A review on the association between inflammatory myopathies and vaccination.
Several viruses and vaccines are among the environmental factors implicated as triggers of autoimmune inflammatory myopathies. Case histories report on the onset of dermatomyositis/polymyositis after immunization with various vaccines of patients with probable genetic predisposition. However, retrospective and epidemiological studies failed to ascertain an association between DM/PM and vaccines: no significant increase in the incidence of DM/PM was reported after large vaccination campaigns. The risk for vaccine-induced adverse events may be enhanced by adjuvants. Macrophagic myofasciitis is a novel inflammatory myopathy ascribed to an ongoing local immune reaction to a vaccine adjuvant. Isolated prospective studies showed that the administration of unadjuvanted, non-live vaccine to patients with DM/PM caused no short-term harmful effects to DM/PM immune processes. However, more research is warranted to clarify the incidence of vaccine-preventable infections, harmful effects of vaccination, and the influence of any immunomodulating agents on vaccination efficacy. Vaccination is an important disease prevention tool in modern medicine. This review does not address risk-benefit or cost-benefit analyses, and does not advocate the use of specific vaccines or vaccination programs. Despite a great deal of scientific uncertainty, the concept of a possible causal link between immunization and inflammatory myopathies should not be totally rejected.
Nutrition, inflammation and liver-spleen axis.
Barrea Luigi,Di Somma Carolina,Muscogiuri Giovanna,Tarantino Giovanni,Tenore Gian Carlo,Orio Francesco,Colao Annamaria,Savastano Silvia
Critical reviews in food science and nutrition
Chronic low-grade systemic inflammation represents a mechanism common to many diseases linked to atherosclerosis-related pathways. There is a growing body of evidence indicating that the combination of food quantity and quality along with genetic susceptibility are able to induce the aberrant activation of innate immune signalling, which initially contributes to chronic low-grade inflammation. Liver represents the central player to inflammatory response. Dietary/metabolic factors contribute to the pathogenesis of Non-alcoholic Fatty Liver Disease (NAFLD), the main causes of liver disease in the Western world. Enlargement of the spleen, central organ in regulating the inflammation-related immune response, is commonly seen in patients with of NAFLD, depicting the so called "liver-spleen axis." The aim of this review was to provide an at-a-glance overview of the possible bi-directional mechanisms linking nutrition and inflammation, particularly pinpointing the inflammatory effects stemmed by nutrition on "liver-spleen axis." In particular, the role of unhealthy diet, healthy dietary patterns, such as the Mediterranean diet style, dietary vitamins and micronutrients, such as vitamin D or Magnesium, and Glucagon-Like Peptide-1, a well-known incretin released in response to meal intake, will be discussed. The highly variability of the inflammatory response highlights the role of expert nutritionists in refining methodologies apt to assess nutritional epidemiology and to apply appropriate dietary intervention to counteract diet-induced inflammation mechanisms.
Esposito Susanna,Longo Maria Roberta
The term Guillain-Barré syndrome (GBS), the most frequent cause of acute paralytic neuropathy, covers a number of recognisably distinct variants. The exact cause of GBS is unknown, but 50-70% of cases appear 1-2weeks after a respiratory or gastrointestinal infection, or another immune stimulus that induces an aberrant autoimmune response targeting peripheral nerves and their spinal roots. The interplay between the microbial and host factors that dictate whether and how the immune response shifts towards autoreactivity is still unclear, and nothing is known about the genetic and environmental factors that affect an individual's susceptibility to the disease. All patients with GBS need meticulous monitoring, and can benefit from supportive care and the early start of specific treatment. This review summarises the clinical features and diagnostic criteria of GBS and proposes an algorithm for its management. An analysis of the literature showed that, about one century after it was first described, new information concerning its etiopathogenesis has allowed the development of new treatment strategies that should be started immediately after diagnosis; however, the available therapies are not sufficient in many patients, especially in the presence of the acute inflammatory demyelinating polyneuropathy. New post-infectious forms, such as those caused by Zika virus and enterovirus D68, need to be carefully analysed and, in order to improve patient outcomes, research should continue to aim at identifying new biomarkers of disease severity and better means of avoiding axonal injury.
The immunometabolic role of indoleamine 2,3-dioxygenase in atherosclerotic cardiovascular disease: immune homeostatic mechanisms in the artery wall.
Ketelhuth Daniel F J
Coronary heart disease and stroke, the two most common cardiovascular diseases worldwide, are triggered by complications of atherosclerosis. Atherosclerotic plaques are initiated by a maladaptive immune response triggered by accumulation of lipids in the artery wall. Hence, disease is influenced by several non-modifiable and modifiable risk factors, including dyslipidaemia, hypertension, smoking, and diabetes. Indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme in the kynurenine pathway of tryptophan (Trp) degradation, is modulated by inflammation and regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. A large body of evidence indicates that IDO-mediated Trp metabolism is involved directly or indirectly in atherogenesis. This review summarizes evidence from basic and clinical research showing that IDO is a major regulatory enzyme involved in the maintenance of immunohomeostasis in the vascular wall, as well as current knowledge about promising targets for the development of new anti-atherosclerotic drugs.
