Adrenomedullin mediates pro-angiogenic and pro-inflammatory cytokines in asthma and COPD.

PURPOSE: Adrenomedullin (AM) is a pluripotent peptide hormone with contradictory effects in human health and disease. In chronic inflammatory lung diseases, such as asthma and COPD, AM has been shown to inhibit inflammation and cell proliferation. In the present study, we aimed to investigate the effect of AM on pro-angiogenic and pro-inflammatory cytokines in asthma and COPD. PATIENTS AND METHODS: Serum levels of pro-AM were measured in patients with asthma, COPD and matched controls. The effect of AM on intracellular signaling proteins and cytokine secretion was assessed in primary cultures of epithelial cells (EC) and airway smooth muscle cells (ASMC) established from endo-bronchial biopsies of patients with asthma, COPD and controls. RESULTS: Serum pro-AM was higher in patients with asthma and COPD, compared to controls. AM stimulated cAMP in ASMC but not in EC. In EC, AM decreased Erk1/2 MAPK expression and activation but in ASMC, AM activated Erk1/2. This effect was similar in asthma, COPD and controls. AM stimulated the secretion of pro-angiogenic CXCL1 by EC of controls and CXCL5 by EC of asthma patients. AM did not affect the secretion of IL-6 or IL-8 by EC but stimulated the secretion of IL-6 by ASMC. In EC, AM inhibited the stimulatory effect of TGF-ß and IL-4 on the secretion of IL-6 and IL-8 but had an additive stimulatory effect with TGF-ß in ASMC. CONCLUSIONS: These data suggest that AM mediates the secretion of pro-angiogenic and pro-inflammatory cytokines in a cell-type and/or a disease-specific way, explaining its association with clinical outcomes in COPD.

Treatment with long acting muscarinic antagonists stimulates serum levels of irisin in patients with COPD.

Long acting muscarinic antagonists (LAMA) are currently considered the therapeutic mainstay for patients with COPD and have been shown to improve clinical outcomes including symptoms, exercise capacity and airflow limitation. Irisin, is a newly discovered hormone-like myokine generated by skeletal muscle cells in response to exercise and it is suggested to regulate energy expenditure and exercise capacity. The aim of the present study was to investigate if treatment with LAMA alters serum irisin levels in patients with COPD. Irisin was assessed by ELISA in the serum of 506 patients with COPD, GOLD II-IV, with a smoking history >10 PY, who were included in the PROMISE-COPD cohort. The effect of inhaled LAMA on serum irisin levels was evaluated in a proof-of-concept cohort of 40 COPD patients. Univariate linear regression analysis revealed that there was a significant negative association of irisin with age-adjusted Charlson score (p = 0.003) and a positive association of irisin with 6-min walking distance (6MWD) (p = 0.018) and treatment with LAMA (p = 0.004) but not with LABA or ICS. Multivariate analysis revealed that the association of irisin with LAMA treatment remains significant after adjustment for age-adjusted score and 6MWD. In the proof-of-concept cohort a single inhalation of LAMA stimulated serum irisin levels after 4 h. These findings imply that treatment of COPD patients with LAMA increase circulating irisin, thus explaining some of the beneficial extra-pulmonary effects of these drugs when used in the treatment of COPD.

IFNΛ3/4 locus polymorphisms and IFNΛ3 circulating levels are associated with COPD severity and outcomes.

BACKGROUND: Interferon lambdas (IFNLs) have important anti-viral/bacterial and immunomodulatory functions in the respiratory tract. How do IFNLs impact COPD and its exacerbations? METHODS: Five hundred twenty eight patients were recruited in a prospective observational multicentre cohort (PROMISE) study. The genetic polymorphisms (rs8099917 and rs12979860) within the IFNL3/4 gene region and circulating levels of IFNL3 in COPD patients were determined and associated with disease activity and outcome during a median follow-up of 24 months. RESULTS: The GG genotype significantly influenced severe exacerbation rate (42 vs. 23%; p = 0.032) and time to severe exacerbation (HR = 2.260; p = 0.012). Compared to the TT or TG genotypes, the GG genotype was associated with severe dyspnoea (modified medical research council score ≥ median 3; 22 vs 42%, p = 0.030). The CC genotype of the rs12979860 SNP was associated with a poorer prognosis (body mass index, airflow obstruction, dyspnea and exercise capacity index ≥ median 4; 46 vs. 36% TC vs. 20.5% TT; p = 0.031). Patients with stable COPD and at exacerbation had significantly lower circulating IFNL3 compared to healthy controls (p < 0.001 and p < 0.001, respectively). Circulating IFNL3 correlated to post-bronchodilator FEV1%predicted and the tissue maturation biomarker Pro-collagen 3. CONCLUSION: IFNL3/4 polymorphisms and circulating IFNL3 may be associated with disease activity and outcomes in COPD. TRIAL REGISTRATION: Clinical Trial registration http://www.isrctn.com/ identifier ISRCTN99586989 on 16 April 2008.

