Allergic rhinitis

Summary

Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. Signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes. The fluid from the nose is usually clear. Symptom onset is often within minutes following allergen exposure, and can affect sleep and the ability to work or study. Some people may develop symptoms only during specific times of the year, often as a result of pollen exposure. Many people with allergic rhinitis also have asthma, allergic conjunctivitis, or atopic dermatitis. Allergic rhinitis is typically triggered by environmental allergens such as pollen, pet hair, dust, or mold. Inherited genetics and environmental exposures contribute to the development of allergies. Growing up on a farm and having multiple siblings decreases this risk. The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. It causes mucous membranes in the nose, eyes and throat to become inflamed and itchy as they work to eject the allergen. Diagnosis is typically based on a combination of symptoms and a skin prick test or blood tests for allergen-specific IgE antibodies. These tests, however, can give false positives. The symptoms of allergies resemble those of the common cold; however, they often last for more than two weeks and, despite the common name, typically do not include a fever. Exposure to animals early in life might reduce the risk of developing these specific allergies. Several different types of medications reduce allergic symptoms, including nasal steroids, antihistamines, such as diphenhydramine, cromolyn sodium, and leukotriene receptor antagonists such as montelukast. Oftentimes, medications do not completely control symptoms, and they may also have side effects.

Official source

https://en.wikipedia.org/wiki/Allergic_rhinitis

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Related publications (2)

Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis

Eva Sabrina Gollwitzer, Nicola Harris, Benjamin John Marsland

Metabolites from intestinal microbiota are key determinants of host-microbe mutualism and, consequently, the health or disease of the intestinal tract. However, whether such host-microbe crosstalk influences inflammation in peripheral tissues, such as the lung, is poorly understood. We found that dietary fermentable fiber content changed the composition of the gut and lung microbiota, in particular by altering the ratio of Firmicutes to Bacteroidetes. The gut microbiota metabolized the fiber, consequently increasing the concentration of circulating short-chain fatty acids (SCFAs). Mice fed a high-fiber diet had increased circulating levels of SCFAs and were protected against allergic inflammation in the lung, whereas a low-fiber diet decreased levels of SCFAs and increased allergic airway disease. Treatment of mice with the SCFA propionate led to alterations in bone marrow hematopoiesis that were characterized by enhanced generation of macrophage and dendritic cell (DC) precursors and subsequent seeding of the lungs by DCs with high phagocytic capacity but an impaired ability to promote T helper type 2 (TH2) cell effector function. The effects of propionate on allergic inflammation were dependent on G protein-coupled receptor 41 (GPR41, also called free fatty acid receptor 3 or FFAR3), but not GPR43 (also called free fatty acid receptor 2 or FFAR2). Our results show that dietary fermentable fiber and SCFAs can shape the immunological environment in the lung and influence the severity of allergic inflammation.

Nature Publishing Group2014

Dysregulation of Allergic Airway Inflammation in the Absence of Microbial Colonization

Nicola Harris, Benjamin John Marsland, Tina Herbst

RATIONALE: The incidence of allergic disorders is increasing in developed countries and has been associated with reduced exposure to microbes and alterations in the commensal bacterial flora. OBJECTIVES: To ascertain the relevance of commensal bacteria upon the development of an allergic response, we utilized a model of allergic airway inflammation in germ-free (GF) mice that lack any exposure to pathogenic or non-pathogenic microorganisms. METHODS: Allergic airway inflammation was induced in GF, specific pathogen free (SPF) or recolonized mice by sensitization and challenge with ovalbumin (OVA). The resulting cellular infiltrate and cytokine production were measured. MEASUREMENTS AND MAIN RESULTS: Our results show that the total number of infiltrating lymphocytes and eosinophils were elevated in the airways of allergic GF mice as compared to control SPF mice, and that this increase could be reversed by re-colonization of GF mice with the complex commensal flora of SPF mice. Exaggerated airway eosinophilia correlated with increased local production of Th2 associated cytokines, elevated IgE production and an altered number and phenotype of conventional dendritic cells (cDC). Regulatory T cell populations and regulatory cytokine levels were unaltered but GF mice exhibited an increased number of basophils and decreased numbers of alveolar macrophages (AM) and plasmacytoid dendritic cells (pDC). CONCLUSIONS: These data demonstrate that the presence of commensal bacteria is critical for ensuring normal cellular maturation, recruitment and control of allergic airway inflammation.

2011

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