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…)

The induction of immune tolerance and specific immune suppression are essential processes in the control of immune responses. Regulatory T cells (Treg) play a central role in immune control in the periphery. Two broad categories of Treg have been described: naturally occurring Treg that are present in all individuals and antigen-induced Treg that secrete inhibitory cytokines such as interleukin (IL)-10 and/or transforming growth factor (TGF)-ß. (more…)

Routes by which infectious organisms gain entry into the body include the skin, respiratory tract, gastro-intestinal (GI) tract and GU tract. There are fundamentally two ways in which infectious agents cross the physical and chemical barriers: either they are able to penetrate the intact barriers at one or more anatomical sites, or the physical barriers are damaged and breached, allowing entry of the organism.

Bellow are some possibles pathogens entry into human body:

Penetration of intact skin or mucosa

• Skin. Few organisms are able to penetrate intact skin. However, some parasites (e.g. hookworm) or their larvae (e.g. schistosoma) can do this. Other agents, such as wart viruses, set up infection in the skin and do not enter further into the body.

• Mucosa. Mucosa, being softer and damper than skin, are much more frequent sites of entry and all intact mucosa can be penetrated by some organisms. Examples are shown in table bellow. Pathogens can cross epithelia by passing through epithelial cells, as in the case of the meningococcus (a bacteria causing meningitis), or by passing between the epithelial cells, seen with Haemophilus influenzae.

Mucosal Sites of Entry for Pathogens

Penetration of damaged skin or mucosa

There are many ways in which skin or mucosa can be damaged, allowing entry of infectious organisms that could not cross intact skin or mucosa. Damage to skin is a particularly important route of infection and can occur in a number of ways:

• Burns. Burns, especially severe ones, pose a major risk for infection, particularly with Staphylococcus, Streptococcus, Pseudomonas and Clostridium tetanus.

• Cuts and wounds. These can allow entry of similar organisms to those seen after burns.

• Insect bites. Numerous infections pathogenesis are transmitted via insect bites. These include malaria, typhus and plague.

• Animal bites. Animal bites can provide direct transmission of infection, such as in rabies. Because they cause significant damage to the skin, bites can allow the entry of the same environmental pathogens as burns, cuts and wounds (see above).

• Human behaviour. Various aspects of uniquely human behaviour can result in the skin being penetrated. Sharing of syringes by intravenous (IV) drug users exposes them to risk of hepatitis and human immunodeficiency virus (HIV). A number of viral infections (hepatitis, HIV) have been transmitted by blood transfusion and blood products (e.g. factor VIII for haemophiliacs) before appropriate screening procedures were developed. Transplantation has also resulted in transmission of infection before the introduction of appropriate donor screening.

Damage to mucosa may not increase the likelihood of infection to the same extent as damage to the skin. However, physical or chemical damage may allow entry of some organisms (e.g. smoking increases the risk of respiratory bacterial infections or respiratory allergies). Furthermore, infection of the mucosa with a virus may cause damage and facilitate the entry of bacterial pathogens spread.

Normally present at very low levels in plasma, antibodies of the immunoglobulin E (IgE) isotype were first discovered in 1967, decades after the description of IgA, IgG, and IM. IgE antibodies are produced primarily by plasma cells in mucosal-associated lymphoid tissue and their levels are uniformly elevated in patients suffering from atopic conditions like allergic rhinitis, asthma and atopic dermatitis. Production of allergen-specific IgE in atopic individuals is driven both by a genetic predisposition to the synthesis of this isotype as well as by environmental factors, including chronic allergen exposure. (more…)

CD14 is part of the receptor complex for endotoxin, which is a component of tobacco smoke. The CD14 gene is located on chromosome 5q, a region previously demonstrated to be linked to asthma when stratified for smoke exposure. This study was designed to extend these findings by determining whether polymorphisms in the CD14 gene are related to this gene–environment interaction on asthma. Puerto Rican (n = 362 trios) and Mexican (n = 259 trios) families ascertained through a child with asthma were studied. (more…)

Asthma is characterized by Th2-dominant cytokine profiles. The risk of developing asthma is lower in children attending day care in the first year of life. Therefore, this study was conducted to assess the interaction between day-care attendance, T-cell cytokine profiles and atopic phenotypes in early childhood. Children (n = 208) in the Childhood Onset of Asthma (COAST) study were genotyped for 72 polymorphisms in 45 immune response genes. The COAST cohort was selected on the basis of a high risk of asthma. Measurements of IFN-y (Th1), IL-5 and IL-13 (Th2), and IL-10 (Treg) were made at birth and at age 1 year and the children were stratified by day-care attendance. Wheeze and atopic dermatitis phenotypes were documented in the first year. (more…)

The Tcell Ig domain and mucin domain (TIM) proteins, the genes for which are located on chromosome 5q, have been suggested to be involved in allergic disease. This study examined allergies genetic association of sequence variants of the TIM1 and TIM3 genes in an African-American population. Case–control and family based association analyses were performed for three SNPs each in the TIM1 and TIM3 genes, and an insertion/deletion polymorphism in Tcell Ig domain and mucin domain 1. (more…)

Avoidance of any one of the individual risk factors associated with childhood asthma has not been successful in preventing its development. The purpose of this study was to determine the effectiveness of a multifaceted intervention programme for the primary prevention of asthma in high-risk infants at 7 years of age. Five hundred and forty-five high-risk infants with an immediate family history of asthma and allergies were prospectively randomized into intervention and control groups pre-natally. (more…)

The geographical variation in the prevalence of asthma in children does not coincide with variations in air pollution levels. The increase in the prevalence of asthma and allergies seen over the last decades was paralleled by a decrease in emissions of SO2 and particles from coal combustion, and an increase of emissions from motor vehicle traffic. There is a growing number of studies suggesting that increased exposure to traffic exhausts, particularly diesel exhausts, may be a risk factor for the new onset of asthma. (more…)