- Email: [email protected]
Early Skin Care By “Experienced Mothers” May Prevent Sensitization In Infants With Atopic Dermatitis
Abstracts AB195
J ALLERGY CLIN IMMUNOL VOLUME 133, NUMBER 2
674
Early Skin Care By ''Experienced Mothers'' May Prevent Sensitization In Infants With Atopic Dermatitis Dr. Atsushi Yamashita, Dr. Mizuho Nagao, MD, Ms. Kanae Furuya, Dr. Junya Hirayama, Dr. Keigo Kainuma, MD, Dr. Takao Fujisawa, MD, FAAAAI; Institute for Clinical Research, Mie National Hospital. RATIONALE: Caregivers of infants with severe atopic dermatitis (AD) usually learn pivotal importance of skin care when they receive proper treatment and experience favorable outcome of AD by the treatment. Then, an ‘experienced’ mother tends to start skin care very early for her next child hoping to prevent bad outcome she went through with her first one. Since it has been suggested that epidermal barrier dysfunction in AD promotes allergen sensitization, we hypothesized that early skin care by ’experienced’ mothers may alleviate sensitization of infants with AD, possibly through protection of skin barrier function. METHODS: To investigate whether IgE sensitization levels to food and house dust mite (HDM) in AD infants of ‘experienced’ mothers are lower than those of ‘na€ıve’ mothers who first experienced AD in their child. Retrospective analysis of 55 infants with AD was performed. They were divided into 2 groups; 45 infants who were first-born children or had elder siblings without AD, designated as ‘na€ıve’ group and 10 infants who had elder siblings with severe AD, designated as ‘experienced’ group. RESULTS: Severity and age at initial presentation was higher in ‘na€ıve’ group than in ‘experienced’ group. Serum IgE, egg white-specific IgE and HDM-specific IgE levels from 6 months to 18 months old tended to be higher in ‘na€ıve’ group than in ‘experienced’ group. CONCLUSIONS: Early skin care presumably done by ‘experienced’ mothers may be beneficial to protect AD infants from ‘sensitization spreading’.
675
Association Of Bathing Habits To Pruritus and Allergic Disease Dr. Kanwaljit K. Brar, MD1, Dr. Rauno O. Joks, MD, FAAAAI2, Dr. Hamid Moallem, MD1; 1SUNY Downstate Medical Center, Brooklyn,
NY, 2Center for Allergy and Asthma Research, State University of New York Downstate Medical Center, Brooklyn, NY. RATIONALE: Traditionally, physicians have advised limiting bathing frequency and duration for patients with pruritis. Our patient population is primarily Afro-Caribbean immigrants, whose practice of frequent bathing to stave off heat persists after migration to the cooler climate of Brooklyn. We sought to evaluate for an association between bathing habits and pruritis in our adult allergy patients. We report preliminary data from our pilot study. METHODS: IRB approval was obtained, patients (n5 17) were recruited from the adult allergy clinic of University Hospital of Brooklyn, and King’s County Hospital. Our survey addressed demographics, bathing habits, medical, and environmental history. Bathing exposure time was determined by multiplying frequency of bathing with the duration of bath or shower. Pruritis was measured using a 5-D itch scale, a validated tool used to measure pruritis. Scores ranged from 5 (absent pruritis) to 25 (very severe pruritis). RESULTS: Among the 17 patients, 16 (94%) were female; 11 (65%) originated from the Caribbean Islands or South America. Average bath exposure time was 33 minutes/day. Patients who had a bath exposure time of greater than 10 minutes had a mean pruritis score of 12.75, compared with patients who had a bath exposure time of less than 10 minutes who had a mean pruritis score of 10. A correlation with bath exposure time and pruritis score was not found (p50.83). CONCLUSIONS: This is the first study to evaluate bathing habits and their association to pruritis. Bath exposure time is a novel method of quantifying bathing duration and bathing frequency.
