Current Clinical Microbiology Reports最新文献

Purpose of review: Colonization of the gastrointestinal (GI) tract with Candida albicans (CA), the most common human fungal pathogen, is the first step towards the development of invasive infection. Yet the fungal virulence factors and host factors that modulate CA GI colonization are still poorly understood. In this review, we will review emerging evidence of the importance of select CA genetic determinants and CA's interaction with the host that contribute to its successful adaptation as a pathobiont in the human GI tract.

Recent findings: Recent data reveal the importance of 1) CA genetic determinants; 2) host factors; and 3) environmental factors in modulating CA GI colonization in humans.

Summary: As evidence continues to grow supporting the notion that the GI tract and its resident microbiota are an integral part of the host immune system, it will be critical for studies to interrogate the interaction of CA with the host (including both the host innate and adaptive immune system as well as the endogenous gut microbiota) in order to dissect the mechanisms of CA pathogenesis and thus lay the foundation for novel therapeutic approaches to prevent and/or treat invasive fungal infections.

Purpose of review: Mucormycosis is an emerging opportunistic fungal infection whose causative agents are found within the Mucorales family. A recent increase in immunocompromised cohorts with solid organ transplants, diabetes mellitus, and other medical conditions have resulted in increased fungal infections including mucormycosis. Our current knowledge about Mucoralean fungi is in its infancy compared to other fungal pathogens, which may be due to lack of robust genetic tools for Mucorales. In this review we summarize recent advances in genetic tools to study the two most prevalent and genetically amenable Mucoralean fungi, Mucor circinelloides and Rhizopus delemar.

Recent findings: There have been advances made in the study of Mucorales family genetics. These findings include the construction of recyclable markers to manipulate the genome, as well as silencing vectors, and the adaptation of the CRISPR/Cas9 gene editing system.

Summary: We present how these genetic methods have been applied to understand basic biology, morphogenesis, pathogenesis, and host-pathogen interactions in the two Mucoralean fungi, M. circinelloides and R. delemar. With these advances in Mucorales the opportunity to further understand the pathogenesis of these organisms is opened.

Purpose of review: Despite the increasing number of clinical reports on immune reconstitution inflammatory syndrome (IRIS), mechanistic understanding of IRIS is still largely limited. The main focus of this review is to summarize animal studies, which were performed to better understand the cellular and molecular mechanisms underlying the pathology of IRIS.

Recent findings: Three IRIS animal models have been reported. They are Mycobacterial IRIS (M-IRIS), cryptococcal IRIS (C-IRIS) and Pneumocystis-IRIS. M-IRIS animal model suggested that, rather than lymphopenia itself, the failure to clear the pathogen by T cells results in excessive priming of the innate immune system. If this happens before T cell reconstitution, hosts likely suffer IRIS upon T cell reconstitution. Interestingly, T cells specific to self-antigens, not only pathogen-specific, could drive IRIS as well.

Summary: The mechanism to develop IRIS is quite complicated, including multiple layers of host immune responses; the innate immune system that detects pathogens and prime host immunity, and the adaptive immune system that is reconstituted but hyper-activated particularly through CD4⁺ T cells. Animal models of IRIS, although there are still small numbers of studies available, have already provided significant insights on the mechanistic understanding of IRIS.