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Biomedical subjects

A S Kemp

Publications and source records attributed to A S Kemp.

At least 19 recordsLinked to original sources
PubMed2003

Age-related T cell responses to allergens in childhood.

BACKGROUND: T cell priming, as determined by allergen-induced proliferative responses, is believed to occur principally in early childhood in both atopic and non-atopic infants under the influence of multiple factors including environmental allergen exposure. It is considered that T cell priming with expansion of Th2 cells is a crucial factor in the development of atopic disease. OBJECTIVE: To examine T cell priming to commonly encountered allergens in childhood in relation to age. METHODS: In a cross-sectional study T cell proliferation in relation to age was examined for three common allergens, ovalbumin (OVA), house dust mite (HDM) and rye grass pollen (RYE), in atopic and non-atopic children. The effect of age on Th1 (IFN-gamma) and Th2 (IL-5 and IL-13) cytokine production in response to these allergens was investigated to examine the possibility of immune deviation with time. RESULTS: A significant increase in T cell proliferation with age was observed with RYE among atopic children only. However, the same was not observed with the two other allergens studied (i.e. OVA and HDM). In addition, RYE-induced (but not HDM or OVA) cytokine production showed an increased Th2 deviation with age as reflected in the increasing IL-5/IFN-gamma and IL-13/IFN-gamma ratios only among the atopic subjects with rye grass pollen sensitivity. CONCLUSION: These findings suggest that grass pollen sensitivity in childhood is accompanied by a progressive accumulation of allergen-primed T cells and progressive deviation of the allergen-induced cytokine response towards a Th2 response in atopic subjects throughout childhood.

Adolescent↗
PubMed2003

EpiPen epidemic: suggestions for rational prescribing in childhood food allergy.

There has been a marked increase in community concerns of the risk of food induced anaphylaxis in children and a consequent increase in the provision of the self or carer injectable epinephrine (EpiPen) (CSL Ltd, Parkville, Victoria, Australia)). The Australian use of EpiPens in children under 10 years has increased by 300% over 5 years with a crude rate of EpiPen provision of 1 per 544 Australian children aged under 10 years. However, the risk of a fatal reaction to food, particularly in preschool children, is remote (in Australia, an estimated one fatality in 30 years in the under 5-year-old population and two deaths in 10 years in the entire child population). It is therefore important to provide a perspective on the risk of death from food induced anaphylactic to parents and carers in view of the anxiety generated on this issue. The indications for provision of an EpiPen to children are not well defined. Six risk factors, which can be considered in evaluating the risk of a life-threatening reaction (age over 5 years; a history of respiratory tract involvement with the initial or subsequent reactions; a history of asthma requiring preventer medication; peanut or tree nut sensitivity; reactions induced by traces or small amounts of allergen; a strongly positive skin prick test) are proposed. It is suggested that the greater the number that are positive, the lower the threshold for provision of an EpiPen. In addition, instruction in EpiPen administration and the provision of both a clear and simple anaphylaxis action plan and a rational perspective on the remote risk of death is just as important as the provision of the device itself.

Anaphylaxis↗
PubMed2002

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-gamma responses to allergens in atopic subjects. OBJECTIVE: To examine childhood polyclonal and allergen-induced cytokine responses in parallel to evaluate cytokine imbalances in childhood atopic disease. METHODS: PBMC cytokine responses were examined in response to a polyclonal stimulus, staphylococcal superantigen (SEB), in parallel with two inhalant allergens, house dust mite (HDM) and rye grass pollen (RYE), and an ingested allergen, ovalbumin (OVA), in (a) 35 healthy children (non-atopic) and (b) 36 children with atopic disease (asthma, eczema and/or rhinitis) (atopic). RESULTS: Atopic children had significantly reduced IFN-gamma and increased IL-4 and IL-5 but not IL13 production to SEB superantigen stimulation when compared with non-atopic children. HDM and RYE allergens stimulated significantly increased IFN-gamma, IL-5 and IL-13, while OVA stimulated significantly increased IFN-gamma production in atopic children. CONCLUSION: We show that a polyclonal stimulus induces a reduced Th1 (IFN-gamma) and increased Th2 (IL-4 and IL-5) cytokine pattern. In contrast, the allergen-induced cytokine responses in atopic children were associated with both increased Th1 (INF-gamma) and Th2 (IL-5 and IL-13) cytokine production. The increased Th1 response to allergen is likely to reflect prior sensitization and indicates that increases in both Th1 and Th2 cytokine production to allergens exists concomitantly with a decreased Th1 response to a polyclonal stimulus in atopic children.

