http://www.clinicalmolecularallergy.com The most accessed research articles published by Clinical and Molecular Allergy 2012-01-04T00:00:00Z In Asian countries where the Buddhism and Taoism are mainstream religions, incense burning is a daily practice. A typical composition of stick incense consists of 21% (by weight) of herbal and wood powder, 35% of fragrance material, 11% of adhesive powder, and 33% of bamboo stick. Incense smoke (fumes) contains particulate matter (PM), gas products and many organic compounds. On average, incense burning produces particulates greater than 45 mg/g burned as compared to 10 mg/g burned for cigarettes. The gas products from burning incense include CO, CO2, NO2, SO2, and others. Incense burning also produces volatile organic compounds, such as benzene, toluene, and xylenes, as well as aldehydes and polycyclic aromatic hydrocarbons (PAHs). The air pollution in and around various temples has been documented to have harmful effects on health. When incense smoke pollutants are inhaled, they cause respiratory system dysfunction. Incense smoke is a risk factor for elevated cord blood IgE levels and has been indicated to cause allergic contact dermatitis. Incense smoke also has been associated with neoplasm and extracts of particulate matter from incense smoke are found to be mutagenic in the Ames Salmonella test with TA98 and activation. In order to prevent airway disease and other health problem, it is advisable that people should reduce the exposure time when they worship at the temple with heavy incense smokes, and ventilate their house when they burn incense at home. http://www.clinicalmolecularallergy.com/content/6/1/3 Ta-Chang Lin Guha Krishnaswamy David Chi Clinical and Molecular Allergy 2008, null:3 2008-04-25T00:00:00Z doi:10.1186/1476-7961-6-3 Health risks posed by incense smoke Incense burning in Buddhist and Taoist temples is regular practice, however inhalation of incense gas products can cause respiratory disease and other health problems, so worshippers are advised to reduce exposure times, and ventilate their houses when they burn incense at home. /content/figures/1476-7961-6-3-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 3 2008-04-25T00:00:00Z XML Autoimmune progesterone dermatitis (APD) is a condition in which the menstrual cycle is associated with a number of skin findings such as urticaria, eczema, angioedema, and others. In affected women, it occurs 3–10 days prior to the onset of menstrual flow, and resolves 2 days into menses. Women with irregular menses may not have this clear correlation, and therefore may be missed. We present a case of APD in a woman with irregular menses and urticaria/angioedema for over 20 years, who had not been diagnosed or correctly treated due to the variable timing of skin manifestations and menses. In addition, we review the medical literature in regards to clinical features, pathogenesis, diagnosis, and treatment options. http://www.clinicalmolecularallergy.com/content/2/1/10 Alan Baptist James Baldwin Clinical and Molecular Allergy 2004, null:10 2004-08-02T00:00:00Z doi:10.1186/1476-7961-2-10 /content/figures/1476-7961-2-10-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 10 2004-08-02T00:00:00Z XML Tinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. The practicing allergist may be called upon to treat this disease for various reasons. Sometimes tinea infection may be mistaken for atopic dermatitis or allergic eczema. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease. Patients with recurrent cellulitis may be referred to the allergist/immunologist for an immune evaluation and discovered to have tinea pedis as a predisposing factor. From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Very often, protracted topical and/or oral antifungal agents are required to treat this often frustrating and morbid disease. An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease. http://www.clinicalmolecularallergy.com/content/2/1/5 Muhannad Al Hasan S. Matthew Fitzgerald Mahnaz Saoudian Guha Krishnaswamy Clinical and Molecular Allergy 2004, null:5 2004-03-29T00:00:00Z doi:10.1186/1476-7961-2-5 /content/figures/1476-7961-2-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2004-03-29T00:00:00Z XML Background: Cow's milk allergy is one of the most common food allergies among younger children. We investigated IgE antibodies to milk, and IgE and IgG4 antibodies to casein, alpha-lactalbumin and beta-lactoglobulin in cow's milk allergic (CMA) and non-allergic (non-CMA) children in order to study their clinical usefulness. Methods: Eighty-three children with suspected milk allergy (median age: 3.5 years, range: 0.8-15.8 years) were diagnosed as CMA (n=61) or non-CMA (n=22) based on an open milk challenge or convincing clinical history. Their serum concentrations of allergen-specific (s) IgE and IgG4 antibodies were measured using ImmunoCAP. For the sIgG4 analysis, 28 atopic and 31 non-atopic control children were additionally included (all non-milk sensitized). Results: The CMA group had significantly higher levels of milk-, casein- and beta-lactoglobulin-sIgE antibodies as compared