Food Additives, a Key Environmental Factor in the Development of IBD through Gut Dysbiosis

Diet is a key environmental factor in inflammatory bowel disease (IBD) and, at the same time, represents one of the most promising therapies for IBD. Our daily diet often contains food additives present in numerous processed foods and even in dietary supplements. Recently, researchers and national authorities have been paying much attention to their toxicity and effects on gut microbiota and health. This review aims to gather the latest data focusing on the potential role of food additives in the pathogenesis of IBDs through gut microbiota modulation. Some artificial emulsifiers and sweeteners can induce the dysbiosis associated with an alteration of the intestinal barrier, an activation of chronic inflammation, and abnormal immune response accelerating the onset of IBD. Even if most of these results are retrieved from in vivo and in vitro studies, many artificial food additives can represent a potential hidden driver of gut chronic inflammation through gut microbiota alterations, especially in a population with IBD predisposition. In this context, pending the confirmation of these results by large human studies, it would be advisable that IBD patients avoid the consumption of processed food containing artificial food additives and follow a personalized nutritional therapy prescribed by a clinical nutritionist.

Recurrent herpes zoster with IgD deposits, multinucleated keratinocytes and overexpression of galectin and glypican 3 in a patient with SARS-COVID-19 infection

The novel coronavirus disease (COVID-19) that currently plagues the world and caused by SARS-CoV-2, has spread internationally since late 2019. The dermatologic manifestations of this virus are currently being identified. We describe a 73-year-old Caucasian female who presented to many physicians for recurrent Herpes zoster episodes that persisted, despite treatment with multiple antiviral medications. The patient was diagnosed with COVID-19 before an onset of vesicular pustular lesions. The clinical diagnoses were recurrent herpes zoster and recurrent varicella. A skin biopsy was obtained and stained with hematoxylin and eosin to confirm a diagnosis. Immunohistochemical stains for Ki-67, Phospho-Histone H3, galectin 3, glypican and IgD were positive in multinucleated cells of the skin, where the viral lesions were detected. Recidivated herpes zoster and varicella are currently being clinically associated with COVID- 19; the abnormal immune response in patients with COVID-19 may be due to the overexpression of molecules that facilitate the outbreak of these viruses.

Kawasaki Disease Triggered by Epstein-Barr Virus Infection: A Case Report

Kawasaki disease (KD) is the most common cause of acquired heart disease today. An important and enduring complication of KD is a coronary aneurysm, whose early diagnosis and treatment can reduce the risk from 25% to 3%. Diagnosis of this disease is mainly clinical, although leukocytosis, increased erythrocyte sedimentation rate, and echocardiography are helpful in diagnosis. The cause of KD remains unknown, but the most common hypothesis is an abnormal immune response that is likely caused by an infectious agent, possibly in a favorable genetic background, and leads to vasculitis of the middle arteries, especially coronary arteries of the heart. Numerous infectious agents have been suggested in this regard. Co-infection with KD can also delay diagnosis. In this article, we introduce five years and seven months child who developed Kawasaki disease within a few days of the onset of Epstein-Barr virus infection.

Paraneoplastic and Other Autoimmune Neurologic Disorders

A paraneoplastic disorder arises from remote effects of malignancy, rather than direct tumor invasion. Paraneoplastic neurologic disorders occur because of the vigorous immune responses directed against antigens expressed in tumors. The vigor of the immune response usually ensures that neoplasm is confined to the primary organ and regional lymph nodes. However, in the clinical setting of paraneoplastic disease, the immune response may attack any part of the nervous system (brain, spinal cord, nerve, neuromuscular junction, or muscle), and antibodies are either directed at intracellular neuronal proteins or against neuronal cell surface or synaptic proteins. Treatment is often aimed at the cancer and suppression of the abnormal immune response.

Primary biliary cirrhosis associated with myasthenia gravis after postpartum: a case report

Background Autoimmune diseases refers to a class of diseases involving abnormal immune response of human body and tissue damage caused by the dysregulation of autoimmune balance or destruction of immune tolerance. Recent research has revealed that the occurrence of autoimmune diseases is influenced by genetic, hormonal, immunological, and environmental factors. As sex hormone levels change obviously during pregnancy and postpartum, the morbidity and recurrence rate of autoimmune diseases increase during this period. Case presentation A 31-year-old Asian woman was admitted to our hospital for myasthenia gravis and treated with methylprednisolone and pyridostigmine bromide 3 months postpartum. Physical examination and laboratory inspection after admission suggested that the patient had primary biliary cirrhosis. Subsequently, azathioprine was added to the treatment, and the symptoms of both diseases were successfully controlled. Conclusions This case exhibits a rare condition of myasthenia gravis combined with primary biliary cirrhosis postpartum. Given the fluctuation of the immune status during the postpartum period, combined autoimmune diseases need to be taken into account when patients develop clinical symptoms of an autoimmune disease. Therefore, detailed physical and laboratory examination can help to prevent the missed diagnosis of these diseases.