Adolescent↗
PubMed2002

Polyclonal and allergen-induced cytokine responses in children with elevated immunoglobulin E but no atopic disease.

BACKGROUND: Reduced Th1 and elevated Th2 cytokine responses are considered to be a principal mechanism in the generation of the inflammation leading to the manifestations of atopic disease in the skin of atopic dermatitis and in the airways of asthma. If reduced Th1 and elevated Th2 responses are principal determinants of the manifestation of atopic disease it might be expected that subjects with established disease would exhibit differences in their cytokine profiles as compared with atopic patients without clinical disease. OBJECTIVE: To determine whether asymptomatic atopic children exhibit a cytokine imbalance similar to that seen in patients with established atopic disease or if they behave like non-atopic controls. Cytokine responses in a group of children with elevated IgE but no clinical manifestations of disease, atopic children with established disease and non-atopic controls were compared. METHODS: We examined allergen-induced (house dust mite, HDM, rye grass pollen and RYE) cytokine responses in parallel with polyclonal (staphylococcal enterotoxin B, SEB) cytokine responses in a group of children with elevated serum IgE levels without current or past evidence of atopic disease (median age 6.6 years) and compared these with a non-atopic control group (median age 6.5 years) and a group of children with atopic disease (median age 6.7 years). RESULTS: Symptomatic atopic children had reduced SEB-induced IFN-gamma and increased SEB-induced IL-4 and IL-5 as compared with non-atopic controls. In contrast, SEB-induced IFN-gamma, IL-4 and IL-5 production in asymptomatic atopics was not significantly different from the non-atopic control subjects. Allergen-induced Th1 (IFN-gamma) and Th2 (IL-5 and IL-13) cytokine production was increased in both symptomatic atopics and asymptomatic atopics when compared with non-atopic controls. CONCLUSION: The defect in polyclonally induced IFN-gamma production was associated with the clinical manifestation of atopic disease but not the atopic stateper se. This suggests that the global reduction in IFN-gamma is the key determinant of the development of overt atopic disease. In contrast, elevated allergen-induced Th2 cytokine responses in children related to the atopic state per se irrespective of the presence of clinical atopic disease.

Adolescent↗
PubMed2001

Ontogeny of T-helper 1 and T-helper 2 cytokine production in childhood.

Compared to adults, infants and young children demonstrate differences in their immune response, indicating that there is maturation or change over time and it is probable that this may be reflected in cytokine production. Cytokine responses have been demonstrated to be different in atopic and non-atopic individuals. In this study, we examined T-helper 1 (Th1) (interferon-gamma [IFN-gamma]) and T-helper 2 (Th2) (interleukin [IL]-4, IL-5, and IL-13) cytokine release from atopic and non-atopic children in response to the staphylococcal superantigen, staphylococcal enterotoxin B (SEB). In non-atopic and atopic children, IFN-gamma, IL-4, and IL-5 release was significantly related to age. Non-atopic children younger than 2 years of age were found to have significantly reduced Th2 (IL-4, IL-5, and IL-13) responses when compared with older, non-atopic children. Atopic children had a reduced IFN-gamma response when compared with non-atopics in early childhood; however, the decreased IFN-gamma response seen in early childhood did not persist after 10 years. These age-related changes in cytokine production provide further support for the concept that cytokine deviations may determine the natural history of atopic disease during early childhood. In addition, the present study indicates the necessity of age-matched controls when examining children for both Th1 (IFN-gamma) and Th2 (IL-4) cytokine release.

Aging↗
PubMed2001

Clinical correlates of response to pneumococcal immunization.