676
A Molecular Mechanism Underlying Atopic Dermatitis In Hyper-IgE Syndrome Masako Saito, PhD1, Dr. Hajime Karasuyama, MD, PhD2, Dr. Yoshiyuki Minegishi, MD, PhD3; 1Division of Molecular Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan, 2Tokyo Medical and Dentistry Graduate School, Tokyo, Japan, 3Division of Molecular Medicine, Institute for Genome Research, The University of Tokushima. RATIONALE: Hyper-IgE syndrome (HIES) is a primary immunodeficiency characterized by extremely high serum IgE levels, atopic dermatitis, staphylococcal infections and eosinophilia. Dominant negative (DN) mutations in the STAT3 gene is a major genetic origin of the HIES. We recently established STAT3-DN knock-in mice, which did not develop atopic dermatitis spontaneously under SPF conditions. METHODS: Mice were sensitized with oxazolone (Ox) on day -6, and challenged every other day from day 0. Ear thickness was measured and cells recovered from the ear skin were evaluated immunologically. RESULTS: Ox-sensitized and challenged STAT3-DN mice showed significantly greater ear swelling after day 10 compared to STAT3-WT mice. More CD4+ T cells, eosinophils and basophils but less neutrophils were infiltrated in STAT3-DN mice compared to STAT3WT mice at day 15. STAT3-DN mice have significantly higher Oxspecific IgE levels compared to STAT3-WT mice. In the skin lesion, the expression of IFNg, IL-4, CXCL9, CCL17, CCL22, and CCL5 was increased in STAT3-DN mice. IFNg was predominantly expressed by CD4+ T cells, and IL-4 was expressed by basophils. CCL17 and CCL22 were expressed by DCs, and CXCL9 was expressed by CD45 negative cells. CCL5, which can recruit eosinophils, was expressed mainly by DCs. Although eosinophilia in HIES is considered to be associated with the development of atopic dermatitis, eosinophil deficient STAT3-DN mice showed equivalent ear swelling compared to eosinophil sufficient STAT3-DN mice. CONCLUSIONS: These results suggest that eosinophilia is not involved in the development of atopic dermatitis in HIES.
MONDAY
673
Mycotoxin Aggravates Atopic Dermatitis Via TSLP Induced Th2 Inflammation Ms. Seung-Hwa Lee1, Ms. Ha-Jung Kim1, Prof. Soo-Jong Hong, MD. PhD2,3; 1 Asan Institute for Life Sciences, University of Ulsan College of Medicine, 2 Department of Pediatrics, Asan Medical Center, Childhood Asthma Atopy Center, South Korea, 3Research Center for Standardization of Allergic Disease, University of Ulsan College of Medicine, Seoul, Korea. RATIONALE: Mycotoxins, secondary metabolites of molds, have an effect on impairment of immune system. The exposure of mycotoxin is associated with the development of atopic dermatitis (AD). However, the precise mechanisms of the allergy-promoting effect of mycotoxins remain unclear. This study was to investigate the effect of mycotoxin exposure on AD in a mouse model. METHODS: To investigate the effect of mycotoxin in AD, SKH-1 hairless mice were exposed via skin to patulin (mycotoxin) during ovalbumin (OVA) sensitization for developing the mouse model of AD. Evaluation of clinical signs (erythema), transepidermal water loss (TEWL), histopathology (H&E stain), and immunohistochemistry of TSLP and IL-4 on skin was performed. In addition, serum OVA-specific IgE and OVA-specific IgG1 were measured to confirm systemic immunization. RESULTS: Patulin exposure of OVA-induced mice exacerbated the phenotypes (e.g., clinical score, TEWL and skin inflammation) of AD compared to only OVA-induced mice. In addition, the levels of OVAspecific IgE and OVA-specific IgG1 in serum were significantly increased after the application of patulin with OVA. Furthermore, the exposure of patulin with OVA increased the skin expression of TSLP and IL-4 compared to only OVA-induced mice. CONCLUSIONS: The application of patulin aggravates symptoms and inflammation of AD. Exposure of mycotoxin might increases the inflammatory response in AD by systemic Th2 immunity via a TSLP dependent mechanism.