Targeting Inflammatory Cytokines to Improve Type 2 Diabetes Control

Type 2 diabetes (T2D) is one of the most common chronic metabolic disorders in adulthood worldwide, whose pathophysiology includes an abnormal immune response accompanied by cytokine dysregulation and inflammation. As the T2D-related inflammation and its progression were associated with the balance between pro and anti-inflammatory cytokines, anticytokine treatments might represent an additional therapeutic option for T2D patients. This review focuses on existing evidence for antihyperglycemic properties of disease-modifying antirheumatic drugs (DMARDs) and anticytokine agents (anti-TNF-α, anti-interleukin-(IL-) 6, -IL-1, -IL-17, -IL-23, etc.). Emphasis is placed on their molecular mechanisms and on the biological rationale for clinical use. Finally, we briefly summarize the results from experimental model studies and promising clinical trials about the potential of anticytokine therapies in T2D, discussing the effects of these drugs on systemic and islet inflammation, beta-cell function, insulin secretion, and insulin sensitivity.

When Leptin Is Not There: A Review of What Nonsyndromic Monogenic Obesity Cases Tell Us and the Benefits of Exogenous Leptin

Obesity is a pandemic condition of complex etiology, resulting from the increasing exposition to obesogenic environmental factors combined with genetic susceptibility. In the past two decades, advances in genetic research identified variants of the leptin-melanocortin pathway coding for genes, which are related to the potentiation of satiety and hunger, immune system, and fertility. Here, we review cases of congenital leptin deficiency and the possible beneficial effects of leptin replacement therapy. In summary, the cases presented here show clinical phenotypes of disrupted bodily energy homeostasis, biochemical and hormonal disorders, and abnormal immune response. Some phenotypes can be partially reversed by exogenous administration of leptin. With this review, we aim to contribute to the understanding of leptin gene mutations as targets for obesity diagnostics and treatment strategies.

Coenzyme Q10 and Vitamin D Interventions Could Ameliorate COVID-19 Related Cellular Bioenergetic Dysfunction and Cytokine Storms

The immune response to SARS-CoV-2 varies from asymptomatic or mild symptoms of high temperature, muscle aches and coughs lasting 7 to 14 days to lower respiratory tract infections leading to pneumonia and serious respiratory distress as well as long COVID-19. Complications occur due to an abnormal immune response which involves upregulation of multiple cytokines leading to sustained inflammation which results in the spread of infection to vital organs. The double vaccine roll out has been rapid however vaccine mediated antibodies are not 100% effective against future coronavirus variants which may become increasingly more resistant and easily transmissible to overcome host immunity. Invariably supportive therapies will be needed. Research has shown that coenzyme Q10 and vitamin D deficiencies can have detrimental effects on immune cell defence, function and cytokine secretion promoting inflammation and sepsis especially against microbes. Early interventions including supplementation of these factors could mitigate cellular dysfunction especially in relation to mitochondria bioenergetics and help maintain cell immunity. This is particularly important as chronically ill COVID-19 patients seem to display abnormal immune cell phenotypes in infected organs indicating this could contribute to disease progression. The immune response and proposed roles of Vitamin D and Coenzyme Q10 in COVID-19 are discussed.

Correlation between Coronavirus Disease 2019 and Heart Failure: A Review

Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) led to the coronavirus disease 2019 (COVID-19) pandemic, which has resulted in devastating conditions worldwide. In addition to affecting the respiratory system, COVID-19 affects other systemic organs, and in particular, cardiovascular failure is related to the worsening of symptoms and death. Among these, cardiac insufficiency seems to be an important prognostic factor. Methods and Findings: We reviewed the association between COVID-19 and heart failure by searching Google Scholar and PubMed for reports related to COVID-19 and heart failure and selected those qualitatively and quantitatively established. The presence of heart failure may cause increased susceptibility to SARS-CoV-2 due to an abnormal immune response, which may aggravate COVID-19. In addition, myocardial injury, cytokine storm, endothelial dysfunction, blood coagulation abnormality, and hypoxemia due to respiratory injury may lead to worsening heart failure. Conclusions: Heart failure and COVID-19 are closely related, and their mechanisms are diverse. Multidisciplinary treatment is required to control the progression of cardiac insufficiency, which complicates COVID-19. Further elucidation of the pathology and establishment of efficacious therapy is desirable.