Disruption of the gut-microbiome-brain axis contributes to the development of chronic inflammation, impaired intestinal barrier integrity, and progressive tissue damage, ultimately reducing quality of life and increasing risk of comorbidities, including neurodegenerative diseases. Current therapies are often limited by adverse effects and insufficient long-term efficacy, highlighting the need for more comprehensive therapeutic approaches. Berberine (BRB), a plant-derived isoquinoline alkaloid, has attracted growing attention due to its pleiotropic immunomodulatory, neuroprotective, and gut-homeostasis-modulating properties, which involve reshaping the gut microbiota and underscore its therapeutic relevance within the gut–microbiome–brain axis. The aim of this review is to synthesize current scientific evidence regarding the anti-inflammatory mechanisms of BRB in inflammatory bowel disease (IBD). We compare its activity with first-line therapies and discuss its impact on microbial composition, including the bidirectional regulation of specific bacterial taxa relevant to intestinal and systemic disorders that originate in the gut. Furthermore, we emphasize that gut bacteria convert BRB into bioactive metabolites, contributing to its enhanced intraluminal activity despite its low systemic bioavailability. By integrating molecular and microbiological evidence, this review fills a critical knowledge gap regarding the comprehensive therapeutic potential of BRB as a promising candidate for future IBD interventions. The novelty of this work lies in unifying fragmented findings into a framework that explains how BRB acts simultaneously at the levels of host immunity, microbial ecology, and neuroimmune communication—thus offering a new conceptual model for its role within the gut–microbiome–brain axis.

Pertussis is an infectious disease that contributes to hundreds of thousands of deaths worldwide each year. Despite the prevalence of preventive vaccination programs, there has been an increasing number of new cases of the disease over the past few decades. This poses a particular problem for the pediatric population among whom the highest mortality from the disease is recorded. Several reasons for this phenomenon can be mentioned, but what is particularly important from the microbiological point of view is the correlation of the increased number of pertussis cases with the introduction of a new form of vaccine—the acellular vaccine in place of the whole-cell vaccine. In this review, we summarized the current state of knowledge on potential factors that may contribute to the decline in immunization efficacy against the pathogen. The post-vaccination response profile, symptomatic of vaccination with vaccination-acellular, is characterized by recruitment of Th₂ and Th₁₇ lymphocytes; it has been reported that in the long term, this results in insufficient activation of B cells and low titers of antibodies to key bacterial antigens (hemagglutinin, pertactin). Moreover, the immune response proceeds by bypassing the recruitment of tissue-resident memory T cells, resulting in a lack of protection against colonization of the nasal cavity by the bacterium despite vaccination. The decline in vaccination efficacy should also be attributed to the phenotypic variability of Bordetella. The popularization of the PtxP3 strain, characterized by its ability to incompletely activate immune mechanisms, poses a real threat to public health. The growing resistance of B. pertussis to standardly used antibiotics including macrolides also remains a problem. This makes it difficult to eradicate pathogens from the nasal cavity area and increases the pool of bacterial carriers in the population area. The increasing prevalence of the disease prompts reflection on more effective methods of prevention. Particularly promising in this field seem to be new vaccines, especially mucosally implemented, e.g., intranasal, or developed on the basis of B. pertussis antigens other than those used so far.

Biofilm-associated infections pose a significant clinical challenge due to their increased antibiotic tolerance and strong association with multidrug-resistant pathogens. The biofilm protects bacteria against antimicrobial agents and host immune response through a complex matrix, altered cell metabolism, activation of quorum sensing, and overexpression of efflux pumps. Despite the availability of numerous therapeutic strategies, the effectiveness of treatment of these infections remains limited, justifying the search for new pharmaceutics, e.g., compounds of natural origin. Berberine, an isoquinoline alkaloid from the plants of the Berberidaceae family, is of growing interest due to its broad spectrum of antimicrobial and antibiofilm activities. This review summarizes the current state of knowledge regarding the molecular mechanisms of action of berberine against the biofilm forming Gram-(+) and Gram-(−) bacteria. Its effect on bacterial cell adhesion, modulation of quorum sensing, inhibition of extracellular matrix synthesis, disruption of biofilm maturation, and the dispersion process are discussed. The role of berberine as an adjuvant to antibiotic therapy was also analyzed, in particular, its ability to restore bacterial sensitivity to different classes of antibiotics. The pharmacokinetic limitations of berberine and the prospects for the use of modern delivery systems are also considered. The collected data indicate that berberine is a promising factor supporting the treatment of biofilm-related infections.

Chronic inflammation and the associated dysbiosis of the gut microbiota are increasingly recognized as key factors contributing to the development of inflammatory bowel disease (IBD) and colorectal cancer (CRC). The diet–gut microbiota–immune system–cancer axis is considered a key regulator of these processes. Among the bioactive compounds found in the diet, ellagitannins have garnered significant scientific interest due to their conversion by the gut microbiota into biologically active metabolites known as urolithins. Urolithin A (UroA), one of the best characterized compounds, exhibits broad anti-inflammatory, antioxidant, immunomodulatory, and anticancer properties. It modulates signaling pathways associated with inflammation, oxidative stress, mitochondrial dysfunction, and cell proliferation. Furthermore, UroA has been shown to improve intestinal barrier integrity, regulate immune cell activity, and induce mitophagy, thereby contributing to the restoration of mitochondrial and cellular homeostasis. A growing body of evidence also suggests that UroA may inhibit cancer cell proliferation, induce apoptosis, and disrupt the molecular pathways involved in colorectal carcinogenesis. This review summarizes the current state of knowledge regarding the biosynthesis and bioavailability of UroA, its molecular mechanisms of action in IBD, and its potential role in the prevention and treatment of CRC. Furthermore, the limitations of UroA-based therapies and future research directions are discussed. Although further, well-designed clinical trials are necessary, current findings suggest that UroA may represent a promising microflora-targeted therapeutic strategy in chronic inflammatory and CRC diseases.

Chronic rhinosinusitis (CRS) has traditionally been viewed as a chronic inflammatory disease in which microbial factors are implicated. However, increasing evidence suggests that CRS may be better understood as a disruption of sinonasal microbial homeostasis rather than as a chronic infection caused by a single pathogen. This review summarizes current knowledge on healthy sinonasal microbiome composition and function as well as microbial alterations in CRS. Particular attention is given to dysbiosis involving potentially pathogenic microorganisms, including Staphylococcus aureus and Pseudomonas aeruginosa, as well as biofilm formation and its interactions with the epithelial barrier and host immune response. We also discuss host-related, therapeutic, hormonal, and environmental factors that may contribute to microbial imbalance. Current evidence does not clearly establish whether dysbiosis is a cause or consequence of chronic inflammation. Based on the evidence synthesized here, we propose that CRS may be understood as a dynamic, bidirectional interaction between microbial imbalance and chronic inflammation, whereby microbial alterations may contribute to epithelial and immune dysregulation, while changes in the host environment influence the sinonasal ecosystem. By integrating these microbiological and host-related perspectives, this review provides a boarder framework for understanding CRS pathophysiology and guiding future research into individual patterns of sinonasal microbial homeostasis.