Recently, multiple studies regarding the human microbiota and its role on the development of disease have emerged. Current research suggests that the nasal cavity is a major reservoir for opportunistic pathogens, which can then spread to other sections of the respiratory tract and be involved in the development of conditions such as allergic rhinitis, chronic rhinosinusitis, asthma, pneumonia, and otitis media. However, our knowledge of how nasal microbiota changes originate nasopharyngeal and respiratory conditions is still incipient. Herein, we describe how the nasal microbiome in healthy individuals varies with age and explore the effect of nasal microbiota changes in a range of infectious and immunological conditions. We also describe the potential health benefits of human microbiota modulation through probiotic use, both in disease prevention and as adjuvant therapy. Current research suggests that patients with different chronic rhinosinusitis phenotypes possess distinct nasal microbiota profiles, which influence immune response and may be used in the future as biomarkers of disease progression. Probiotic intervention may also have a promising role in the prevention and adjunctive treatment of acute respiratory tract infections and allergic rhinitis, respectively. However, further studies are needed to define the role of probiotics in the chronic rhinosinusitis.

In the area of drug delivery, novel tools and technological approaches have captured the attention of researchers in order to improve the performance of conventional therapeutics and patient compliance to pharmacological therapy. Stimuli-responsive drug delivery systems (DDS) appear as a promising approach to control and target drug delivery. When these DDS are administered, the drug release is activated and then modulated through some action or external input and facilitated by the energy supplied externally. The stimuli responsible to activate the drug release can be classified into three types according to their nature or the type of energy applied: physical (e.g. magnetic field, electric field, ultrasound, temperature and osmotic pressure); chemical (e.g. pH, ionic strength and glucose); and biological (enzymes and endogenous receptors). The present review gives an overview of the most significant physical and chemical stimuliresponsive DDS and elucidates about their current and relevant applications in controlled and targeted drug delivery attending different routes of administration.

Background: The human gut microbiota is defined as the microorganisms that collectively inhabit the intestinal tract. Its composition is relatively stable; however, an imbalance can be precipitated by various factors and is known to be associated with various diseases. Humans are daily exposed to ionizing radiation from ambient and medical procedures, and gastrointestinal side effects are not rare. Methods: A systematic search of PubMed, EMBASE, and Cochrane Library databases was conducted. Primary outcomes were changes in composition, richness, and diversity of the gut microbiota after ionizing radiation exposure. Standard methodological procedures expected by Cochrane were used. Results: A total of 2929 nonduplicated records were identified, and based on the inclusion criteria, 11 studies were considered. Studies were heterogeneous, with differences in population and outcomes. Overall, we found evidence for an association between ionizing radiation exposure and dysbiosis: reduction in microbiota diversity and richness, increase in pathogenic bacteria abundance (Proteobacteria and Fusobacteria), and decrease in beneficial bacteria (Faecalibacterium and Bifidobacterium). Conclusions: This review highlights the importance of considering the influence of ionizing radiation exposure on gut microbiota, especially when considering the side effects of abdominal and pelvic radiotherapy. Better knowledge of these effects, with larger population studies, is needed.

Background: For almost a century it has been recognized that human possess a varied and dens microbial ecosystem called the human microbiota, yet we are still beginning to understand many of the roles that these microorganisms play in human health and development. It is thought that under certain circumstances such as dysbiosis, the microbiota can cause diseases, where the central nervous system (CNS) has an important relevance and where the “gut-brain axis” will play a major role. Aims: This review investigated the influence of the gut microbiota on brain function, trying to demonstrate whether dysbiosis influences CNS diseases or whether it is the disease that causes dysbiosis, highlighting the existing literature within this field. Methods: We performed a systematic literature search in EMBASE, PubMed, and Cochrane combining the terms “gut microbiota,” “dysbiosis,” and “CNS diseases” to identify those whom reported some influence or relation between dysbiosis of gut microbiota and CNS diseases. For the present systematic review, we only included systematic reviews or meta-analysis. Results: The EMBASE, PubMed, and Cochrane were systematically searched, considering only systematic reviews or meta-analysis. Nine studies comprising 705 articles were included in this review. Those 9 systematic reviews consist in 2 about autism spectrum disorder, 1 in dementia, 1 in depression, 2 in autoimmune diseases, 1 in schizophrenia, and 2 in some altered brain function. Available data characterizing several neural diseases demonstrate a significant correlation between dysbiosis and CNS diseases, strengthen the evidence that dysbiosis of gut microbiota may correlate with abnormalities in CNS patients. Conclusions: Although there is a clear need for more investigations to better understand the role of the gut microbiota in CNS diseases, the modulation of the nervous system by the microbiota is clear, continuing to be the subject of continuous research. We need to fully understand the mechanisms by which the microbiota interacts with the human brain, and therefore what's the connection between dysbiosis and pathologies such depression, dementia, autism, or schizophrenia.