No abstract available.
Child* ; Humans ; Rhinitis*

Chronic rhinosinusitis (CRS) is a multifactorial and heterogeneous disease, and variousfactors, such as inflammation, infection, fungus, and superantigens, have been proposed to play crucial roles in its pathogenesis. Recently, the dominant mechanismof CRS pathogenesis has shiftedfrom microbial infection and environmental factors to host susceptibility. Host susceptibility relies not only on adaptive immunity, but also on innate immunity, and there has recently been much research into innate immunity. Innate immunity is an evolutionally conserved immune system that recognizes microbial signature molecules via pattern recognition receptors and is a primary defense system that elicits inflammatory and bactericidal responses. Dysfunction of the host response to pathogens is suggested to be involved in pathogenesis of CRS and an irrelevant response of the host's innate immunity could cause a failure toeradicate the pathogens, thereby contributing to CRS pathogeneses. Among these innate immune systems, toll-like receptors and epithelial barrier functions have been studied extensively, and new players, such as innate lymphoid cells,have beensurfacing. Betterunderstanding of innate immunity couldhelp to investigateand treat this complex disease. In this review, toll-like receptors, epithelial barrier functions, and innate lymphoid cells,among many subjects related to innate immunity,will be discussed in terms of pathogenesis.
Adaptive Immunity ; Fungi ; Immune System ; Immunity, Innate* ; Inflammation ; Receptors, Pattern Recognition ; Superantigens ; Toll-Like Receptors

As society industrializes and develops, people become increasingly concerned about quality of life and sleep-related disorders. Sleep disordered breathing (SDB) includes obstructive sleep apnea (OSA) and upper airway resistance syndrome. Most of the patients that snore have OSA, and OSA can result in not only cardiovascular and neuro-cognitive diseases but also in severe morbidities and mortalities; therefore, its importance cannot be emphasized too strongly. The mechanism by which OSA induces such morbidities is related to sleep fragmentation and intermittent hypoxia, which result in sympathetic activation, endothelial dysfunction, and metabolic dysregulation. All of these conditions produce a humoral imbalance, a hypercoagulable state, and atherosclerosis, which finally result in multi-morbidities. These comorbidities include cardiovascular, respiratory, neurologic, metabolic, and genitourinary disorders. The clinical relevance of OSA is mainly due to its strong association with morbidities such as hypertension, metabolic syndrome, diabetes, heart failure, coronary artery disease, arrhythmias, stroke, pulmonary hypertension, and neurocognitive and mood disorders. A high mortality rate has also been associated with OSA. It is important to acknowledge the comorbidities of OSA to achieve a better understanding of the disease and for better treatment of patients with OSA. In this review, the comorbidities of OSA will be discussed in detail.
Airway Resistance ; Anoxia ; Arrhythmias, Cardiac ; Atherosclerosis ; Comorbidity ; Coronary Artery Disease ; Heart Failure ; Humans ; Hypertension ; Hypertension, Pulmonary ; Mood Disorders ; Mortality ; Quality of Life ; Sleep Apnea Syndromes ; Sleep Apnea, Obstructive* ; Sleep Deprivation ; Stroke

Allergic rhinitis is a one of the most prevalent disease and its prevalence has been increasing these days. Many researchers have used the mouse models to study the mechanism of allergic rhinitis and development of anti-allergic medications. In the fields of allergic disease, several models such as allergic asthma, allergic contact dermatitis, and allergic rhinitis etc are introduced and several modifications are used. In case of mouse models of allergic rhinitis, it has been developed and modified from allergic asthma model. Most commonly used allergic rhinitis models are acute models and chronic models are used less. Ovalbumin, house dust mite and fungus are most commonly used allergens. Usually, mouse are sensitized with allergen and adjuvant such as aluminum hydroxide gel or Freund adjuvant for 2-3 weeks (once/week) then are challenged with allergen intranasally every day for 1 week. Mouse are sacrificed within 24 hours after final challenge and several parameters of allergic rhinitis are evaluated. They include nasal rubbing and sneezing count, eosinophil count in the nasal mucosa, total and allergen specific immunoglobulin E, nasal cytokine level and splenic cytokine level by splenocyte culture. By revealing those parameters, researchers could identify the allergic status of the mouse. However, there are many variables in mouse model of allergic rhinitis such as mouse strain, type of allergen, sensitization time, adjuvant, acute or chronic type, and allergen administration route etc. In this review, several variables and protocols of mouse model of AR will be discussed in detail.
Allergens ; Aluminum Hydroxide ; Animals ; Asthma ; Dermatitis, Allergic Contact ; Eosinophils ; Freund's Adjuvant ; Fungi ; Immunoglobulin E ; Immunoglobulins ; Mice* ; Nasal Mucosa ; Ovalbumin ; Prevalence ; Pyroglyphidae ; Rhinitis* ; Sneezing

No abstract available.
Otorhinolaryngologic Diseases ; Particulate Matter

No abstract available.
Hormone Replacement Therapy ; Humans ; Incheon* ; Osteoporosis* ; Physicians, Primary Care* ; Primary Health Care*

Recently, air pollution has become more and more severe globally and has decreased the quality of life significantly in subjects with or without allergic diseases. Air pollution more severely affects patients with allergic diseases, including allergic rhinitis (AR); therefore, it could devastate quality of life. Many epidemiological studies have shown that air pollutants increased outpatient clinic visits as well as the prevalence/severity of AR and decreased quality of life in patients with AR. Traffic-related air pollution also increases the severity and occurrence rate of AR, and heavy traffic is also associated with an increased prevalence of AR. Immunologically, air pollutants increase airway inflammation and mucin production by triggering the generation of reactive oxygen species and inducing the nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome and apoptosis. Since air pollution affects both the upper and lower airways and is known to be a risk factor for AR, proper diagnosis and treatment should be applied. In this review article, we will address several epidemiological and clinical studies about the effects of air pollution on AR, mechanisms by which air pollutants aggravate AR, and treatment of AR triggered by air pollutant.

The novel SARS-CoV-2 virus that causes COVID-19 has emerged rapidly and the virus has caused a global pandemic since it was first diagnosed in December 2019. SARS-CoV-2 is the seventh virus associated with human transmission among corona viruses. Otorhinolaryngologists could be vulnerable to this viral transmission due to the high viral load in the nasal cavity and nasopharynx. Hence, it is essential to understand the novel COVID-19 from the perspective of otorhinolaryngologists. We provide literature reviews of previous human coronaviruses and the novel COVID-19 with clinical hallmarks, diagnostic approaches, and possible treatment options. Further study is necessary to elucidate viral features and standardize treatment protocols with curable anti-viral agents and vaccines.

No abstract available.
Cell Differentiation