to the non-CMA group. The casein test showed the best discriminating performance with a clinical decision point of 6.6 kUA/L corresponding to 100% specificity. All but one of the CMA children aged >5 years had casein-sIgE levels >6.6 kUA/L. The non-CMA group had significantly higher sIgG4 levels against all three milk allergens compared to the CMA group. This was most pronounced for casein-sIgG4 in non-CMA children without history of previous milk allergy. These children had significantly higher casein-sIgG4 levels compared to any other group, including the non-milk sensitized control children. Conclusions: High levels of casein-sIgE antibodies are strongly associated with milk allergy in children and might be associated with prolonged allergy. Elevated casein-sIgG4 levels in milk-sensitized individuals on normal diet indicate a modified Th2 response. However, the protective role of IgG4 antibodies in milk allergy is unclear. http://www.clinicalmolecularallergy.com/content/10/1/1 Komei Ito Masaki Futamura Robert Moverare Akira Tanaka Tsutomu Kawabe Tatsuo Sakamoto Magnus Borres Clinical and Molecular Allergy 2012, null:1 2012-01-02T00:00:00Z doi:10.1186/1476-7961-10-1 /content/figures/1476-7961-10-1-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 1 2012-01-02T00:00:00Z PDF Chronic Granulomatous Disease is the most commonly encountered immunodeficiency involving the phagocyte, and is characterized by repeated infections with bacterial and fungal pathogens, as well as the formation of granulomas in tissue. The disease is the result of a disorder of the NADPH oxidase system, culminating in an inability of the phagocyte to generate superoxide, leading to the defective killing of pathogenic organisms. This can lead to infections with Staphylococcus aureus, Psedomonas species, Nocardia species, and fungi (such as Aspergillus species and Candida albicans). Involvement of vital or large organs can contribute to morbidity and/or mortality in the affected patients. Major advances have occurred in the diagnosis and treatment of this disease, with the potential for gene therapy or stem cell transplantation looming on the horizon. http://www.clinicalmolecularallergy.com/content/9/1/10 EunKyung Song Gayatri Jaishankar Hana Saleh Warit Jithpratuk Ryan Sahni Guha Krishnaswamy Clinical and Molecular Allergy 2011, null:10 2011-05-31T00:00:00Z doi:10.1186/1476-7961-9-10 /content/figures/1476-7961-9-10-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 10 2011-05-31T00:00:00Z XML Macrolides, a class of antimicrobials isolated from Streptomycetes more than 50 years ago, are used extensively to treat sinopulmonary infections in humans. In addition, a growing body of experimental and clinical evidence indicates that long-term (years), low (sub-antimicrobial)-dose 14- and 15-membered ring macrolide antibiotics, such as erythromycin, clarithromycin, roxithromycin and azithromycin, express immunomodulatory and tissue reparative effects that are distinct from their anti-infective properties. These salutary effects are operative in various lung disorders, including diffuse panbronchiolitis, cystic fibrosis, persistent chronic rhinosinusitis, nasal polyposis, bronchiectasis, asthma and cryptogenic organizing pneumonia.The purpose of this overview is to outline the immunomodulatory effects of macrolide antibiotics in patients with asthma. http://www.clinicalmolecularallergy.com/content/2/1/4 Umur Hatipoglu Israel Rubinstein Clinical and Molecular Allergy 2004, null:4 2004-03-16T00:00:00Z doi:10.1186/1476-7961-2-4 /content/figures/1476-7961-2-4-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 4 2004-03-16T00:00:00Z XML Dysregulated immune response results in inflammatory symptoms in the respiratory mucosa leading to asthma and allergy in susceptible individuals. The T helper type 2 (Th2) subsets are primarily involved in this disease process. Nevertheless, there is growing evidence in support of T cells with regulatory potential that operates in non-allergic individuals. These regulatory T cells occur naturally are called natural T regulatory cells (nTregs) and express the transcription factor Foxp3. They are selected in the thymus and move to the periphery. The CD4 Th cells in the periphery can be induced to become regulatory T cells and hence called induced or adaptive T regulatory cells. These cells can make IL-10 or TGF-b or both, by which they attain most of their suppressive activity. This review gives an overview of the regulatory T cells, their role in allergic diseases and explores possible interventionist approaches to manipulate Tregs for achieving therapeutic goals. http://www.clinicalmolecularallergy.com/content/7/1/5 Subhadra Nandakumar Christopher Miller Uday Kumaraguru Clinical and Molecular Allergy 2009, null:5 2009-03-12T00:00:00Z doi:10.1186/1476-7961-7-5 /content/figures/1476-7961-7-5-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 5 2009-03-12T00:00:00Z XML ObjectiveThe phenomena manifested during inflammation require interplay between circulating effector cells, local resident cells, soluble mediators and genetic host factors to establish, develop and maintain