OBJECTIVE: The inability to form antibodies to polysaccharide antigens may occur as a part of a more significant immunodeficiency or as an isolated defect. The latter has been reported in some children with recurrent upper and lower respiratory tract infections and evaluation of the responsiveness of such patients to polysaccharide antigens is indicated as part of their assessment. The present study evaluated the pattern of antibody responses of patients immunized with pneumococcal vaccine as part of the investigation of recurrent upper and lower respiratory tract infections to determine if any correlation exists between these responses and clinical presentation. METHODOLOGY: An analysis was performed of antibody responses to pneumococcal serotypes 3, 4 and 6 following immunization with a 23-valent vaccine in 42 children with normal IgG levels who were evaluated for recurrent infections. Antibody responses were assessed in relation to clinical features and the results of other immunological investigations. RESULTS: Of the 42 patients evaluated, 25 (59%) were responders to all serotypes tested. Failure to respond to serotype 3 alone was the least common pattern of non-response. Recurrent pneumonia, but not otitis media with discharge or chronic productive cough, was significantly associated with a lack of response to two or three serotypes. Failure to respond to serotype 3 alone or in combination with other serotypes was associated with more significant immune abnormalities. CONCLUSION: In a selected population of children with recurrent bacterial infections, pneumococcal serotype 3 is a strong immunogen. In this clinical group recurrent pneumonia is associated with a defect in response to multiple pneumococcal serotypes.

Antibodies, Bacterial↗
PubMed2001

Immune response to infection with Mycobacterium ulcerans.

Mycobacterium ulcerans is a slow-growing, acid-fast bacillus that causes chronic necrotizing skin ulcers known as Buruli ulcers. Previously reported information on immunity to this mycobacterium is limited. We examined immune responses to M. ulcerans and M. bovis BCG in patients with M. ulcerans disease and in 20 healthy control subjects (10 tuberculin test positive and 10 tuberculin test negative). Cell-mediated immunity was assessed by stimulating peripheral blood mononuclear cells (PBMC) with whole mycobacteria and then measuring PBMC proliferation and the production of gamma interferon (IFN-gamma). Humoral immunity was assessed by immunoblotting. PBMC from all subjects showed significantly greater proliferation and IFN-gamma production in response to stimulation with living mycobacteria compared with killed cells. However, PBMC from subjects with past or current M. ulcerans disease showed significantly reduced proliferation and production of IFN-gamma in response to stimulation with live M. ulcerans or M. bovis than PBMC from healthy, tuberculin test-positive subjects (P < 0.001) and showed results in these assays comparable to those of tuberculin test-negative subjects (P > 0.2). Serum from 9 of 11 patients with M. ulcerans disease, but no control subject, contained antibodies to M. ulcerans. The results indicate that patients with M. ulcerans infection mount an immune response to M. ulcerans as evidenced by antibody production, but they demonstrate profound systemic T-cell anergy to mycobacterial antigens. These findings may explain some of the distinct clinical and pathological features of M. ulcerans-induced disease.

Adolescent↗
PubMed1999

Pooled human immunoglobulin inhibits IL-4 but not IFN-gamma or TNF-alpha secretion following in vitro stimulation of mononuclear cells with Staphylococcal superantigen.

Intravenous immunoglobulin preparations have been successfully used in many disorders, where immunomodulation rather than immunoglobulin replacement has been the goal of therapy. The exact mechanisms by which immunoglobulin exerts its immunomodulatory effects are unclear. Proposed mechanisms include modification of T cell activation and alteration to cytokine production. As intravenous immunoglobulin therapy has been used in a number of disorders where superantigens are proposed to play a role in the disease pathogenesis, we have examined the effect of in vitro human pooled immunoglobulin on cytokine production from peripheral blood mononuclear cells in response to activation with the Staphylococcal superantigen Staphylococcal enterotoxin B. The authors found inhibition of secretion of interleukin 4 (IL-4) (P<0.001) but not interferon gamma (IFN-gamma) (P=0.13) or tumour necrosis factor alpha (TNF-alpha) (P=0.66) by pooled immunoglobulin at concentrations (6 g/l) which approximate the rise in serum immunoglobulin following in vivo IVIG therapy. Mononuclear cell proliferation was also inhibited by addition of pooled immunoglobulin to superantigen stimulated cultures. These effects do not relate to specific anti-staphylococcal enterotoxin B antibodies in the immunoglobulin preparation. The authors show that pooled human immunoglobulin can differentially modulate the secretion of IL-4 and IFN-gamma in response to superantigen stimulation.

