Exposure and allergic sensitization to cockroach was associated with a significantly greater risk of asthma hospitalization and greater healthcare utilization among 476 children aged 4 to 9 years who participated in the National Cooperative Inner-City Asthma Study. Allergic sensitization to the mold Alternaria has been identified as a significant allergen in terms of increasing airway hyperresponsiveness and was associated with a nearly 200-fold increased risk of respiratory arrest due to asthma, emphasizing the importance of determining underlying allergic sensitivities in patients with asthma and providing patients with accurate and practical advice on allergen avoidance techniques. (more…)

A role for Leukotriene B4 in the induction of airway hyper-responsiveness was explored through the use of transgenic mice deficient in the BLT1 receptor for LTB4 . Ovalbumin challenge of sensitized wild-type mice resulted in the usual features of experimental asthma, including goblet cell hyperplasia, hyper-responsiveness to inhaled methacholine and elevated BAL fluid concentrations of the Th2 cytokine IL-13. In contrast, BLT1 –/– mice (i.e. genetically modified mice lacking the gene coding for the BLT1 receptor) exhibited significantly lower responses. BLT1 –/– mice also exhibited lower numbers of IL-13-positive T lymphocytes of both the helper (CD4 T Cells) and cytotoxic/suppressor (CD8 + ) types. (more…)

Current internationally recognized guidelines indicate that symptomatic asthmatics using a low to medium inhaled corticosteroid dose (400–800 µg/day of beclomethasone or equivalent) alone should preferentially be commenced on a long-acting agonist ß2 prior to an leukotriene receptor antagonists LTRA (British guideline on the management of asthma 2003; GINA Workshop Report 2004). However, two recent large trials have performed head to-head comparisons of add-on long-acting ß2 agonist versus LTRA as therapeutic adjuncts to inhaled corticosteroids, using exacerbation frequency (rather than lung function and symptoms) as the primary end point. (more…)

Negative family characteristics such as family conflict and family dysfunction discriminated children who died of asthma from children with equally severe asthma who did not die. Parenting difficulties have been associated with a higher risk for the development of asthma early in life. In addition, children with the highest risk of developing early-onset asthma were those in families with both parenting problems and high stress. Evidence for a asthma and stress link has been demonstrated through temporal studies, as experiencing an acute negative life event increased children’s risk for an asthma attack 4 to 6 weeks after the occurrence of the event. (more…)

Histamine is a low-molecular-weight monoamine that binds to four different G-protein-coupled receptors, and has recently been demonstrated to regulate several essential events in the immune response. The histamine receptor type 2 (HR2) is coupled to adenylate cyclase and studies in different species and several human cells have demonstrated that inhibition of characteristic features of the cells by primarily cAMP formation dominates in HR2-dependent effects of histamine. (more…)

The immunologic mechanisms of sublingual immunotherapy are less established. In Cochrane analysis, the authors concluded that there was an increase in IgG4 but no stable effect on IgE levels in adults. In addition, the induction of allergen-specific IgA has been reported. There are conflicting data concerning lympho-proliferative responses. So far the evidence on changes in Th1/Th2/Treg activity induced by sublingual immunotherapy need to be confirmed. The effects on T-cell reactivity and cytokine secretion show strong variation in a number of studies. (more…)

The genetic basis of asthma heritability has been extensively studied and the studies are yielding some understanding. There is, as yet, no set genetic pattern that predicts presence of asthma or defines it severity. There are usually reasons or risk of asthma factors that makes someone susceptible to asthma and respiratory allergy problems. Asthma doesn’t just happen randomly to anyone without asthma gene factors risk factors.

Let’s consider some asthma risk factors and see how they increase the chance that a individual will have the asthma signs or symptoms of cough, wheezing, as well as shortness of breathing associated with the disease. After determining your personal risk factors for asthma, decide on the ones you can control as well as try to make some lifestyle changes. Avoidance of the risk factors you can control is important in preventing asthma symptoms. While you cannot change your own gender to family history, you can avoid smoking with asthma, breathing polluted air, and obesity. Take control of your asthma by controlling the asthma risk factors. By understanding all of the risk factors, you are able to prevent to control your asthma.

Genetic factors cannot explain the rise in asthma prevalence, morbidity, or mortality. However, a small change in the prevalence of relevant environmental exposures could explain a significant rise in disease prevalence among genetically susceptible individuals. Gene-environment interaction, defined as the co-participation of genetic and environmental factors, is particularly relevant to the etiology of asthma morbidity, especially in individuals who experience a disproportionate burden of environmental exposures. Relevant exposures include smoking, stress, nutritional factors, infections, allergens, and occupational asthma exposures. In addition, racial/ethnic variability in the distribution of genetic polymorphisms can potentially modify the response to pharmacotherapeutic agents, such as the ß 2 -adrenergic receptor. A genetic polymorphism in the ß 2 -adrenergic receptor gene has been associated with asthma severity, as well as with the susceptibility to develop asthma among individuals who smoked.

Childhood asthma happens more frequently in boys than in girls. It is still not known precisely why this occurs even though some experts find a young male’s airway size is small compared to the female’s airway, that may contribute to increased risk of wheezing after a cold or perhaps other viral infection. Around age 20, the ratio of asthma between people is the same. At age 40, more females than men have adult asthma.

The inherited genetic makeup predisposes you to having asthma. In fact, it’s thought that three-fifths of all asthma cases are hereditary. Based on CDC report, if a person has a parent with asthma, there is 3 to 6 times more probably to develop asthma than someone who does definitely not have a parent with asthma.

Treg cells or regulatory T cells constitute a large population of cellular infiltrate in atopic/allergic inflammation and a dysregulated immune response appears to be an important pathogenetic factor. Cardinal events during allergic inflammation can be classified as activation, organ-selective homing, survival and reactivation, and effector functions of immune system cells. T cells are activated by aeroallergens, food antigens, autoantigens, and bacterial exotoxins superantigens in allergic inflammation. They are under the influence of the skin, lung, or nose-related chemokine network and show organ-selective homing. (more…)

Allergen-specific immunotherapy is highly effective in the treatment of IgE-mediated allergy diseases such as rhinitis, conjunctivitis, asthma, and venom allergy hypersensitivity. It is the only treatment that leads to lifelong tolerance against previously disease-causing allergens due to restoration of the normal immunity. (more…)

An emerging concept is that pro-inflammatory signals lead to loss of Regulatory T Cells (Treg) function. Pasare and Medzhitov (2003) demonstrated that activation of DCs through TLRs led to the production of signals, including IL-6, which blocked the suppressive effect of CD4+CD25+ Treg. Subsequent studies support these observations. For example in a mouse model of allergic airway disease, IL-6 is proposed to act via two mechanisms to promote disease: direct enhancement of Th2 responses and by overcoming the suppressive function of CD4+CD25+ Treg. Tumor necrosis factor (TNF) as well as IL-7 and IL-15 have also been proposed to overcome regulatory activity in other human immunologic diseases. (more…)