itself. Of the molecues involed in the initiation and perpetuation of acute allergic inflammation in asthma, the involvement of effector cells in redox reactions for producing O2- (superoxide anion) through the mediation of NADPH oxidase is a critical step. Prior data suggest that reactive oxygen species (ROS) produced by NADPH oxidase homologues in non-phagocytic cells play an important role in the regulation of signal transduction, while macrophages use a membrane-associated NADPH oxidase to generate an array of oxidizing intermediates which inactivate MMPs on or near them.Materials and Methods and TreatmentTo clarify the role of gp91phox subunit of NADPH oxidase in the development and progression of an acute allergic asthma phenotype, we induced allergen dependent inflammation in a gp91phox-/- single knockout and a gp91phox-/-MMP-12-/- double knockout mouse models. Results: In the knockout mice, both inflammation and airway hyperreactivity were more extensive than in wildtype mice post-OVA. Although OVA-specific IgE in plasma were comparable in wildtype and knockout mice, enhanced inflammatory cell recruitment from circulation and cytokine release in lung and BALf, accompanied by higher airway resistance as well as Penh in response to methacholine, indicate a regulatory role for NADPH oxidase in development of allergic asthma. While T cell mediated functions like Th2 cytokine secretion, and proliferation to OVA were upregulated synchronous with the overall robustness of the asthma phenotype, macrophage upregulation in functions such as proliferation, and mixed lymphocyte reaction indicate a regulatory role for gp91phox and an overall non-involvement or synergistic involvement of MMP12 in the response pathway (comparing data from gp91phox-/- and gp91phox-/-MMP-12-/- mice). http://www.clinicalmolecularallergy.com/content/10/1/2 Ena Ray Banerjee William Henderson Clinical and Molecular Allergy 2012, null:2 2012-01-04T00:00:00Z doi:10.1186/1476-7961-10-2 /content/figures/1476-7961-10-2-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 2 2012-01-04T00:00:00Z XML A 25-year-old, with type I Diabetes Mellitus with a previous diagnosis of Protamine Allergy but not to human Insulin, started to notice anaphylactic reactions inmmediatly after bolus with Insulin. Skin prick and intradermal test were positive to all insulins. Skin tests to other potential allergens resulted negative. Examination after bolus of Human Insulin revealed urticaria. Daily insulin requirement were around 2-2,4 U/Kg/day. Slow desensitisation with Aspart insulin, the insulin with lowest size of skin test, was performed using subcutaneous insulin pump. Six months after the end of desensitisation his daily insulin requirement decreased to 0.8 U/Kg/day and oral corticosteroids are being reduced with no symptoms. http://www.clinicalmolecularallergy.com/content/3/1/16 Victor Matheu Eva Perez Marta Hernandez Elisa Diaz Ricardo Darias Inmaculada Sanchez Abel Gonzalez Jose Garcia Laura Feliciano Agueda Caballero Fernando de la Torre Clinical and Molecular Allergy 2005, null:16 2005-12-23T00:00:00Z doi:10.1186/1476-7961-3-16 /content/figures/1476-7961-3-16-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 16 2005-12-23T00:00:00Z XML Asthma belongs to the category of classical allergic diseases which generally arise due to IgE mediated hypersensitivity to environmental triggers. Since its prevalence is very high in developed or urbanized societies it is also referred to as "disease of civilizations". Due to its increased prevalence among related individuals, it was understood quite long back that it is a genetic disorder. Well designed epidemiological studies reinforced these views. The advent of modern biological technology saw further refinements in our understanding of genetics of asthma and led to the realization that asthma is not a disorder with simple Mendelian mode of inheritance but a multifactorial disorder of the airways brought about by complex interaction between genetic and environmental factors. Current asthma research has witnessed evidences that are compelling researchers to redefine asthma altogether. Although no consensus exists among workers regarding its definition, it seems obvious that several pathologies, all affecting the airways, have been clubbed into one common category called asthma. Needless to say, genetic studies have led from the front in bringing about these transformations. Genomics, molecular biology, immunology and other interrelated disciplines have unearthed data that has changed the way we think about asthma now. In this review, we center our discussions on genetic basis of asthma; the molecular mechanisms involved in its pathogenesis. Taking cue from the existing data we would briefly ponder over the future directions that should improve our understanding of asthma pathogenesis. http://www.clinicalmolecularallergy.com/content/7/1/7 Amrendra Kumar Balaram Ghosh Clinical and Molecular Allergy 2009, null:7 2009-05-06T00:00:00Z doi:10.1186/1476-7961-7-7 /content/figures/1476-7961-7-7-toc.gif Clinical and Molecular Allergy 1476-7961 ${item.volume} 7 2009-05-06T00:00:00Z XML