Our digestive system, particularly our intestines, harbors a vast amount of microorganisms, whose genetic makeup is referred to as the microbiome. Clostridium difficile is a spore-forming Gram-positive bacterium, which can cause an infection whose symptoms range from asymptomatic colonization to fearsome complications such as the onset of toxic megacolon. The relationship between gut microbiota and Clostridium difficile infection has been studied from different perspectives. One of the proposed strategies is to be able to specifically identify which types of microbiota alterations are most at risk for the onset of CDI. In this article, we understood once again how crucial the role of the human microbiota is in health and especially how crucial it becomes, in the case of its alteration, for the individual’s disease. Clostridium difficile infection is an emblematic example of how a normal and physiological composition of the human microbiome can play a very important role in immune defense against such a fearsome disease.
Myopericarditis is an inflammatory heart condition involving the pericardium and myocardium. It can lead to heart failure, dilated cardiomyopathy, arrhythmia and sudden death. Its pathogenesis is mainly mediated by viral infections but also can be induced by bacterial infections, toxic substances and immune mediated disorders. All these conditions can produce severe inflammation and myocardial injury, often associated with a poor prognosis. The specific roles of these different pathogens (in particular viruses), the interaction with the host, the interplay with gut microbiota, and the immune system responses to them are still not completely clear and under investigation. Interestingly, some research has demonstrated the contribution of the gut microbiota, and its related metabolites (some of which can mimic the cardiac myosin), in cardiac inflammation and in the progression of this disease. They can stimulate a continuous and inadequate immune response, with a subsequent myocardial inflammatory damage. The aim of our review is to investigate the role of gut microbiota in myopericarditis, especially for the cardiovascular implications of COVID-19 viral infection, based on the idea that the modulation of gut microbiota can be a new frontier in the cardiological field to prevent or treat inflammatory cardiomyopathies.
Cigarette smoke is a classic risk factor for many diseases. The microbiota has been recently indicated as a new, major player in human health. Its deregulation—dysbiosis—is considered a new risk factor for several illnesses. Some studies highlight a cross-interaction between these two risk factors—smoke and dysbiosis—that may explain the pathogenesis of some diseases. We searched the keywords “smoking OR smoke AND microbiota” in the title of articles on PubMed®, UptoDate®, and Cochrane®. We included articles published in English over the last 25 years. We collected approximately 70 articles, grouped into four topics: oral cavity, airways, gut, and other organs. Smoke may impair microbiota homeostasis through the same harmful mechanisms exerted on the host cells. Surprisingly, dysbiosis and its consequences affect not only those organs that are in direct contact with the smoke, such as the oral cavity or the airways, but also involve distant organs, such as the gut, heart, vessels, and genitourinary tract. These observations yield a deeper insight into the mechanisms implicated in the pathogenesis of smoke-related diseases, suggesting a role of dysbiosis. We speculate that modulation of the microbiota may help prevent and treat some of these illnesses.
There is much evidence confirming the crucial role played by the gut microbiota in modulating the immune system in the onset of autoimmune diseases. In this article, we focus on the relationship between alterations in the microbiome and the onset of diabetes mellitus type 1 and LADA, in light of the latest evidence. We will then look at both how the role of the gut microbiota appears to be increasingly crucial in the pathogenesis of these disorders and how this aspect may be instrumental in the development of new potential therapeutic strategies that modulate the gut microbiota, such as probiotics, prebiotics, and fecal microbiota transplantation.
I would like to thank my collaborators, Prof. Emilian Dudas, Cezar Condeescu and Prof. Ioannis Florakis, for the stimulating discussions that expanded my knowledge and opened new perspectives on the topics I have been working on.A special thank is deserved to my collaborator and friend, Ivano Basile, who taught me a lot of new physics I did not know of and opened my eyes to new worlds to be explored, as well as for his kindness and availability even outside physics. His passion and enthusiasm have been stimulating and inspirational in my research activity.During these years I had the opportunity to be involved in interesting conversations, from which my work undoubtedly benefited, with many brilliant colleagues and senior scientists including Prof.
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