Constitutive high expression of protein arginine methyltransferase 1 in asthmatic airway smooth muscle cells is caused by reduced microRNA-19a expression and leads to enhanced remodeling.

BACKGROUND: In asthma remodeling airway smooth muscle cells (ASMCs) contribute to airway wall thickness through increased proliferation, migration, and extracellular matrix deposition. Previously, we described that protein arginine methyltransferase 1 (PRMT1) participates in airway remodeling in pulmonary inflammation in E3 rats. OBJECTIVE: We sought to define the asthma-specific regulatory mechanism of PRMT1 in human ASMCs. METHODS: ASMCs from healthy subjects and asthmatic patients were activated with platelet-derived growth factor (PDGF)-BB. PRMT1 was localized by means of immunohistochemistry in human lung tissue sections and by means of immunofluorescence in isolated ASMCs. PRMT1 activity was suppressed by the pan-PRMT inhibitor AMI-1, signal transducer and activator of transcription 1 (STAT1) was suppressed by small interfering RNA, and extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein kinase (MAPK) was suppressed by PD98059. MicroRNAs (miRs) were assessed by using real-time quantitative PCR and regulated by miR mimics or inhibitors. RESULTS: PRMT1 expression was significantly increased in lung tissue sections and in isolated ASMCs of patients with severe asthma. PDGF-BB significantly increased PRMT1 expression through ERK1/2 MAPK and STAT1 signaling in control ASMCs, whereas in ASMCs from asthmatic patients, these proteins were constitutively expressed. ASMCs from asthmatic patients had reduced miR-19a expression, causing upregulation of ERK1/2 MAPK, STAT1, and PRMT1. Inhibition of PRMT1 abrogated collagen type I and fibronectin deposition, cell proliferation, and migration of ASMCs from asthmatic patients. CONCLUSIONS: PRMT1 is a central regulator of tissue remodeling in ASMCs from asthmatic patients through the pathway: PDGF-BB-miR-19a-ERK1/2 MAPK and STAT1. Low miR-19a expression in ASMCs from asthmatic patients is the key event that results in constitutive increased PRMT1 expression and remodeling. Therefore PRMT1 is an attractive target to limit airway wall remodeling in asthmatic patients.

Mannose-binding lectin protein and its association to clinical outcomes in COPD: a longitudinal study.

BACKGROUND: Functional deficiency of mannose-binding lectin (MBL) may contribute to the pathogenesis of chronic obstructive pulmonary disease. We hypothesized that specific MBL2 gene polymorphisms and circulating MBL protein levels are associated with clinically relevant outcomes in the Predicting Outcome using systemic Markers In Severe Exacerbations of COPD PROMISE-COPD cohort. METHODS: We followed 277 patients with stable COPD GOLD stage II-IV COPD over a median period of 733 days (IQR 641-767) taking survival as the primary outcome parameter. Patients were dichotomized as frequent (≥ 2 AECOPD/year) or infrequent exacerbators. Serum MBL levels and single nucleotide polymorphisms of the MBL2 gene were assessed at baseline. RESULTS: The MBL2-HYPD haplotype was significantly more prevalent in frequent exacerbators (OR: 3.33; 95% CI, 1.24-7.14, p = 0.01). The median serum MBL concentration was similar in frequent (607 ng/ml, [IQR; 363.0-896.0 ng/ml]) and infrequent exacerbators (615 ng/ml, [IQR; 371.0-942.0 ng/ml]). Serum MBL was not associated with lung function characteristics or bacterial colonization in sputum. However, high serum MBL at stable state was associated with better survival compared to low MBL (p = 0.046, log rank test). CONCLUSIONS: In COPD, the HYPD haplotype of MBL2 gene is associated with frequent exacerbations and high serum MBL is linked to increased survival. The PROMISE-COPD study was registered at www.controlled-trials.com under the identifier ISRCTN99586989.

Longitudinal Measurement of Serum Vascular Endothelial Growth Factor in Patients with Chronic Obstructive Pulmonary Disease.

