91桃色

Human microbiome; Fungal infections; Microbiota dysbiosis; Candidiasis; Aspergillosis; Cryptococcosis; Gut microbiome; Immune regulation; Probiotics; Antifungal resistance

Introduction

The human microbiome, a complex ecosystem of bacteria, viruses, fungi, and other microorganisms, plays a vital role in maintaining immune homeostasis and protecting against pathogenic infections [1]. Among its many functions, the microbiome helps regulate fungal colonization by limiting the overgrowth of opportunistic fungi such as Candida spp., Aspergillus spp., and Cryptococcus spp. However, disturbances in microbiome composition—caused by factors such as antibiotic use, immunosuppression, chronic disease, or dietary changes—can lead to dysbiosis, increasing susceptibility to fungal infections [2].

The gut, oral, and skin microbiomes are particularly influential in fungal disease susceptibility. Commensal bacteria such as Lactobacillus and Bifidobacterium produce antimicrobial compounds that inhibit fungal growth, while the immune system relies on microbial signals to distinguish between commensal and pathogenic fungi. When microbial diversity is reduced, fungi can proliferate unchecked, leading to infections such as candidiasis, aspergillosis, and cryptococcosis. The growing incidence of antifungal resistance further complicates treatment, highlighting the need for microbiome-targeted therapeutic strategies [3].

Understanding the intricate relationship between the microbiome and fungal pathogens is critical for developing innovative approaches to disease prevention and treatment. This paper explores the role of the human microbiome in fungal disease susceptibility, emphasizing the impact of microbiome dysbiosis, immune interactions, and potential microbiome-based therapies in managing fungal infections [4].

Discussion

The interplay between the human microbiome and fungal pathogens is a critical factor in determining susceptibility to fungal infections. The microbiome, particularly in the gut, oral cavity, and skin, plays a protective role by maintaining microbial balance and preventing the overgrowth of opportunistic fungi. Commensal bacteria such as Lactobacillus and Bifidobacterium contribute to fungal regulation by producing antimicrobial peptides and modulating immune responses [5]. However, disruptions in microbiome composition, known as dysbiosis, can weaken these protective mechanisms, creating an environment that favors fungal proliferation. Antibiotic overuse, immunosuppressive therapies, chronic diseases such as diabetes, and dietary changes have all been implicated in altering microbial communities, thereby increasing the risk of infections such as candidiasis, aspergillosis, and cryptococcosis [6].

The gut microbiome, in particular, exerts significant control over fungal populations. Studies suggest that a healthy gut microbiome maintains a delicate equilibrium between bacteria and fungi, preventing fungal overgrowth [7]. However, dysbiosis often triggered by prolonged antibiotic use can lead to excessive fungal colonization, increasing the risk of systemic infections. Similarly, the oral microbiome plays a vital role in preventing fungal infections such as oral candidiasis, as bacterial-fungal interactions help maintain a balanced microbial environment. In immunocompromised individuals, such as those undergoing chemotherapy or organ transplantation, microbiome disturbances can significantly enhance fungal virulence and resistance to antifungal treatments [8].

Emerging research suggests that microbiome-targeted therapies could serve as innovative strategies for preventing and managing fungal infections. Probiotics and prebiotics have shown promise in restoring microbial diversity and enhancing antifungal resistance, while fecal microbiota transplantation (FMT) has been explored as a potential intervention in severe dysbiosis-related infections. Additionally, manipulating microbial metabolites to suppress fungal growth represents a novel therapeutic avenue [9]. However, challenges remain in fully understanding the complex interactions between the microbiome and fungal pathogens, as well as optimizing microbiome-based interventions for clinical use. Overall, the relationship between the human microbiome and fungal disease susceptibility underscores the importance of maintaining microbial balance for infection prevention. Further research into microbiome-driven antifungal strategies is needed to develop effective, personalized approaches for individuals at high risk of fungal infections, particularly in the era of rising antifungal resistance [10].

Conclusion

The human microbiome plays a pivotal role in regulating fungal colonization and preventing opportunistic infections. A balanced microbiome, particularly in the gut, oral cavity, and skin, helps suppress fungal overgrowth through microbial competition, immune modulation, and the production of antimicrobial compounds. However, factors such as antibiotic overuse, immunosuppression, chronic diseases, and dietary changes can disrupt microbial homeostasis, leading to dysbiosis and increased susceptibility to fungal infections such as candidiasis, aspergillosis, and cryptococcosis. Understanding the intricate relationship between the microbiome and fungal pathogens is essential for developing new therapeutic strategies. Microbiome-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation (FMT), offer promising avenues for restoring microbial balance and reducing fungal disease risk. Despite these advancements, further research is needed to optimize these approaches and fully elucidate the mechanisms underlying microbiome-fungus interactions. As antifungal resistance continues to rise, integrating microbiome-based therapies into clinical practice could revolutionize the prevention and management of fungal infections. Future studies focusing on personalized microbiome modulation, microbial metabolite interactions, and novel antifungal strategies will be crucial in mitigating the global burden of fungal diseases and improving patient outcomes.

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