During the course of an infection, a sinusitis sufferer’s nasal mucosa becomes inflamed, resulting in mucus backup. This inflammation blocks the normal drainage of mucus from the nose and sinuses, and can also affect the sinuses’ ability to drain. Symptoms can include a foul taste in the mouth, pain in the face and throat, and congestion.후비루치료
Chronic rhinosinusitis (CRS) is a common health condition that affects approximately 31 million people in the United States each year. Although the etiology of CRS remains unclear, its pathophysiology is thought to be multi-factorial. In addition to the immune response, environmental factors, such as pollution, may play an important role in the development of CRS.
Recent research has revealed an active role for airway immunity in CRS. The mucus blanket of the sinonasal epithelium plays a critical role in the defense against inhaled particulates. In addition to being a passive mechanical barrier, the epithelium is a complex system of immune pathways that interacts with the host to suppress infectious threats. This relationship has been characterized by multiple innate pathways, such as b-defensin expression, which increases the production of innate immune effectors. This process is initiated by the poly(I:C) complex, which also promotes the expression of matrix metalloproteinase.
A defect in innate immunity has been implicated in the development of chronic inflammation. IL-4 and IL-13 downregulate multiple antimicrobial innate immune markers in vitro. It has been suggested that viral proteins, such as adenovirus, may stimulate secretion of these antimicrobials. This idea is supported by data from a study of bronchial lavage fluid from patients with COPD. The authors found that inflammatory markers increased after a 10-day period following onset of symptoms. During an exacerbation of the disease, the levels of these markers rose further.
The innate and adaptive immune systems work cooperatively to prevent and eradicate infectious threats from the sinuses. Inflammation in CRS results from abnormal mucosal immune function, which disrupts homeostasis. The inflammatory responses are triggered by a combination of host and environmental factors, including viruses and bacteria. In addition to the innate immune system, the adaptive immune system provides a second line of defense, which aims to block the influx of microbial material and to control the inflammatory response. This interaction between the innate and adaptive immune systems is bidirectional, with the innate immune pathway driving a Th2-biased inflammatory response and the adaptive immune system regulating Th1 and Th17 cytokines. This is thought to contribute to the pathogenesis of CRSwNP.
In addition to these innate immune mechanisms, the epithelium also functions as a host’s first line of defense against inhaled particulates. This function is facilitated by the presence of the mucus blanket, which helps to entrap and retain foreign materials. A deviated nasal septum or other medical conditions may cause nasal blockage, resulting in inflammation. In recalcitrant forms, the disease may be associated with eosinophilic asthma. Regulatory T cells, known as Tregs, are essential in controlling mucosal immune responses. In addition to suppressing the Th2 inflammatory response, Tregs can modulate the innate and adaptive immune pathways in the epithelium.라경찬한의원