J ALLERGY CLIN IMMUNOL VOLUME 133, NUMBER 2
674
Early Skin Care By ''Experienced Mothers'' May Prevent Sensitization In Infants With Atopic Dermatitis Dr. Atsushi Yamashita, Dr. Mizuho Nagao, MD, Ms. Kanae Furuya, Dr. Junya Hirayama, Dr. Keigo Kainuma, MD, Dr. Takao Fujisawa, MD, FAAAAI; Institute for Clinical Research, Mie National Hospital. RATIONALE: Caregivers of infants with severe atopic dermatitis (AD) usually learn pivotal importance of skin care when they receive proper treatment and experience favorable outcome of AD by the treatment. Then, an ‘experienced’ mother tends to start skin care very early for her next child hoping to prevent bad outcome she went through with her first one. Since it has been suggested that epidermal barrier dysfunction in AD promotes allergen sensitization, we hypothesized that early skin care by ’experienced’ mothers may alleviate sensitization of infants with AD, possibly through protection of skin barrier function. METHODS: To investigate whether IgE sensitization levels to food and house dust mite (HDM) in AD infants of ‘experienced’ mothers are lower than those of ‘na€ıve’ mothers who first experienced AD in their child. Retrospective analysis of 55 infants with AD was performed. They were divided into 2 groups; 45 infants who were first-born children or had elder siblings without AD, designated as ‘na€ıve’ group and 10 infants who had elder siblings with severe AD, designated as ‘experienced’ group. RESULTS: Severity and age at initial presentation was higher in ‘na€ıve’ group than in ‘experienced’ group. Serum IgE, egg white-specific IgE and HDM-specific IgE levels from 6 months to 18 months old tended to be higher in ‘na€ıve’ group than in ‘experienced’ group. CONCLUSIONS: Early skin care presumably done by ‘experienced’ mothers may be beneficial to protect AD infants from ‘sensitization spreading’.
675
Association Of Bathing Habits To Pruritus and Allergic Disease Dr. Kanwaljit K. Brar, MD1, Dr. Rauno O. Joks, MD, FAAAAI2, Dr. Hamid Moallem, MD1; 1SUNY Downstate Medical Center, Brooklyn,
NY, 2Center for Allergy and Asthma Research, State University of New York Downstate Medical Center, Brooklyn, NY. RATIONALE: Traditionally, physicians have advised limiting bathing frequency and duration for patients with pruritis. Our patient population is primarily Afro-Caribbean immigrants, whose practice of frequent bathing to stave off heat persists after migration to the cooler climate of Brooklyn. We sought to evaluate for an association between bathing habits and pruritis in our adult allergy patients. We report preliminary data from our pilot study. METHODS: IRB approval was obtained, patients (n5 17) were recruited from the adult allergy clinic of University Hospital of Brooklyn, and King’s County Hospital. Our survey addressed demographics, bathing habits, medical, and environmental history. Bathing exposure time was determined by multiplying frequency of bathing with the duration of bath or shower. Pruritis was measured using a 5-D itch scale, a validated tool used to measure pruritis. Scores ranged from 5 (absent pruritis) to 25 (very severe pruritis). RESULTS: Among the 17 patients, 16 (94%) were female; 11 (65%) originated from the Caribbean Islands or South America. Average bath exposure time was 33 minutes/day. Patients who had a bath exposure time of greater than 10 minutes had a mean pruritis score of 12.75, compared with patients who had a bath exposure time of less than 10 minutes who had a mean pruritis score of 10. A correlation with bath exposure time and pruritis score was not found (p50.83). CONCLUSIONS: This is the first study to evaluate bathing habits and their association to pruritis. Bath exposure time is a novel method of quantifying bathing duration and bathing frequency.