BACKGROUND: Impaired vascular endothelial growth factor (VEGF) signaling causes emphysema in animal models. In chronic obstructive pulmonary disease (COPD) patients, alterations in VEGF tissue expression have been observed. We hypothesize that circulating VEGF may be a biomarker to phenotype COPD patients. OBJECTIVE: The aim of this study was to investigate VEGF serum levels in stable and exacerbated COPD. METHODS: VEGF serum levels as well as parameters of short- and long-term outcome were assessed and analyzed in two COPD cohorts [PROMISE, n = 117; ProCOLD (PC), n = 191]. RESULTS: VEGF serum levels at stable COPD were neither related to forced expiratory volume in 1 s nor to the Modified Medical Research Council dyspnea score, 6-min walking distance or BODE index. There was no association between single VEGF levels and COPD exacerbation frequency or mortality at 1 and 2 years of follow-up. In PC an increase in VEGF over time (ΔVEGF) was associated with the exacerbation frequency as well as the 1- and 2-year hospitalization rate (p = 0.046, 0.009 and 0.006, respectively). Furthermore, in PC ΔVEGF was associated with 1- and 2-year survival (p = 0.009 and 0.041, respectively). CONCLUSIONS: Single serum VEGF levels, at stable and exacerbated COPD, were not associated with clinically significant outcomes in COPD. Conversely, the VEGF course seems related to COPD prognosis.

Vasoactive Intestinal Peptide for Diagnosing Exacerbation in Chronic Obstructive Pulmonary Disease.

BACKGROUND: Vasoactive intestinal peptide (VIP) is the most abundant neuropeptide in the lung. VIP has been linked to pulmonary arterial hypertension and hypoxia. OBJECTIVES: We aimed to assess circulating VIP levels at exacerbation and at stable chronic obstructive pulmonary disease (COPD) and to evaluate the diagnostic performance in a well-characterized cohort of COPD patients. METHODS: The nested cohort study included patients with Global Initiative for Chronic Obstructive Lung Disease stage II-IV. Patients were examined at stable state and at acute exacerbation of COPD (AE-COPD), and dedicated serum was collected at both conditions. Serum VIP levels were determined by enzyme-linked immunosorbent assay. Diagnostic accuracy was analyzed by receiver operating characteristic curve and area under the curve (AUC). RESULTS: Patients with acute exacerbation (n = 120) and stable COPD (n = 163) had similar characteristics at baseline. Serum VIP levels did not correlate with oxygen saturation at rest (p = 0.722) or at exercise (p = 0.168). Serum VIP levels were significantly higher at AE-COPD (130.25 pg/ml, 95% CI 112.19-151.83) as compared to stable COPD (40.07 pg/ml, 95% CI 37.13-43.96, p < 0.001). The association of increased serum VIP with AE-COPD remained significant after propensity score matching (p < 0.001). Analysis of the Youden index indicated the optimal serum VIP cutoff value as 56.6 pg/ml. The probability of AE-COPD was very low if serum VIP was ≤35 pg/ml (sensitivity >90%) and very high if serum VIP was ≥88 pg/ml (specificity >90%). Serum VIP levels presented a robust performance to diagnose AE-COPD (AUC 0.849, 95% CI 0.779-0.899). CONCLUSIONS: Increased serum VIP levels are associated with AE-COPD.

Anti-fibrotic effects of nintedanib in lung fibroblasts derived from patients with idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis. The kinase inhibitor nintedanib specific for vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and fibroblast growth factor receptor (FGFR) significantly reduced the rate of decline of forced vital capacity versus placebo. AIM: To determine the in vitro effect of nintedanib on primary human lung fibroblasts. METHODS: Fibroblasts were isolated from lungs of IPF patients and from non-fibrotic controls. We assessed the effect of VEGF, PDGF-BB and basic FGF (bFGF) ± nintedanib on: (i) expression/activation of VEGFR, PDGFR, and FGFR, (ii) cell proliferation, secretion of (iii) matrix metalloproteinases (MMP), (iv) tissue inhibitor of metalloproteinase (TIMP), and (v) collagen. RESULTS: IPF fibroblasts expressed higher levels of PDGFR and FGFR than controls. PDGF-BB, bFGF, and VEGF caused a pro-proliferative effect which was prevented by nintedanib. Nintedanib enhanced the expression of pro-MMP-2, and inhibited the expression of TIMP-2. Transforming growth factor-beta-induced secretion of collagens was inhibited by nintedanib. CONCLUSION: Our data demonstrate a significant anti-fibrotic effect of nintedanib in IPF fibroblasts. This effect consists of the drug's anti-proliferative capacity, and on its effect on the extracellular matrix, the degradation of which seems to be enhanced.

