The interaction between the host and microorganisms in chronic rhinosinusitis (CRS) is poorly understood and is a growing area of interest. More recently, methodologies have been developed to assess the microbiome without the use of culture by analyzing the bacterial 16S ribosomal RNA gene. We reviewed the microbiome literature to better understand the role of microbes in CRS.
The development of culture-independent bacterial DNA sequencing techniques and integration into research practice has led to a burgeoning interest in the microbiome and its relevance to human health and disease. Introduction into the study of chronic rhinosinusitis in the past few years has shaped current thinking on the role of bacteria in the disease process.
Rich and diverse populations of bacteria inhabit the sinonasal cavity at all times. Decreased bacterial richness and diversity may be associated with disease state and outcomes.
Although there is much to be explored, the sinus microbiome appears to have potentially promising roles in many aspects of sinus health and disease.
Chronic rhinosinusitis (CRS) is an inflammatory disorder of the paranasal sinuses that is defined based on the presence of characteristic sinonasal symptoms such as nasal and extranasal symptoms for at least 12 weeks. CRSâ€associated symptoms are differentially associated with the downstream disease consequences of decreased quality of life (QOL) and decreased productivity. A wide range of hypotheses have been described with regard to the pathogenesis of CRS, with both environmental and innate host defense mechanisms implicated in the etiology of the disease. Local environmental and microbial factors within the paranasal sinuses that could drive or modulate the CRS disease process include presence of biofilms, Staphylococcal superantigens, fungi, and more recently, dysbiosis of the microbiome.
The concept of dysbiosis is a complex entity but has been defined as microbial imbalance, change in the microbiota, or misrecognition of normal microbiota that may contribute to disease. Dysbiosis has been implicated in various inflammatory diseases including CRS and respiratory disease as well as inflammatory bowel disease, rheumatoid arthritis, and psoriasis. Specifically, in the CRS population, colonization by pathogenic organisms, and resultant microbial imbalance have been cited as triggers of a dysfunctional and chronic immune response. On the other hand, dysbiosis may be a result of dysfunctional immune barriers and resultant inflammation that establish an environment amenable to overgrowth of pathogenic bacteria that then promote a state of dysbiosis.
Microbiology: Current Research