676
A Molecular Mechanism Underlying Atopic Dermatitis In Hyper-IgE Syndrome Masako Saito, PhD1, Dr. Hajime Karasuyama, MD, PhD2, Dr. Yoshiyuki Minegishi, MD, PhD3; 1Division of Molecular Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan, 2Tokyo Medical and Dentistry Graduate School, Tokyo, Japan, 3Division of Molecular Medicine, Institute for Genome Research, The University of Tokushima. RATIONALE: Hyper-IgE syndrome (HIES) is a primary immunodeficiency characterized by extremely high serum IgE levels, atopic dermatitis, staphylococcal infections and eosinophilia. Dominant negative (DN) mutations in the STAT3 gene is a major genetic origin of the HIES. We recently established STAT3-DN knock-in mice, which did not develop atopic dermatitis spontaneously under SPF conditions. METHODS: Mice were sensitized with oxazolone (Ox) on day -6, and challenged every other day from day 0. Ear thickness was measured and cells recovered from the ear skin were evaluated immunologically. RESULTS: Ox-sensitized and challenged STAT3-DN mice showed significantly greater ear swelling after day 10 compared to STAT3-WT mice. More CD4+ T cells, eosinophils and basophils but less neutrophils were infiltrated in STAT3-DN mice compared to STAT3WT mice at day 15. STAT3-DN mice have significantly higher Oxspecific IgE levels compared to STAT3-WT mice. In the skin lesion, the expression of IFNg, IL-4, CXCL9, CCL17, CCL22, and CCL5 was increased in STAT3-DN mice. IFNg was predominantly expressed by CD4+ T cells, and IL-4 was expressed by basophils. CCL17 and CCL22 were expressed by DCs, and CXCL9 was expressed by CD45 negative cells. CCL5, which can recruit eosinophils, was expressed mainly by DCs. Although eosinophilia in HIES is considered to be associated with the development of atopic dermatitis, eosinophil deficient STAT3-DN mice showed equivalent ear swelling compared to eosinophil sufficient STAT3-DN mice. CONCLUSIONS: These results suggest that eosinophilia is not involved in the development of atopic dermatitis in HIES.
MONDAY
673
Mycotoxin Aggravates Atopic Dermatitis Via TSLP Induced Th2 Inflammation Ms. Seung-Hwa Lee1, Ms. Ha-Jung Kim1, Prof. Soo-Jong Hong, MD. PhD2,3; 1 Asan Institute for Life Sciences, University of Ulsan College of Medicine, 2 Department of Pediatrics, Asan Medical Center, Childhood Asthma Atopy Center, South Korea, 3Research Center for Standardization of Allergic Disease, University of Ulsan College of Medicine, Seoul, Korea. RATIONALE: Mycotoxins, secondary metabolites of molds, have an effect on impairment of immune system. The exposure of mycotoxin is associated with the development of atopic dermatitis (AD). However, the precise mechanisms of the allergy-promoting effect of mycotoxins remain unclear. This study was to investigate the effect of mycotoxin exposure on AD in a mouse model. METHODS: To investigate the effect of mycotoxin in AD, SKH-1 hairless mice were exposed via skin to patulin (mycotoxin) during ovalbumin (OVA) sensitization for developing the mouse model of AD. Evaluation of clinical signs (erythema), transepidermal water loss (TEWL), histopathology (H&E stain), and immunohistochemistry of TSLP and IL-4 on skin was performed. In addition, serum OVA-specific IgE and OVA-specific IgG1 were measured to confirm systemic immunization. RESULTS: Patulin exposure of OVA-induced mice exacerbated the phenotypes (e.g., clinical score, TEWL and skin inflammation) of AD compared to only OVA-induced mice. In addition, the levels of OVAspecific IgE and OVA-specific IgG1 in serum were significantly increased after the application of patulin with OVA. Furthermore, the exposure of patulin with OVA increased the skin expression of TSLP and IL-4 compared to only OVA-induced mice. CONCLUSIONS: The application of patulin aggravates symptoms and inflammation of AD. Exposure of mycotoxin might increases the inflammatory response in AD by systemic Th2 immunity via a TSLP dependent mechanism.