Distribution and identification of culturable airborne microorganisms in a Swiss milk processing facility.

Airborne communities (mainly bacteria) were sampled and characterized (concentration levels and diversity) at 1 outdoor and 6 indoor sites within a Swiss dairy production facility. Air samples were collected on 2 sampling dates in different seasons, one in February and one in July 2012 using impaction bioaerosol samplers. After cultivation, isolates were identified by mass spectrometry (matrix-assisted laser desorption/ionization-time-of-flight) and molecular (sequencing of 16S rRNA and rpoB genes) methods. In general, total airborne particle loads and total bacterial counts were higher in winter than in summer, but remained constant within each indoor sampling site at both sampling times (February and July). Bacterial numbers were generally very low (<100 cfu/m(3) of air) during the different steps of milk powder production. Elevated bacterial concentrations (with mean values of 391 ± 142 and 179 ± 33 cfu/m(3) of air during winter and summer sampling, respectively; n=15) occurred mainly in the "logistics area," where products in closed tins are packed in secondary packaging material and prepared for shipping. However, total bacterial counts at the outdoor site varied, with a 5- to 6-fold higher concentration observed in winter compared with summer. Twenty-five gram-positive and gram-negative genera were identified as part of the airborne microflora, with Bacillus and Staphylococcus being the most frequent genera identified. Overall, the culturable microflora community showed a composition typical and representative for the specific location. Bacterial counts were highly correlated with total airborne particles in the size range 1 to 5 µm, indicating that a simple surveillance system based upon counting of airborne particles could be implemented. The data generated in this study could be used to evaluate the effectiveness of the dairy plant's sanitation program and to identify potential sources of airborne contamination, resulting in increased food safety.

Aerobiological, clinical, and immunobiochemical studies on Alstonia scholaris pollen from Eastern India.

Alstonia scholaris or Indian devil tree is a common, evergreen, tropical tree of the Apocynaceae family. The objectives of this study were (a) to observe the seasonal variation of A. scholaris pollen in the atmosphere of an industrial and rural area of West Bengal, India by conducting a 2-year aerobiological survey with a Burkard personal volumetric sampler, (b) to study its allergenicity in the local population by in vivo (skin-prick test) and in vitro tests (enzyme-linked immunosorbent assay and dot blotting), (c) to identify the immunoglobulin E (IgE)-binding proteins present in the pollen extract (sodium dodecyl sulphate-polyacrylamide gel electrophoresis and immunoblotting), (d) to study its chemical composition. A. scholaris pollen were present in the air from September until November. They contained 14.3 % carbohydrate, 9.2 % lipid, and 4.3 % protein. Among 140 respiratory allergic local patients, 28.57 % showed positive skin reaction to A. scholaris pollen extract. Twelve protein bands in the range of 94.4-13.3 kDa were observed in the pollen extract. Seven IgE-binding proteins were found. Among them, one component of 29.9 kDa was the most important in A. scholaris pollen extract. This component could be purified and would be helpful in the diagnosis and therapy of A. scholaris pollen-susceptible patients.

Airborne load of Cassia pollen in West Bengal, eastern India: its atmospheric variation and health impact.

A Burkard personal volumetric sampler was used at Sriniketan, a town about 150 km northwest of Calcutta, in the state of West Bengal, in eastern India to record the frequency of three common airborne Cassia pollen types, Cassia tora, Cassia occidentalis, and Cassia fistula for two consecutive years (2004-2006). Correlation was made between the meteorological factors and the pollen concentration in the atmosphere. The study reports Cassia pollinosis by in vivo skin prick test in respiratory allergic patients. The highest positive reactions were exhibited by C. tora (34.7 %), C. fistula (33.3 %), and C. occidentalis (28.5 %). The allergic potential of these was investigated by in vitro enzyme linked immunosorbent assay test. Their protein components were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, in the range of 15.8-81.5 kDa. In C. occidentalis and C. fistula, 11 bands were found, while it was 10 in C. tora. The results show that the Cassia pollen occur significantly in the atmosphere with the potential to elicit an allergic response in susceptible patients.

Clinical and immunobiochemical characterization of airborne Peltophorum pterocarpum (yellow gulmohar tree) pollen: a dominant avenue tree of India.