Antigens, Bacterial↗
PubMed1999

Cutaneous lymphocyte-associated antigen expression in children with atopic dermatitis and non-atopic healthy children.

Cutaneous lymphocyte-associated antigen (CLA) is a cell surface glycoprotein which has been implicated in the homing of lymphocytes to cutaneous sites. It is postulated to play an important role in T-cell migration to skin in atopic dermatitis; however, the expression of CLA in both normal children and children with atopic dermatitis has not been extensively studied. If CLA expression on T cells were important in the traffic of lymphocytes to atopic dermatitis skin lesions, it might be expected that the proportion of CLA+ T cells in unstimulated peripheral blood from children with atopic dermatitis would be elevated. We have examined the proportion of CLA+ T cells in children with atopic dermatitis and non-atopic age-matched controls. The proportion of CLA+ T cells in non-atopic children was highly associated with and increased with increasing age (r = 0.88, p < 0.001). There was no difference between the proportion of T cells expressing CLA in the unstimulated peripheral blood mononuclear cells from children with severe (p = 0.18) or with mild/moderate (p = 0.3) atopic dermatitis and age-matched non-atopic controls. Despite this, children with atopic dermatitis did show evidence of perturbation of CLA expression, as unlike the non-atopic children the proportion of CLA+ T cells in the atopic children did not correlate with age. These findings suggest that while CLA expression may play a role in atopic dermatitis, other as yet undefined surface markers are likely to principally determine the migration of T cells to skin in atopic dermatitis.

Adult↗
PubMed1999

Intracellular interferon-gamma (IFN-gamma) production in normal children and children with atopic dermatitis.

A reduction in the in vitro production of IFN-gamma has been consistently described in atopic dermatitis (AD). Whether this reduction is due to a decrease in the population of peripheral blood mononuclear cells (PBMC) producing IFN-gamma or reduced IFN-gamma production per cell, or a combination of both is not clear. We have examined the intracellular production of IFN-gamma in children with AD and in healthy non-atopic controls. As Staphylococcus aureus colonization is a feature of childhood AD, and is postulated to contribute to the cutaneous inflammation in atopic dermatitis, S. aureus and Staphylococcal enterotoxin B (SEB) were used to activate PBMC. Stimulated PBMC from subjects with AD had significantly fewer IFN-gamma-containing cells in response to SEB (P < 0.001) and S. aureus (P < 0.01) than normal non-atopic children. In addition, SEB-stimulated PBMC from children with AD had less IFN-gamma per cell than normal non-atopic children (P < 0.01). Reduction in the proportion of cells containing IFN-gamma was seen in CD4+, CD8+ and natural killer (NK) cells in PBMC from children with AD. Our findings indicate that reduced production of IFN-gamma observed in childhood AD is due to both a decrease in the number of IFN-gamma-producing cells and a reduced amount of IFN-gamma production per cell. Furthermore, we found that this defect was not confined to CD4+ T cells, suggesting a more generalized defect in IFN-gamma production in childhood AD.

Case-Control Studies↗
PubMed1999

Atopic eczema: its social and financial costs.

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 $A1142 per child per year with mild atopic dermatitis, to $A6099 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.

Adolescent↗
PubMed1998

The Melbourne House Dust Mite Study: long-term efficacy of house dust mite reduction strategies.

