Antibacterial resistance has become a challenging situation worldwide. The increasing emergence of multidrug-resistant pathogens stresses the need for developing alternative or complementary antimicrobial strategies, which has led the scientific community to study substances, formulas or active ingredients used before the antibiotic era. Honey has been traditionally used not only as a food, but also with therapeutic purposes, especially for the topical treatment of chronic-infected wounds. The intrinsic characteristics and the complex composition of honey, in which different substances with antimicrobial properties are included, make it an antimicrobial agent with multiple and different target sites in the fight against bacteria. This, together with the difficulty to develop honey-resistance, indicates that it could become an effective alternative in the treatment of antibiotic-resistant bacteria, against which honey has already shown to be effective. Despite all of these assets, honey possesses some limitations, and has to fulfill a number of requirements in order to be used for medical purposes.

Epidemiological and translational data increasingly implicate environmental pollutants in inflammatory bowel disease (IBD). Indeed, the global incidence of IBD has been rising, particularly in developing countries, in parallel with the increased use of chemicals and synthetic materials in daily life and escalating pollution levels. Recent nationwide and ecological studies have reported associations between agricultural pesticides and IBD, particularly Crohn’s disease. Exposure to other chemical categories has also been linked with an increased risk of IBD. To synthesise available data and identify knowledge gaps, we conducted a systematic review of human studies that reported on the impact of environmental pollutants on IBD risk and outcomes. Furthermore, we summarised in vitro data and animal studies investigating mechanisms underlying these associations. The 32 included human studies corroborate that heavy and transition metals, except zinc, air pollutants, per- and polyfluorinated substances, and pesticides are associated with an increased risk of IBD, with exposure to air pollutants being associated with disease-related adverse outcomes as well. The narrative review of preclinical studies suggests several overlapping mechanisms underlying these associations, including increased intestinal permeability, systemic inflammation and dysbiosis. A consolidated understanding of the impact of environmental exposures on IBD risk and outcomes is key to the identification of potentially modifiable risk factors and to inform strategies towards prediction, prevention and mitigation of IBD.

Background and objective: Probiotics show promise in inflammatory bowel disease (IBD), yet knowledge gaps persist. We performed an overview of systematic reviews and an updated metanalysis of randomized controlled trials (RCT) assessing the effect of probiotics on Crohn's disease (CD) and ulcerative colitis (UC). Methods: MEDLINE, Web of Science, and the Cochrane Central Register of Controlled Trials were searched up to September 2023. Primary outcomes were clinical remission and recurrence; secondary outcomes included endoscopic response and remission, and adverse events. We calculated odds ratios (OR) using a random‐effects model in R. The quality of systematic reviews was assessed using the AMSTAR‐2; the trials' risk of bias was evaluated using the Cochrane Collaboration tool. Evidence certainty was rated using the GRADE framework. Results: Out of 2613 results, 67 studies (22 systematic reviews and 45 RCTs) met the eligibility criteria. In the updated meta‐analysis, the OR for clinical remission in UC and CD was 2.00 (95% CI 1.28–3.11) and 1.61 (95% CI 0.21–12.50), respectively. The subgroup analysis suggested that combining 5‐ASA and probiotics may be beneficial for inducing remission in mild‐to‐moderate UC (OR 2.35, 95% CI 1.29–4.28). Probiotics decreased the odds of recurrence in relapsing pouchitis (OR 0.03, 95% CI 0.00–0.25) and trended toward reducing clinical recurrence in inactive UC (OR 0.65, 95% CI 0.42–1.01). No protective effect against recurrence was identified for CD. Multi‐strain formulations appear superior in achieving remission and preventing recurrence in UC. The use of probiotics was not associated with better endoscopic outcomes. Adverse events were similar to control. However, the overall certainty of evidence was low. Conclusion: Probiotics, particularly multi‐strain formulations, appear efficacious for the induction of clinical remission and the prevention of relapse in UC patients as well as for relapsing pouchitis. Notwithstanding, no significant effect was identified for CD. The favorable safety profile of probiotics was also highlighted.

Recently, the gut microbiome has become an important field of interest. Indeed, the microbiome has been associated to numerous drug interactions and it is thought to influence the efficacy of pharmacologic treatments. Although statins are widely prescribed medications, there remains considerable variability in its therapeutic response. In this context, we aimed to investigate how statins modulate the gut microbiome and, reversely, how can the microbiome influence the course of anti‐hypercholesterolemic treatment. We conducted a systematic review by searching four online databases, in accordance with PRISMA guidelines. Studies addressing gut microbiome changes following statin treatment and those assessing statins’ response and associating it with patients’ microbiome were included. Due to the limited number of results, we decided to include studies enrolling both humans and animals. We summarized information from three human and seven animal studies and aimed to assess the influence of gut microbiome composition on statin response (Outcome 1) and to evaluate the impact of statin treatment on the gut microbiome (Outcome 2). An association between a certain microbiome composition that promoted the lipid‐lowering effect of statins was found. However, what kind of microorganisms and how they can exert this effect remains uncertain. Furthermore, statins might have a role in the modulation of the gut microbiome, but then again, it is still unknown whether this change is directly caused by the drug or another metabolic mechanism. Even though gut microbiota may have several potential therapeutic implications, its use as a personalized predictive biomarker requires further studies.