Antibiotic treatment duration in critically ill patients has undergone major reevaluation. Historically concerns for short therapy included a lower cure rate and emergence of resistance, whereas prolonged courses raised risks of microbiome disruption, superinfection, Clostridioides difficile colitis, and resistance. Defining optimal duration of therapy in sepsis and severe infections remains challenging due to heterogeneity in host immunity, pathogen virulence, infection site and source control. Mechanistic insights from microbiology and PK/PD highlight how bacterial inoculum, biofilms, mutant selection windows and altered drug distribution in critical illness influence bacterial clearance and resistance selection. Experimental models and PK-optimized dosing strategies underscore the potential to shorten therapy by accelerating pathogen eradication. Across a range of serious infections, randomized trials consistently show that short course therapy (<7 days) is noninferior to longer courses, including bacteremia, intra-abdominal infections and ventilator-associated pneumonia. Biomarker guided strategies-particularly procalcitonin-based algorithms-might further individualize duration of therapy and safely reduce exposure. Uncertainty remains for S. aureus bacteremia, infections caused by non-fermenting Gram-negative bacilli, difficult to treat multidrug-resistant organisms, invasive candidiasis and immunocompromised patients. Robust evidence supports markedly reduced duration of therapy for uncomplicated bloodstream infections after effective source control, intra-abdominal infections and ventilator-associated pneumonia. Infections involving retained prosthetic material or devices often require prolonged therapy or long-term suppressive regimens. Future research must include adequately powered trials across diverse populations, and evaluate rapid diagnostics, host-response profiling, and individualized response-guided strategies. Optimizing antibiotic duration in critically ill patients ultimately requires integrating mechanistic understanding, individual clinical evolution, and stewardship principles to balance potential efficacy and potential harm.

Inflammatory bowel disease is a significant health concern not only in humans but also in companion animals and livestock, where it manifests as chronic diarrhoea, abdominal pain, and mucosal injury. Probiotics have gained increasing attention as potential therapeutic agents due to their immunomodulatory effects and ability to restore intestinal homeostasis. This study investigated the therapeutic efficacy of Bacillus coagulans and Lactobacillus acidophilus in an acetic acid-induced ulcerative colitis model in Wistar rats. Forty male rats were randomly assigned to control, colitis, mesalazine, B. coagulans, and L. acidophilus treatment groups. Disease severity was evaluated by macroscopic and histopathological scoring, colon length and weight, pro-inflammatory cytokine levels (IL-1β, IL-17), and inflammasome-associated gene expression (NLRP3, Caspase-1, IL-18, TNF-α). The results showed that colitis induction significantly increased pro-inflammatory cytokine expression and histological damage compared with controls. Both probiotics markedly reduced inflammatory markers, improved colon morphology, and attenuated inflammasome activation. Their protective effects were comparable to mesalazine, the standard treatment. These findings suggest that B. coagulans and L. acidophilus can serve as effective adjunct therapies for ulcerative colitis in veterinary practice, with potential translational applications for companion animals and livestock.

Background: The incidence of ulcerative colitis (UC) continues to rise, and food-derived bioactive peptides have attracted increasing attention as potential nutritional interventions for intestinal inflammation. This study investigated the preventive effects of the adzuki bean-derived peptide IFNNDPNNHP (IP10 peptide) on dextran sulfate sodium (DSS)-induced acute colitis in mice and explored the involvement of the gut microbiota. Methods: Mice received prophylactic IP10 peptide at 100 or 200 mg·kg[-1]. Colitis severity was assessed based on body weight, disease activity index, colon length, histopathology, and inflammatory cytokine levels. Gut microbiota composition was analyzed by 16S rRNA gene sequencing, and fecal short-chain fatty acid (SCFA) levels were quantified. Antibiotic-mediated microbiota depletion and fecal microbiota transplantation (FMT) were used to further evaluate the role of the gut microbiota. Results: Prophylactic IP10 peptide administration attenuated DSS-induced colitis, with the 200 mg·kg[-1] dose more effectively attenuating body weight loss and colon shortening, reducing disease activity index scores, and modulating inflammatory cytokine levels. IP10 peptide increased microbial richness and diversity, decreased the relative abundance of Escherichia-Shigella, and increased the relative abundances of SCFA-associated taxa, including norank_f__Muribaculaceae and Lachnospiraceae_NK4A136_group. It also increased fecal SCFA levels, particularly acetate and butyrate; the high dose additionally restored propionate and valerate. When the gut microbiota was depleted using antibiotics, the protective effects of the IP10 peptide were no longer detectable, whereas FMT using fecal microbiota from donors receiving the high dose of IP10 peptide attenuated colitis and increased fecal SCFA levels in recipient mice. Conclusions: IP10 peptide alleviates DSS-induced acute colitis, and this effect may be partly associated with alterations in the gut microbiota, including the enrichment of SCFA-associated taxa and increased fecal SCFA levels. These findings support its potential as a functional food ingredient for intestinal health.

Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea and pseudomembranous colitis and remains one of the most common healthcare-associated infections. Clostridioides difficile sequence types 1 and 11 (ST1 and ST11), which belong to multilocus sequence typing (MLST) clades 2 and 5, respectively, are widely recognized as epidemic-associated lineages. Both lineages harbor virulence-associated genetic features, including truncating variants in tcdC and carriage of the binary toxin locus (CdtLoc). ST37 (clade 4) has been an epidemic lineage in East Asia, whereas ST17 (clade 1) has been reported as a predominant lineage in the Republic of Korea and Japan. We performed short-read whole-genome sequencing (WGS) on 61 clinical isolates collected at a university-affiliated hospital in the Republic of Korea between February 2016 and April 2019. Long-read sequencing was additionally performed for 24 isolates, generating complete genomes by hybrid assembly. ST17 was the most prevalent sequence type (n = 16, 26.2%), followed by ST1 (n = 10, 16.4%). ST1 and ST11 isolates harbored the genetic features reported for these lineages, including truncating variants in tcdC. Genomic profiling further identified virulence-associated genes and antimicrobial resistance (AMR) determinants in diverse lineages. These findings characterize the genomic features of co-circulating C. difficile lineages and reveal the local presence of epidemic-associated strains.

Crohn's disease (CD) is a subtype of inflammatory bowel disease characterized by discontinuous lesions and transmural inflammation. Delayed diagnosis may lead to fistula formation between the intestine and adjacent organs. However, most CD-associated fistulas are enteroenteric or perianal, and abdominal wall abscesses are rarely reported in pediatric patients. We report a case of CD presenting as an abdominal wall abscess in a 15-year-old girl with autism spectrum disorder. Contrast-enhanced computed tomography revealed a fistulous communication between the abscess cavity and the transverse colon. Percutaneous drainage and antibiotic therapy were performed to control the infection. Colonoscopy demonstrated skip lesions with longitudinal ulcers, cobblestone-like mucosa, and inflammatory polyps. Histopathological examination showed active chronic colitis compatible with inflammatory bowel disease. Remission induction therapy consisting of elemental diet, 5-aminosalicylic acid, and corticosteroids was initiated after infection control. Her clinical condition gradually improved, and she was discharged on hospital Day 37. During follow-up, her appetite improved and she gradually gained weight. At 18 months after discharge, contrast-enhanced computed tomography showed no recurrence of the abdominal wall fistula, and her clinical condition remained stable. In pediatric patients, CD may present with nonspecific systemic symptoms, which can delay diagnosis. In patients with autism spectrum disorder, communication difficulties may further obscure gastrointestinal symptoms. Clinicians should consider underlying inflammatory bowel disease when children present with unexplained abdominal wall abscesses accompanied by systemic symptoms such as growth failure or malnutrition.

Ulcerative colitis (UC) involves epithelial injury, gut microbial dysbiosis, disturbed microbial metabolism, and mucosal inflammation. This study evaluated the protective effect of Schisandra chinensis (SC) against dextran sulfate sodium (DSS)-induced UC and investigated the underlying microbiota-metabolite-host signaling mechanism. UPLC-Q-TOF-MS/MS identified 38 constituents in SC, predominantly lignans, organic and phenolic acids, and terpenoids. SC reduced body weight loss, disease activity, colon shortening, mucosal and histological injury, and pro-inflammatory cytokine levels, while partially restoring claudin-1 and occludin expression. Metagenomic analysis showed that SC restructured the DSS-disrupted microbiota, enriched Parabacteroides goldsteinii, and increased the predicted abundance of pathways related to valine, leucine, and isoleucine degradation. Untargeted metabolomics and targeted fatty acid analysis showed lower fecal leucine and higher isovalerate levels after SC treatment. Whole-colon transcriptomic and western blot analyses further demonstrated that SC suppressed the mTOR/HIF-1α/STAT3/IL-17 inflammatory program in colonic tissue. Antibiotic pretreatment weakened several protective effects of SC, whereas P. goldsteinii or sodium isovalerate administration partially recapitulated its anti-inflammatory and barrier-restorative effects. Conversely, the mTOR activator MHY1485 attenuated SC-mediated protection. These findings indicate that the protective effects of SC are associated with remodeling of a P. goldsteinii-related leucine-isovalerate metabolic network and attenuation of colonic mTOR/HIF-1α/STAT3/IL-17 signaling. This study provides a microbiota-centered mechanistic basis for the therapeutic potential of SC in UC.