BACKGROUND: Asthma severity among mite-sensitized individuals appears to be related to the degree of mite allergen exposure. OBJECTIVES: The objective of this study was to assess the long-term effectiveness of mite avoidance measures in the homes of asthmatic children in Melbourne, Australia. METHODS: The concentration of house dust mite allergen (Der p 1) was measured on the child's mattress surfaces and bedroom floors in 85 homes on 10 occasions over a 16-month period. After the first three visits, all mattresses were covered with a semipermeable encasement, and carpeted bedroom floors were randomly allocated to regular applications of a placebo or an "anti-mite" shampoo. RESULTS: The concentration of Der p 1 recovered was initially high in the carpeted bedrooms (n = 66) (41.1, 95% confidence interval, 30.7 to 55.0 microg Der p 1 per gm) and mattresses (n = 85) (39.6, 27.2 to 57.7). During the initial observation period the concentration of mite allergen fell in the treatment, placebo, and parental control groups. During the seven treatment periods, no differences were seen between the Der p 1 concentrations in the groups using the "anti-mite" shampoo, placebo shampoo, or the parental control group (e.g., at visit 4; 12.6, 8.2 to 19.5; 14.8, 8.6 to 25.1; and 12.0, 8.1 to 17.7 microg/gm, respectively). In contrast, the concentration of Der p 1 in samples from uncarpeted floors and mattress encasements was low (4.1, 2.1 to 8.0 microg/gm and 4.2, 2.6 to 6.5 microg/gm, respectively) and insufficient dust for analysis was frequently obtained from these sites. CONCLUSIONS: There was no additional benefit from the use of an "anti-mite" shampoo. The absence of carpets and the use of mattress encasements was a useful long-term strategy for mite allergen avoidance.

Animals↗
PubMed1998

Enhanced IL-4 but normal interferon-gamma production in children with isolated IgE mediated food hypersensitivity.

Atopic disorders such as atopic dermatitis and asthma have been characterised by an imbalance in interferon-gamma (INF-gamma) and IL-4. Whether similar imbalances are found in atopic disorders with different clinical manifestations, such as IgE mediated immediate food hypersensitivity, is not clear. We have examined the in vitro production of INF-gamma and IL-4 in peripheral blood mononuclear cells (PBMC) following phytohaemagglutinin stimulation from children with isolated immediate IgE mediated food hypersensitivity (egg, milk, "nut"), children with moderate and severe atopic dermatitis, and normal children. Children with immediate food reactions were excluded if they had a history or evidence of atopic dermatitis or asthma. PBMC from children with IgE mediated food hypersensitivity produced significantly more IL-4 (p = 0.013) but equivalent INF-gamma (p = 0.26) compared to PBMC from control children. In contrast, PBMC from children with atopic dermatitis produced significantly less INF-gamma (p < 0.001) and more IL-4 (p < 0.008) than PBMC from normal children. In addition, there was no difference in IL-4 (p = 0.74) but significantly less INF-gamma (p < 0.001) produced by PBMC from the children with atopic dermatitis than food hypersensitivity. We demonstrate that children with IgE mediated food hypersensitivity and no other manifestation of atopic disease have enhanced IL-4 production without the defect in INF-gamma production observed in childhood AD and asthma. We postulate that isolated IL-4 enhancement promotes the development of IgE mediated hypersensitivity disorders such as food allergy, whilst the combination of defective INF-gamma and enhanced IL-4 production promotes inflammatory atopic disorders such as AD and asthma.

Child, Preschool↗
PubMed1998

Production of antibodies to staphylococcal superantigens in atopic dermatitis.

Staphylococcal superantigens (SAG) are implicated in the inflammation of atopic dermatitis. As SAG mediated diseases may be modified by specific antibodies, the antibody response to SAG in atopic dermatitis was investigated. Immunoglobulin (Ig) G to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB), and toxic shock syndrome toxin 1 (TSST-1) were measured by sandwich enzyme linked immunosorbent assay (ELISA) in 74 children with atopic dermatitis and 111 controls. Controls had detectable IgG to SEA, SEB, and TSST-1, which increased with age. Atopic dermatitis subjects had an increased response to SEB at 6 months to 2 years (76% v 42%) and 2 to 7 years (79% v 57%), and equivalent responses to SEA and TSST-1, compared to controls. It is suggested that increased responses to SEB relate to increased colonisation and hence exposure to superantigen producing staphylococcus in atopic dermatitis, and that inflammation of atopic dermatitis is not caused by an inability to make antibody to SAG.