BACKGROUND: Peltophorum pterocarpum (yellow gulmohar, PP) pollen is an important aeroallergen for type I hypersensitivity in the tropics. OBJECTIVE: To isolate and characterize the IgE-binding proteins of PP pollen for the first time. METHODS: Pollen extract was fractionated by a combination of Sephacryl S-200 column and diethylaminoethyl-Sephadex column. Allergen characterization was done by sodium dodecyl sulphate polyacrylamide gel electrophoresis, periodic acid-Schiff staining, enzyme-linked immunosorbent assay, and western blotting. Allergenic activities were determined by in vivo (skin prick test) and in vitro (enzyme-linked immunosorbent assay and histamine release) analyses. To determine whether the carbohydrate chains are involved in immunoreactivity, deglycosylation of PP pollen proteins was performed. RESULTS: SPT results on the respiratory allergic patients of Calcutta showed that 32.77% showed positivity with PP pollen. Eight IgE-reactive protein components were found in crude extract. Optimum IgE-reactive fraction 1 was resolved into five subfractions. The subfraction 1a showed maximum IgE reactivity containing the 28 kDa IgE-reactive component. Periodate oxidation showed that protein component was involved in its IgE binding. Twenty-eight kilodalton IgE reactive protein component was recognized by 75% of PP-sensitive patients in Western blotting. It also induced significant histamine release in sensitive patient sera. CONCLUSIONS: The purified 28 kDa protein is a clinically relevant allergen with a potential for diagnosis and therapy of patients susceptible to PP pollen.

Clinico-immunochemical studies on airborne Areca catechu L. Pollen, a probable risk factor in emergency asthma hospitalization from Eastern India.

BACKGROUND: The pollen grain of the Areca catechu L. tree is airborne and allergenic. This study aimed to know the role of this pollen as a source of aeroallergen with effect on emergency asthma hospitalization, to isolate its important allergic fraction and to check its cross-reaction with betel nut. METHODS: Areca pollen was monitored with a Burkard sampler. Determination of allergenic activities was studied by in vivo and in vitro analyses. Asthma hospitalization data were collected from two nearby hospitals. The pollen extract was fractionated by a combination of DEAE-Sephadex and Sephacryl S-200 column. The protein components were observed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Cross-reactivity of Areca pollen and betel nut was shown by IgE enzyme-linked immunosorbent assay (ELISA) inhibition. RESULTS: The Areca pollen was perennially airborne. Skin test results of respiratory allergic patients showed 38.6% positivity. The detected aeroallergen spots in particle immunoblotting correlated significantly with airborne pollen count. Areca pollen showed a significant positive correlation with asthma hospitalization. There are 6 IgE-reactive protein components in the whole-pollen extract. IgE-reactive fraction 1 was resolved into 4 subfractions. Subfraction 1a showing IgE reactivity contained 3 protein components, among which 2 of 48 and 118 kDa were IgE reactive. The 48-kDa component was reported to be cross-reactive with other palm pollen types. In IgE ELISA inhibition, the betel nut extract showed 50% inhibition with about 110 ng/ml concentration. CONCLUSION: A. catechu pollen is a significant contributor to the aeroallergen load in India. Its partially purified IgE-reactive fraction may be useful in therapeutics. The betel nut extract showed remarkable cross-reactivity with Areca pollen.

PDGF-BB induces PRMT1 expression through ERK1/2 dependent STAT1 activation and regulates remodeling in primary human lung fibroblasts.

Tissue remodeling of sub-epithelial mesenchymal cells is a major pathology occurring in chronic obstructive pulmonary disease (COPD) and asthma. Fibroblasts, as a major source of interstitial connective tissue extracellular matrix, contribute to the fibrotic and inflammatory changes in these airways diseases. Previously, we described that protein arginine methyltransferase-1 (PRMT1) participates in airway remodeling in a rat model of pulmonary inflammation. In this study we investigated the mechanism by which PDGF-BB regulates PRMT1 in primary lung fibroblasts, isolated from human lung biopsies. Fibroblasts were stimulated with PDGF-BB for up-to 48h and the regulatory and activation of signaling pathways controlling PRMT1 expression were determined. PRMT1 was localized by immuno-histochemistry in human lung tissue sections and by immunofluorescence in isolated fibroblasts. PRMT1 activity was suppressed by the pan-PRMT inhibitor AMI1. ERK1/2 mitogen activated protein kinase (MAPK) was blocked by PD98059, p38 MAPK by SB203580, and STAT1 by small interference (si) RNA treatment. The results showed that PDGF-BB significantly increased PRMT1 expression after 1h lasting over 48h, through ERK1/2 MAPK and STAT1 signaling. The inhibition of ERK1/2 MAPK or of PRMT1 activity decreased PDGF-BB induced fibroblast proliferation, COX2 production, collagen-1A1 secretion, and fibronectin production. These findings suggest that PRMT1 is a central regulator of tissue remodeling and that the signaling sequence controlling its expression in primary human lung fibroblast is PDGF-ERK-STAT1. Therefore, PRMT1 presents a novel therapeutic and diagnostic target for the control of airway wall remodeling in chronic lung diseases.