Clostridioides difficile infection (CDI) remains a major cause of antibiotic-associated diarrhea and colitis, with a high rate of recurrence. Current CDI treatments rely largely on antibiotics that perpetuate dysbiosis or on microbiota-based interventions with limited accessibility, emphasizing the need to explore novel, targeted microbiota-derived therapies. Probiotics have emerged as a potential approach for the prevention and management of CDI, owing to their capacity to modulate the gut microbiota and host immune responses. Among them, bifidobacteria are prominent commensal anaerobes of the human gut with well-documented health-promoting properties. Although their role in CDI has been less extensively explored than that of other probiotic microorganisms, accumulating evidence suggests that bifidobacteria may exert both direct antagonistic effects against C. difficile and indirect benefits through the restoration of eubiosis and attenuation of inflammation. This review summarizes recent in vitro, in vivo, and clinical studies investigating the effects of bifidobacteria in the context of CDI. We discuss mechanisms including inhibition of C. difficile growth and toxin activity, modulation of host inflammatory responses, and interactions with the intestinal microbiota. Particular attention is given to studies published over the past decade. Overall, bifidobacteria emerge as promising candidates for future probiotic or microbiota-based interventions targeting CDI, although further well-designed clinical trials are needed to establish their efficacy and optimal modes of use.

Human health is influenced by various factors, including bacteria that surround us ubiquitously. Bacteria constituting normal microbiota of various human body niches, primarily the gut, can confer beneficial effects by aiding food digestion, improving nutrient production, and preventing pathogen colonization. However, bacteria can also have harmful effects as pathogens, especially when the immune system is compromised due to various diseases. In particular, secondary or co-infections caused by pathogenic bacteria have been shown to significantly contribute to illness severity and increased mortality rates. Ginseng, an herb widely used for various medicinal purposes in Asia, including the treatment of cancer and immune-related diseases, has shown substantial effects in modulating the bacterial composition of the human body, including protecting human health against various pathogenic bacterial infections. Furthermore, recent studies have also demonstrated that ginseng can promote the restoration of disrupted gut microbiota composition, caused by various reasons such as intestinal inflammation, obesity, antibiotics-associated diarrhea, colitis and so on. Therefore, this review comprehensively discusses the effects of ginseng on pathogenic bacteria, as well as the recent findings on the impact of ginseng on gut microbiota imbalances caused by various factors.

Plant polysaccharides are functional carbohydrates with diverse structures and close interactions with the gut microbiota. Here, a low-molecular-weight neutral carbohydrate fraction, SMP-1, was isolated from Salvia miltiorrhiza and characterized for molecular weight, monosaccharide composition, linkage features, and selected NMR correlations. SMP-1 showed an apparent molecular weight of approximately 3.3 kDa. Complementary monosaccharide analyses indicated Gal, Glc, and Ara as the main detected sugars, with trace Fru. Methylation analysis mainly described the Galp/Glcp-rich portion and suggested abundant terminal Galp, 6-linked Galp, and 6-linked Glcp residues, whereas Fru-derived linkages were not resolved under the present methylation-GC-MS conditions. NMR analysis supported major Glcp/Galp spin systems and Fruf-containing residues, but a complete repeating-unit structure was not assigned. In a dextran sulfate sodium-induced colitis model, oral SMP-1 alleviated body weight loss, disease activity, colon shortening, and mucosal injury; restored mucus secretion and tight junction integrity; reduced pro-inflammatory cytokines; and suppressed TLR4/NF-κB signaling. SMP-1 also partially restored microbial diversity and reshaped DSS-disrupted gut microbial composition, while antibiotic-mediated microbiota depletion weakened its protective effects. These findings suggest that SMP-1 improves colitis-associated intestinal dysfunction through regulation of gut microbiota, epithelial barrier integrity, and inflammatory responses.