Sepsis is a serious organ dysfunction caused by a dysregulated immune host reaction to a pathogen. The innate immunity is programmed to react immediately to conserved molecules, released by the pathogens (PAMPs), and the host (DAMPs). We aimed to review the molecular mechanisms of the early phases of sepsis, focusing on PAMPs, DAMPs, and their related pathways, to identify potential biomarkers. We included studies published in English and searched on PubMed^® and Cochrane^®. After a detailed discussion on the actual knowledge of PAMPs/DAMPs, we analyzed their role in the different organs affected by sepsis, trying to elucidate the molecular basis of some of the most-used prognostic scores for sepsis. Furthermore, we described a chronological trend for the release of PAMPs/DAMPs that may be useful to identify different subsets of septic patients, who may benefit from targeted therapies. These findings are preliminary since these pathways seem to be strongly influenced by the peculiar characteristics of different pathogens and host features. Due to these reasons, while initial findings are promising, additional studies are necessary to clarify the potential involvement of these molecular patterns in the natural evolution of sepsis and to facilitate their transition into the clinical setting.

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.

Drug abuse (cannabis, cocaine, opiates, and synthetic drugs) is an increasing phenomenon, especially in the younger population, thus leading to more cases of intoxication requiring evaluation in the emergency department and subsequent hospitalization. In 2017, 34.2% of students reported having used an illegal psychoactive substance in their lifetime, while 26% reported having done so over the past year. We made a review about the effectiveness of the role of the temporary observation unit in the emergency department to improve management of acute drugs intoxication. We checked medical literature from the last 10 years (2009–2019). The following electronic databases were systematically searched: MEDLINE-PubMed, Web of Science, Scopus, and the Cochrane Central Register of Controlled Trials. Then, a systematic review was carried out according to the Preferred Reporting Items for Systematic Review standards. Intoxicated patients usually display a favorable medical course, few diagnostic and therapeutic interventions, a short stay in the hospital, and, when hospitalization is needed, semi-intensive therapy is a feasible solution; therefore, intoxicated patients are ideal candidates for a temporary observation unit. The emergency department is very important to manage intoxicated patients; however, the hospitalization of these patients is often not necessary.

Fibrosis, sustained by the transformation of intestinal epithelial cells into fibroblasts (epithelial-to-mesenchymal transition, EMT), has been extensively studied in recent decades, with the molecular basis well-documented in various diseases, including inflammatory bowel diseases (IBDs). However, the factors influencing these pathways remain unclear. In recent years, the role of the gut microbiota in health and disease has garnered significant attention. Evidence suggests that an imbalanced or dysregulated microbiota, along with environmental and genetic factors, may contribute to the development of IBDs. Notably, microbes produce various metabolites that interact with host receptors and associated signaling pathways, influencing physiological and pathological changes. This review aims to present recent evidence highlighting the emerging role of the most studied metabolites as potential modulators of molecular pathways implicated in intestinal fibrosis and EMT in IBDs. These studies provide a deeper understanding of intestinal inflammation and fibrosis, elucidating the molecular basis of the microbiota role in IBDs, paving the way for future treatments.