Zhonghua Qi

Irritable bowel syndrome is a disorder of gut–brain interaction characterized by recurrent abdominal pain and altered bowel habits. Interactions among intestinal microorganisms and their metabolites, the epithelial barrier, mucosal immunity, and gut–brain signaling provide important insights into the heterogeneity of this condition. Engineered micro- and nanoscale carriers may improve the stability of orally administered bioactive agents and facilitate local intestinal delivery while modulating relevant pathological processes through protection of viable microorganisms, delivery of microbial metabolites, or direct regulation of host cells. This review examines major mechanisms underlying microbiota–immune interactions and summarizes advances in colon-targeted delivery, protective carriers for probiotics, plant-derived vesicle-like preparations, and microalgae-based hybrid systems. We further discuss the biological characteristics of different clinical subtypes and key translational challenges, including safety, quality control, and rigorous verification of therapeutic efficacy. In particular, evidence from direct irritable bowel syndrome studies is distinguished from findings in symptom-based models, other disease models, and fundamental mechanistic experiments.

Osteoporosis, a prevalent metabolic bone disorder characterized by reduced bone mass and compromised bone strength, poses a substantial socioeconomic burden worldwide due to its staggering global incidence. Individuals afflicted with osteoporosis face an elevated risk of debilitating fractures, leading to compromised quality of life, disability, and increased mortality. The gut-bone axis, the intricate bidirectional communication between the gut microbiome and skeletal system, has recently emerged as a focal area in bone health research. Accumulating evidence suggests that gut homeostasis, the delicate balance of gut microbial communities, modulates bone metabolism through diverse mechanisms, potentially driving the pathogenesis of osteoporosis. Conversely, gut dysbiosis, the disruption of this equilibrium, may directly or indirectly perturb bone homeostasis, contributing to the onset and progression of osteoporosis. Elucidating the regulatory interplay between gut homeostasis and bone metabolism in the context of osteoporosis holds promising potential for developing novel preventive and therapeutic strategies, bearing profound theoretical and clinical implications.

Pancreatic cancer is a highly invasive and heterogeneous malignancy, with its incidence witnessed a global escalation in recent years. This tumor type is typically asymptomatic in its early stages, and the anatomical location of the pancreas renders it obscured, frequently leading to late detection. Its highly invasive growth pattern can readily invade surrounding tissues and organs, and pancreatic cancer exhibits poor sensitivity to radiotherapy and chemotherapy. Surgical resection remains the primary treatment modality, but due to delayed diagnosis, most patients lose the opportunity for curative resection. Pancreatic cancer is one of the most challenging malignancies, with a grave prognosis, and its incidence and mortality rates continue to rise annually. In recent years, the interplay between intestinal homeostasis and pancreatic cancer development has emerged as a burgeoning area of research. Intestinal homeostasis is a dynamic equilibrium state formed by the intricate interplay between the intestinal barrier and the intestinal environment (including intestinal microbiota). Further elucidating intestinal homeostasis and its association with pancreatic cancer pathogenesis will aid in exploring novel therapeutic strategies to combat this devastating disease.