Risk factors of allergic rhinitis: genetic or environmental? PMID: PMC1661616
Symptoms of allergic rhinitis: rhinorrhea, nasal obstruction, nasal itching, and sneezing Caused by exposure to perennial or seasonal allergens both indoors and outdoors, including dust, molds and pollen IgE mediated immunological mechanisms that cause inflammation of tissue, the balance of Th1 to Th2 thought to be a key component Prevalence has increased in developed and industrialized countries Hygiene Hypothesis Increased atopic disease is inversely proportional to prevalence of communicable disease due to increased health and hygiene standards First suggested by Strachan: risk of developing allergies is inversely related to number of children in family, confirmed by studies that looked at number of older siblings, attendance in daycare, having had orofecal infections, contact with animals A Th1 response to a microbial infection can counter balance a Th2 response, by producing molecules that down regulate Th2 response, that leads to allergies Need to identify what helps protect from allergens and how to manipulate environment to provide that without harming individuals
The pathophysiology of the hygiene hypothesis. PMID: 23701898
A major underlying factor of the hygiene hypothesis is the differentiation of helper T cells into Th1 or Th2 Th1= work in immunological responses by inducing macrophages and producing inflammatory tissue Th2= induce atopy, production of IgE, mast cells that produce an allergic response Increased childhood infections result in a higher ratio if Th1, needed to combat infections and viruses Children in smaller families and less inflammatory conditions produce higher ratios of Th2 to Th1, leading to increased allergic response