Andrew Kemp

Reduced interferon-γ secretion in neonates and subsequent atopy

Abstract Summary Low interferon-γ (IFN-γ) secretion has been found in individuals with active atopic disease. Whether this is a cause or result of the disease process is uncertain. Cord blood IFN-γ secretion was examined in 35 neonates who were then prospectively followed up for 1 year for the development of atopic disease. Infants who developed either symptoms of atopic disease or a positive IgE-mediated skin prick test at 12 months of age produced significantly less IFN-γ at birth compared with those who did not (p = 0·005). This reduced secretion of IFN-γ at birth indicates that the defect in interferon secretion is a primary component of the atopic state rather than an effect of the disease process.

IL-4 and interferon-gamma production in children with atopic disease

In vitro studies have implicated reciprocal roles for IL‐4 and interferon‐gamma (IFN‐γ) in the regulation of IgE production. As elevated IgE is a major feature of atopic disease, an important question is whether an imbalance of IL‐4 and IFN‐γ is present in vivo. The production of IL‐4 and IFN‐γ in phytohaemagglutinin (PHA)‐stimulated peripheral blood mononuclear cell cultures from atopic children was examined to determine if there is an increased production of IL‐4 and/or a reduced production of IFN‐γ. Highly atopic children with IgE >600 U/ml produced significantly more IL‐4 and less IFN‐γin vitro than age‐matched non‐atopic controls. Production of IL‐4 and IFN‐γ in mildly atopic children was equivalent to controls. These findings indicate that highly atopic children have an imbalance of IL‐4 and IFN‐γ production and that the degree of imbalance relates to severity of the atopic state. The ratio of in vitro IL‐4: IFN‐γ production correlated positively with serum IgE, which suggests that the balance of these two cytokines is a factor in the regulation of IgE, in vivo. It remains to be determined whether this imbalance of IL‐4 and IFN‐γ in the highly atopic children is the cause or result of the disease process.

Increased Th1 and Th2 allergen-induced cytokine responses in children with atopic disease.

Background Polyclonal cytokine responses following stimulation of T cells with mitogens or superantigens provides information on cytokine production from a wide range of T cells. Alternatively allergen‐induced T cell responses can provide information on cytokine production by allergen‐reactive T cells. While there is evidence of increased Th2 and reduced Th1 cytokine production following T cell stimulation with non‐specific mitogens and superantigens, the evidence that Th1 cytokine production to allergens is decreased in line with a postulated imbalance in Th1/Th2 responses is unclear, with studies finding decreased, no difference or increased IFN‐γ responses to allergens in atopic subjects.

Interleukin‐4 and interferon‐gamma production in atopic and non‐atopic children with ashma

Previous studies have demonstrated increased production of interleukin‐4 (IL‐4) and reduced production of interferon (IFN)‐γ in stimulated peripheral blood mononuclear cell cultures from children and adults with atopic dermatitis, however, it is unclear whether such an imbalance of cytokine production relates to other childhood atopic diseases such as asthma, and in particular to the presence of the atopic state per se. The production of IL‐4 and IFNγ in phytohaemagglutin‐ (PHA)‐stimulated peripheral blood mononuclear cell (PBMC) cultures from atopic and non‐atopic children with moderately severe chronic persistent asthma, and a group of age‐matched non‐atopic controls who did not have asthma was examined. Atopic children with asthma produced significantly more IL‐4 and less IFNγ than non‐atopic children with asthma and non‐atopic controls who did not have asthma. There was no significant difference in IL‐4 or IFNγ production between non‐atopic children with asthma and controls. These findir. 3 demonstrate that an imbalance of IL‐4 and IFNγ production is present in atopic asthma as previously documented in atopic dermatitis, therefore suggesting that it is a feature of the atopic state per se.

The association between infant feeding practices and subsequent atopy among children with a family history of asthma.

Background Although longer duration of breastfeeding and later introduction of solid foods are both recommended for the prevention of asthma and allergic disease, evidence to support these recommendations is controversial.

Immune deviation and the hygiene hypothesis: A review of the epidemiological evidence

The epidemiological evidence for the proposal that early life immune deviation is the principal mechanism by which microbial agents prevent the development of atopy has been reviewed. Seven criteria are proposed which should ideally be fulfilled. The majority of studies only fulfill two or three criteria. For mycobacteria, measles and respiratory viruses there are studies that demonstrate a significant increase in atopy or allergic disease. Parasite infections, which provide a strong TH2 stimulus, are associated with reduced rather than enhanced allergen sensitization. The available epidemiological evidence does not provide support for a mechanism of early life immune deviation. The principal environmental influences on atopic disease are likely to occur throughout life and involve interactions between microbes and other non‐infective and lifestyle factors.

Cost of illness of atopic dermatitis in children: a societal perspective.

Childhood atopic dermatitis is a disorder with considerable social and financial costs. Consideration of these costs is increasingly important in view of the growing prevalence of atopic dermatitis, particularly in developed countries over recent decades. The family stress related to the care of children with moderate or severe atopic dermatitis is significantly greater than that of the care of children with type 1 diabetes mellitus. The factors contributing to family stress include sleep deprivation, loss of employment, time taken for care of atopic dermatitis and financial costs. The financial costs for the family and community include medical and hospital direct costs of treatments and indirect costs from loss of employment. There are many interventions utilised in the treatment of childhood atopic dermatitis which involve not only medical practitioners but nurses, pharmacists, dieticians, psychologists and purveyors of so-called alternative therapies such as naturopathy, aromatherapy and bioresonance, all of which contribute to the financial burdens on the parents and the community. It is possible that appropriate interventions directed to reducing trigger factors might produce worthwhile savings, although the cost benefit of these measures has not been demonstrated. In conclusion, atopic dermatitis should not be regarded as a minor skin disorder but as a condition which has the potential to be a major handicap with considerable personal, social and financial consequences both to the family and the community.

Atopic eczema: Its social and financial costs

Abstract: Atopic dermatitis is a disorder with considerable social and financial costs. A recent Australian study indicates that the family stress related to the care of a child with moderate or severe atopic dermatitis is significantly greater than that of care of children with insulin‐dependent diabetes mellitus. The factors contributing to family stress include: sleep deprivation; loss of employment; time taken for care of atopic dermatitis; and financial costs. An estimate of the yearly financial costs for a family and community (which includes medical, hospital, direct costs of treatments and indirect costs from loss of employment), range from

Proliferation and production of interferon-gamma (IFN-γ) and IL-4 in response to Staphylococcus aureus and Staphylococcal superantigen in childhood atopic dermatitis

A1142 per child per year with mild atopic dermatitis, to

Management of cow's milk protein allergy in infants and young children: An expert panel perspective

A6099 per child per year for a child with severe atopic dermatitis. As the current prevalence of atopic dermatitis in Australia is 10–15%, this indicates a considerable financial burden on the community. It is possible that appropriate interventions directed to reducing trigger factors, may produce worthwhile savings, in addition to benefits for the individuals and families. Atopic dermatitis should not be regarded as a minor skin disorder but as a condition which has the potential to be a major handicap involving considerable personal, social and financial consequences both for the family and for the community.