The imbalance of microbial composition and diversity in favor of pathogenic microorganisms combined with a loss of beneficial gut microbiota taxa results from factors such as age, diet, antimicrobial administration for different infections, other underlying medical conditions, etc. Probiotics are known for their capacity to improve health by stimulating the indigenous gut microbiota, enhancing host immunity resistance to infection, helping digestion, and carrying out various other functions. Concurrently, the metabolites produced by these microorganisms, termed postbiotics, which include compounds like bacteriocins, lactic acid, and hydrogen peroxide, contribute to inhibiting a wide range of pathogenic bacteria. This review presents an update on using probiotics in managing and treating various human diseases, including complications that may emerge during or after a COVID-19 infection.

Multidrug-resistant Gram-negative bacteria such as Acinetobacter baumannii, Pseudomonas aeruginosa, and members of the Enterobacterales order are a challenging multi-sectorial and global threat, being listed by the WHO in the priority list of pathogens requiring the urgent discovery and development of therapeutic strategies. We present here an overview of the antibiotic resistance profiles and epidemiology of Gram-negative pathogens listed in the ESCAPE group circulating in Romania. The review starts with a discussion of the mechanisms and clinical significance of Gram-negative bacteria, the most frequent genetic determinants of resistance, and then summarizes and discusses the epidemiological studies reported for A. baumannii, P. aeruginosa, and Enterobacterales-resistant strains circulating in Romania, both in hospital and veterinary settings and mirrored in the aquatic environment. The Romanian landscape of Gram-negative pathogens included in the ESCAPE list reveals that all significant, clinically relevant, globally spread antibiotic resistance genes and carrying platforms are well established in different geographical areas of Romania and have already been disseminated beyond clinical settings.

Antibiotic resistance represents a growing public health threat, with airborne drug-resistant strains being especially alarming due to their ease of transmission and association with severe respiratory infections. The respiratory microbiome plays a pivotal role in maintaining respiratory health, influencing the dynamics of antibiotic resistance among airborne pathogenic microorganisms. In this context, this review proposes the exploration of the complex interplay between the respiratory microbiota and antimicrobial resistance, highlighting the implications of microbiome diversity in health and disease. Moreover, strategies to mitigate antibiotic resistance, including stewardship programs, alternatives to traditional antibiotics, probiotics, microbiota restoration techniques, and nanotechnology-based therapeutic interventions, are critically presented, setting an updated framework of current management options. Therefore, through a better understanding of respiratory microbiome roles in antibiotic resistance, alongside emerging therapeutic strategies, this paper aims to shed light on how the global health challenges posed by multi-drug-resistant pathogens can be addressed.

Growing resistance to antimicrobials, combined with pathogens that form biofilms, presents significant challenges in healthcare. Modifying current antimicrobial agents is an economical approach to developing novel molecules that could exhibit biological activity. Thus, five sulfanilamide Schiff bases were synthesized under microwave irradiation and characterized spectroscopically and in silico. They were evaluated for their antimicrobial and antibiofilm activities against both Gram-positive and Gram-negative bacterial strains. Their cytotoxic potential against two cancer cell lines was also determined. Gram-positive bacteria were susceptible to the action of these compounds. Derivatives 1b and 1d inhibited S. aureus’s growth (MIC from 0.014 mg/mL) and biofilm (IC from 0.029 mg/mL), while compound 1e was active against E. faecalis’s planktonic and sessile forms. Two compounds significantly reduced cell viability at 5 μg/mL after 24 h of exposure (1d—HT-29 colorectal adenocarcinoma cells, 1c—LN229 glioblastoma cells). A docking study revealed the increased binding affinities of these derivatives compared to sulfanilamide. Hence, these Schiff bases exhibited higher activity compared to their parent drug, with halogen groups playing a crucial role in both their antimicrobial and cytotoxic effects.

The severe acute respiratory syndrome–related coronavirus 2 (SARS-CoV-2) pandemic has advanced our understanding of the host–microbiome–virus interplay. Several studies in various geographical regions report that SARS-CoV-2 infection disrupts the intestinal microbiota, allowing pathogenic bacteria such as Enterobacteriaceae to thrive, and triggering more severe disease outcomes. Here, we profile the microbiota of 30 individuals, 15 healthy controls and 15 type 2 diabetes (T2D) patients, before and after coronavirus disease 2019 (COVID-19). Despite similar viral loads in both patients and controls, SARS-CoV-2 infection led to exacerbated microbiome changes in T2D patients, characterized by higher levels of Enterobacteriaceae, loss of butyrate producers and an enrichment in fungi such as Candida spp. and Aspergillus spp. Several members of the microbiota were associated with more severe clinical and inflammatory (IL-8 and IL-17) parameters. Future studies to delineate the connection between cytokine release and microbiota disturbances will enhance our understanding of whether these microbial shifts directly impact the cytokine storm in COVID-19 patients or whether they are consecutive to the critical disease.

The gut microbiome is a dynamic ecosystem that plays essential roles in host metabolism, immune regulation, colonization resistance, and maintenance of intestinal homeostasis. Antibiotic exposure profoundly disrupts this ecosystem by reducing microbial diversity, depleting beneficial commensals, reshaping microbial metabolic functions, and remodeling the gut resistome through the selection and dissemination of antibiotic resistance genes (ARGs). Increasing evidence from longitudinal metagenomic, multi-omics, and experimental studies indicates that these perturbations may persist long after antibiotic withdrawal due to incomplete ecological recovery, sustained mobile genetic element-mediated ARG dissemination, and altered microbiome resilience. Beyond antimicrobial resistance, antibiotic-induced dysbiosis has been associated with reduced short-chain fatty acid production, altered bile acid metabolism, impaired epithelial barrier function, and broader disturbances in host metabolic homeostasis, although many of these relationships remain associative rather than causal. This review provides an integrated overview of antibiotic-driven gut microbiome dysbiosis, emphasizing the ecological, functional, metabolic, and resistome-level consequences of antibiotic exposure together with the mechanisms governing microbiome recovery. Current microbiome-targeted restoration strategies, including probiotics, phage therapy, fecal microbiota transplantation, and next-generation microbiome therapeutics, are critically evaluated with particular attention to their evidence maturity, limitations, and translational potential. Finally, key knowledge gaps and future research priorities are discussed to support the development of more effective microbiome-preserving antimicrobial strategies and to limit the long-term dissemination of antimicrobial resistance.