Clinical and immunobiochemical characterization of airborne Delonix regia (Gulmohar tree) pollen and cross-reactivity studies with Peltophorum pterocarpum pollen: 2 dominant avenue trees from eastern India.

BACKGROUND: Delonix regia and Peltophorum pterocarpum pollen are important aeroallergens for type 1 hypersensitivity in the tropics. The IgE-binding proteins of D regia and their cross-allergenity with P pterocarpum pollen have not been evaluated. OBJECTIVES: To isolate and characterize the IgE-binding proteins of D regia pollen for the first time and to investigate the cross-allergenity with P pterocarpum pollen belonging to the same family (Leguminosae). METHODS: Allergenic activities were determined by in vivo and in vitro analyses. Pollen extract was fractionated by a combination of 2 columns (diethyl amino ethyl Sephadex and Sephacryl S-200). Protein components were characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, periodic acid-Schiff staining, and immunoblotting. In vitro inhibition tests were performed to evaluate the cross-reactivity. RESULTS: The skin prick test results of the patients with respiratory allergies in Calcutta, India, showed 31.1% positivity with D regia pollen. Nine IgE-reactive protein components were found in the crude extract. An optimum IgE-reactive fraction was resolved into 4 subfractions. Subfraction A, which showed maximum IgE reactivity, contained 2 (96- and 66-kDa) IgE-reactive protein components. The 66-kDa component was found to be glycoprotein. Remarkable cross-reactivity between D regia and P pterocarpum pollen was found on IgE enzyme-linked immunosorbent assay inhibition and dot blotting. Shared IgE-binding components (66, 56, 32, 28, 25, and 23 kDa) were observed between D regia and P pterocarpum pollen extracts, whereas the 96- and 43-kDa components were specific to D regia. CONCLUSION: The purification of the IgE-binding proteins and the identification of the shared/cross-reactive proteins in these taxonomically related pollen members should be helpful for the diagnosis and therapy of patients susceptible to these pollens.

Immediate hypersensitivity to common food allergens: an investigation on food sensitization in respiratory allergic patients of calcutta, India.

BACKGROUND: : Food allergy may be defined as an immunoglobulin E-mediated immune response to food proteins. Such studies have previously not been done in Calcutta, India. The present study was therefore undertaken to record the sensitivity to commonly consumed foods in patients with allergic rhinitis and asthma. MATERIALS AND METHODS: : A survey of 800 patients (410 males and 390 females) reporting to the Allergy Unit of the Institute of Child Health, Calcutta, were selected for the study conducted from May 2006 to April 2007. Respiratory allergic patients in the age group of 5 to 60 years were evaluated using a standard questionnaire, and skin prick test was performed using common food and aeroallergens. RESULTS/CONCLUSIONS: : Out of the 684 patients with a history of food allergy, most of them, that is, 338, are in the age group 16 to 40 years, 192 of them were in the age group 41 to 60 years, and 154 were in the age group 5 to 15 years. Most of the patients with food allergy had asthma (65.05%), rhinitis and asthma (20.03%), and skin allergies (4.97%), such as itching, eczema, and urticaria. The foodstuffs that were found to elicit symptoms of hypersensitivity were egg, milk, wheat, pulses, vegetables, fishes, and fruits.The patients aged between 16 and 40 years (male-female ratio, 1:1.19) were mostly sensitive to prawn, brinjal, banana, ladyfinger, papaya, wheat, and egg. The age group 41 to 60 years (male-female ratio, 1:1.04) had high skin reactivity to brinjal, egg, banana, fish, and Phaseolus mungo. Patients younger than 16 years (male-female ratio, 1:1.33) were sensitized to brinjal, prawn, banana, spinach, and egg. We observed that food hypersensitivity also reflects different genetic factors and variations in cultural and dietary habits of each individual.