"TRP inflammation" relationship in cardiovascular system.
Numata Tomohiro,Takahashi Kiriko,Inoue Ryuji
Seminars in immunopathology
Despite considerable advances in the research and treatment, the precise relationship between inflammation and cardiovascular (CV) disease remains incompletely understood. Therefore, understanding the immunoinflammatory processes underlying the initiation, progression, and exacerbation of many cardiovascular diseases is of prime importance. The innate immune system has an ancient origin and is well conserved across species. Its activation occurs in response to pathogens or tissue injury. Recent studies suggest that altered ionic balance, and production of noxious gaseous mediators link to immune and inflammatory responses with altered ion channel expression and function. Among plausible candidates for this are transient receptor potential (TRP) channels that function as polymodal sensors and scaffolding proteins involved in many physiological and pathological processes. In this review, we will first focus on the relevance of TRP channel to both exogenous and endogenous factors related to innate immune response and transcription factors related to sustained inflammatory status. The emerging role of inflammasome to regulate innate immunity and its possible connection to TRP channels will also be discussed. Secondly, we will discuss about the linkage of TRP channels to inflammatory CV diseases, from a viewpoint of inflammation in a general sense which is not restricted to the innate immunity. These knowledge may serve to provide new insights into the pathogenesis of various inflammatory CV diseases and their novel therapeutic strategies.
Inflammatory bowel disease and the elderly: a review.
Taleban Sasha,Colombel Jean-Frederic,Mohler M Jane,Fain Mindy J
Journal of Crohn's & colitis
Inflammatory bowel disease among the elderly is common, with growing incident and prevalence rates. Compared with younger IBD patients, genetics contribute less to the pathogenesis of older-onset IBD, with dysbiosis and dysregulation of the immune system playing a more significant role. Diagnosis may be difficult in older individuals, as multiple other common diseases can mimic IBD in this population. The clinical manifestations in older-onset IBD are distinct, and patients tend to have less of a disease trajectory. Despite multiple effective medical and surgical treatment strategies for adults with Crohn's disease and ulcerative colitis, efficacy studies typically have excluded older subjects. A rapidly ageing population and increasing rates of Crohn's and ulcerative colitis make the paucity of data in older adults with IBD an increasingly important clinical issue.
Exploring immune checkpoints as potential therapeutic targets in atherosclerosis.
Kusters Pascal J H,Lutgens Esther,Seijkens Tom T P
In the past decades, the inflammatory nature of atherosclerosis has been well-recognized and despite the development of therapeutic strategies targeted at its classical risk factors such as dyslipidemia and hypertension, atherosclerosis remains a major cause of morbidity and mortality. Additional strategies targeting the chronic inflammatory pathways underlying the development of atherosclerosis are therefore required. Interactions between different immune cells result in the secretion of inflammatory mediators, such as cytokines and chemokines, and fuel atherogenesis. Immune checkpoint proteins have a critical role in facilitating immune cell interactions and play an essential role in the development of atherosclerosis. Although the therapeutic potential of these molecules is well-recognized in clinical oncology, the use of immune checkpoint modulators in atherosclerosis is still limited to experimental models. Here, we review recent insights on the role of immune checkpoint proteins in atherosclerosis. Additionally, we explore the therapeutic potential and challenges of immune checkpoint modulating strategies in cardiovascular medicine and we discuss novel therapeutic approaches to target these proteins in atherosclerosis.
Potential cardiac risk of immune-checkpoint blockade as anticancer treatment: What we know, what we do not know, and what we can do to prevent adverse effects.
Spallarossa Paolo,Meliota Giovanni,Brunelli Claudio,Arboscello Eleonora,Ameri Pietro,Dessalvi Christian Cadeddu,Grossi Francesco,Deidda Martino,Mele Donato,Sarocchi Matteo,Bellodi Andrea,Madonna Rosalinda,Mercuro Giuseppe
Medicinal research reviews
Cancer immunotherapy has become a well-established treatment option for some cancers after the development of a family of drugs targeting the so-called immune checkpoints, such as CTLA4 and PD-1 with PD-L1. These co-receptors/ligands inhibit the activation of T-cell, thus preventing an excessive inflammatory response. Tumors exploit these pathways to induce immune tolerance to themselves. Thus, the main effect of checkpoint-blocking drugs is to awake an immune response primarily directed against cancer cells. Nonetheless, as the immune response elicited by these drugs is not completely tumor-specific, their use may actually cause several adverse effects, including adverse cardiovascular effects. In this review, we will discuss the principles and potentiality of immunotherapy for cancer treatment, the experimental and clinical data on the role of CTLA4 and PD-1 with PD-L1 as immune-checkpoints in the cancer environment and in the cardiovascular system, and strategies aimed at preventing possible cardiovascular adverse effects of immune-checkpoint blockers.