies indicate that its impact is influenced by the presence of concurrent cardiovascular risk factors. The aim of this study is to elucidate the intricate relationship between the prevalence of PAD, diabetic complications, and cardiovascular risk factors among asymptomatic patients with type 2 diabetes mellitus (T2DM)., Methods: Ninety-one patients with T2DM and no symptoms or previous diagnosis of PAD were recruited from the outpatient diabetic clinic. Clinical data were extracted from electronic medical records, and the screening for PAD was conducted using MESI mTABLET., Results: Screening for PAD among asymptomatic individuals with T2DM revealed that 5.49 % of patients exhibit a low ankle-brachial index (ABI). Patients who had previously experienced major adverse cardiovascular events or exhibited albuminuria displayed lower ABI values. Furthermore, a striking 45.05 % of the participants displayed an abnormally high carotid-femoral pulse wave velocity (cfPWV) value, with elevated PWV values correlating with advanced age and longer diabetes duration., Conclusions: The prevalence of elevated cfPWV is more pronounced than that of decreased ABI in T2DM patients with asymptomatic PAD and is associated with older age and longer diabetes duration, therefore measurement of both ABI and PWV is crucial for the cardiovascular risk assessment protocol for patients with T2DM and timely PAD diagnosis., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Memory CD8 T cells play an important role in the protection against breakthrough infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Whether the route of antigen exposure impacts these cells at a functional level is incompletely characterized. Here, we compare the memory CD8 T cell response against a common SARS-CoV-2 epitope after vaccination, infection, or both. CD8 T cells demonstrate comparable functional capacity when restimulated directly ex vivo, independent of the antigenic history. However, analysis of T cell receptor usage shows that vaccination results in a narrower scope than infection alone or in combination with vaccination. Importantly, in an in vivo recall model, memory CD8 T cells from infected individuals show equal proliferation but secrete less tumor necrosis factor (TNF) compared with those from vaccinated people. This difference is negated when infected individuals have also been vaccinated. Our findings shed more light on the differences in susceptibility to re-infection after different routes of SARS-CoV-2 antigen exposure., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

Exercise has many beneficial effects for our body, but can become detrimental at high intensity, especially for our immune system. Little is known about the underlying mechanism of impaired immune functionality under conditions of intense physical strain. Freedivers, people who dive to high depths on a single breath, perform extreme exercise under anaerobic conditions. In this study, we investigated the impact of freediving on the cytotoxic arm of the immune system. At rest, elite freedivers did not display changes in their immunological profile compared to non-diving controls. In contrast, after a freedive, granzyme B and IL-2 production were reduced, whereas IFNγ and TNF secretion were increased by cytotoxic immune cells. Using in vitro models mimicking freedive conditions, we could show that hypoxia in combination with stress hyperglycemia had a negative impact on Granzyme B secretion, whereas IL-2 production was inhibited by stress hormones. Our findings suggest that in response to extreme exercise, cytotoxic immune cells transiently change their functional profile to limit tissue damage., (Copyright © 2022 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.)

The recent pandemic of COVID-19 has made abundantly clear that Type 2 diabetes (T2D) increases the risk of more frequent and more severe viral infections. At the same time, pro-inflammatory cytokines of an anti-viral Type-I profile promote insulin resistance and form a risk factor for development of T2D. What this illustrates is that there is a reciprocal, detrimental interaction between the immune and endocrine system in the context of T2D. Why these two systems would interact at all long remained unclear. Recent findings indicate that transient changes in systemic metabolism are induced by the immune system as a strategy against viral infection. In people with T2D, this system fails, thereby negatively impacting the antiviral immune response. In addition, immune-mediated changes in systemic metabolism upon infection may aggravate glycemic control in T2D. In this review, we will discuss recent literature that sheds more light on how T2D impairs immune responses to viral infection and how virus-induced activation of the immune system increases risk of development of T2D., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Chronic pain is a painful condition defined by its duration where pain persists three months or more. Pain is connected with the high price of health care, work inability and disability. Moreover, it has significant consequences for patients and their families, working organizations and the society as a whole. The prevalence of chronic pain can range between 11.0% and 51.3% in general population. Pain is usually coherent with distress and a range of psychological symptoms such as depression, anxiety, altered attention and cognition manifesting as fear. Comprehensive pain management should always include the treatment of associated psychological symptoms. Multidisciplinary approach in treating chronic pain and its comorbidities and proper education of primary care physicians and different specialists involved in the management of chronic pain are crucial for better clinical outcomes. Topical capsaicin acts as a highly selective agonist of transient receptor potential vanilloid 1 of C and Aδ nociceptors. Repeated applications or high concentrations give rise to a long-lasting effect termed defunctionalisation. In addition, the reduction of central sensitization through reduced C-nociceptor input contributes to capsaicin's indirect mechanism of action. Capsaicin provides effective durable pain relief and reduction of intensity and area of pain in adult patients with chronic pain with a faster onset of analgesia and considerably fewer systemic adverse effects than the conventional treatment. While offering high levels of pain relief, additional improvements in sleep, fatigue, depression and quality of life have been noticed. Topical administration avoids dangerous systemic adverse effects and enables the combination with other drugs and analgesics with limited drug-drug interactions. Adding capsaicin to the standard chronic pain treatment might improve, fasten and ease the challenging path of managing chronic pain consequently providing the patient and their society with better quality of life.