The human microbiome, a complex ecosystem of microorganisms residing in and on the body, plays a pivotal role in the regulation of a wide range of physiological processes, including digestion, immune responses, and metabolic functions. In recent years, the rapidly growing field of microbiome-driven therapeutics has garnered significant attention owing to its potential to revolutionize healthcare. This review explores the evolving landscape of microbiome-based therapies, with a particular focus on the gut microbiome and its implications for both gut health and precision medicine. We highlight recent advances in understanding how microbial communities influence disease pathogenesis and treatment outcomes, spanning conditions such as inflammatory bowel disease (IBD), metabolic disorders, neurological diseases, and even cancer. This article also discusses emerging therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation (FMT), and microbial-based drugs, as well as the challenges associated with their clinical implementation. Additionally, we examined how the integration of microbiome profiling and metagenomic data is advancing the field of precision medicine, paving the way for personalized and effective treatments. This review serves as a comprehensive resource that synthesizes current knowledge, identifies key gaps in microbiome research, and offers insights into the future direction of microbiome-driven therapeutics, thus providing a valuable framework for clinicians, researchers, and policymakers seeking to harness the potential of microbiomes to advance personalized healthcare solutions.

Non-typhoidal Salmonella (NTS) infections in poultry, particularly in commercial-layer chickens, pose a critical risk to food safety and public health worldwide. NTS bacteria can remain undetected in poultry flocks, contaminating products and potentially leading to gastroenteritis in humans. This review examines pre-harvest control strategies for NTS in layer chickens, including biosecurity protocols, vaccinations, feed additives, genetic selection, and environmental management. These strategies have substantially reduced Salmonella colonization and product contamination rates in the commercial layer industry. By evaluating these strategies, this review highlights the importance of integrated control measures to limit NTS colonization, reduce antimicrobial resistance, and improve poultry health. This review aims to provide producers, researchers, and policymakers with insights into effective practices to minimize Salmonella contamination and enhance both animal and human health outcomes.

Tuberculosis caused by the obligate intracellular pathogen, Mycobacterium tuberculosis, is one among the prime causes of death worldwide. An urgent remedy against tuberculosis is of paramount importance in the current scenario. However, the complex nature of this appalling disease contributes to the limitations of existing medications. The quest for better treatment approaches is driving the research in the field of host epigenomics forward in context with tuberculosis. The interplay between various host epigenetic factors and the pathogen is under investigation. A comprehensive understanding of how Mycobacterium tuberculosis orchestrates such epigenetic factors and favors its survival within the host is in increasing demand. The modifications beneficial to the pathogen are reversible and possess the potential to be better targets for various therapeutic approaches. The mechanisms, including histone modifications, DNA methylation, and miRNA modification, are being explored for their impact on pathogenesis. In this article, we are deciphering the role of mycobacterial epigenetic regulators on various strategies like cytokine expression, macrophage polarization, autophagy, and apoptosis, along with a glimpse of the potential of host-directed therapies.

Shiga toxin-producing Escherichia coli (STEC) are notorious foodborne pathogens, capable of causing severe diarrhea and life-threatening complications in humans. Cattle, acting as both primary reservoirs and asymptomatic carriers of STEC, predominantly harbor the pathogen in their rectoanal junction (RAJ), facilitating its transmission to humans through contaminated food sources. Despite the central role of cattle in STEC transmission, the molecular mechanisms governing STEC’s adaptation in the RAJ of the asymptomatic reservoir host and its subsequent infection of human colonic epithelial cells, resulting in diarrhea, remain largely unexplored. This study aims to uncover these complicated dynamics by focusing on the STEC O157:H7 serotype within two distinct host environments, bovine RAJ cells and human colonic epithelial cells, during initial colonization. We employed comparative transcriptomics analysis to investigate differential gene expression profiles of STEC O157:H7 during interactions with these cell types. STEC O157:H7 was cultured either with bovine RAJ cells or the human colonic epithelial cell line CCD CoN 841 to simulate STEC-epithelial cell interactions within these two host species. High-throughput RNA sequencing revealed 829 and 1939 bacterial genes expressed in RAJ and CCD CoN 841, respectively. After gene filtering, 221 E. coli O157:H7 genes were upregulated during initial adherence to CCD CoN cells and 436 with RAJ cells. Furthermore, 22 genes were uniquely expressed with human cells and 155 genes with bovine cells. Our findings revealed distinct expression patterns of STEC O157:H7 genes involved in virulence, including adherence, metal iron homeostasis, and stress response during its initial adherence (i.e., six hours post-infection) to bovine RAJ cells, as opposed to human colonic epithelial cells. Additionally, the comparative analysis highlighted the potential role of some genes in host adaptation and tissue-specific pathogenicity. These findings shed new light on the potential mechanisms of STEC O157:H7 contributing to colonize the intestinal epithelium during the first six hours of infection, leading to survival and persistence in the bovine reservoir and causing disease in humans.