Adolescent↗
PubMed1997

Fatal granulomatous amoebic encephalitis caused by Balamuthia mandrillaris.

Granulomatous amoebic encephalitis caused by Balamuthia mandrillaris is rare (63 human) cases reported worldwide) and fatal. We report a case in a five-year-old boy who had previously been well. For 18 months, he had had a slowly progressive, granulomatous mid facial lesion, but despite extensive investigation definitive diagnosis was made only with the acute onset of neurological signs in the last two weeks of life, when a brain biopsy specimen revealed amoebic trophozoites and cysts. Infection with B. mandrillaris should be considered in the differential diagnosis of chronic skin lesions with non-specific granulomatous histopathology and negative microbiological test results.

Adolescent↗
PubMed1997

Pulmonary diseases in children with severe combined immune deficiency and DiGeorge syndrome.

Pulmonary disease is a common presenting feature and complication of T-cell immunodeficiency. We retrospectively reviewed 15 children with severe combined immune deficiency (SCID) and 19 children with DiGeorge syndrome at the time of their first presentation to the Royal Children's Hospital in the 15-year period from 1981 to 1995. In children with SCID, pulmonary disease was a common (67%) presenting feature and the organisms identified were Pneumocystis carinii (PCP) (n = 7), bacteria (n = 4), viruses (n = 3), and a fungus (n = 1). Late pulmonary complications included lower respiratory tract infections, bronchiolitis obliterans, and lymphointerstitial pneumonitis. Pulmonary infections were common (17 occasions) and the organisms identified were bacteria (n = 7), viruses (n = 6), fungi (n = 3), and Mycobacterium tuberculosis (n = 1). Pulmonary complications were responsible for 5 of 9 deaths. PCP was not identified as a late complication in any child, presumably as a result of effective prophylactic therapy. Although pulmonary disease was not a major presenting feature in children with DiGeorge syndrome, pulmonary complications were common. These included recurrent bacterial and viral infections and bronchomalacia, which complicated management and predisposed to morbidity and mortality, even in those without a T-cell defect. We conclude that pulmonary disease is a common manifestation in children with SCID and DiGeorge syndrome.

CD4 Lymphocyte Count↗
PubMed1997

The Melbourne house dust mite study: eliminating house dust mites in the domestic environment.

BACKGROUND: Hypersensitivity to house dust mite allergens is associated with increased asthma morbidity. Asthma severity appears to be related to the degree of mite allergen exposure. Short-term studies suggest that complete avoidance reduces disease severity. OBJECTIVE: The study was designed to assess the effect of different mattress covers and floor coverings on mite allergen concentrations in the homes of mite-sensitive children with asthma in the city of Melbourne, Australia. METHODS: Mite allergen Der p 1 concentration was measured on mattress covers, mattress surfaces, and carpeted and uncarpeted floors in 107 dwellings; and measurement was performed on three occasions over a 5-month period. After the first sampling, all mattress covers and impermeable encasements were permanently removed. RESULTS: The initial geometric mean concentrations of Der p 1 (micrograms per gram of fine dust) from the surfaces of sheepskin, wool, and cotton mattress coverings were greater than those from the surfaces of impermeable mattress encasements (116, 113, and 19 vs 0.4) (p < 0.001); corresponding concentrations on the underlying mattresses were 142, 38, 20, and 0.6, respectively (p < 0.05 to 0.001). At the end of the study these mattress surface concentrations were 79, 65, 9.7, and 3.1, respectively. In 24 dwellings an uncarpeted room was adjacent to a carpeted room. At each visit the concentration of Der p 1 in uncarpeted rooms was below the reported threshold for sensitization and significantly less than that in the adjacent carpeted room. CONCLUSION: In homes of children with asthma, "asthmogenic" concentrations of Der p 1 were found on nonencased mattresses and carpeted floors, but the use of impermeable mattress encasements and carpet exclusion were associated with concentrations of Der p 1 below the reported threshold for sensitization.

Adolescent↗