11^th International Conference on Allergy, Asthma & Clinical Immunology September 07-08, 2017 Edinburgh, Scotland

Biography:

Professor Jamil received his medical degree from Baghdad University. He holds several postgraduate degrees from England. In 1979 joined Baghdad University, then in 1998 joined Wayne State University and in 2015 joined Michigan State University. He has published 20 books and 191 field research articles. He is one of the founders of "The International Society of Iraqi Scientists" in 2000 and “The AlNahrain International Society of Iraqi Scientists in 2017. Elected in 2002 as President of International Society of Iraqi Scientists until 2015. Professor Jamil received the Teacher Award from Wayne State University in 2006, 2010 and in 2013. 

Abstract:

Background: Gulf war 1991 (GW) syndrome is defined as a group of illnesses including allergy. Although it has been over than two decades since GW, more research is needed to address the impact of GW chemical (Ch) & GW non-chemical (NCh) environmental exposures on the health of Iraqis. The Ch & NCh are the two main etiologies that could explain the high rate of medical conditions, including allergy. However, in 2015, 30 % of adults & 40 % of children in the US reported allergy.

Objective: (1) To examines the prevalence rate of allergy among the study population at different war zone location, (2) To predict risk factors for each type of allergy studied, and self-rated health of Study population, (3) To explore the impact of Ch & NCh agents on different types of allergy & its relation to war zone location.

Methods: In 2002, a cross-sectional study of 1155 Iraqis males, age 18-45, who were residents within 300 Km from GW-1991 were studied. Resident physicians from Basrah University, were trained to implement a structured interview with the participants. The study population were those who accompanied the patients who attend any of the three government outpatient clinics at two provinces general hospitals, which are free of charge to all people. The study population were classified into three zones according to their location during the GW: war zone (Within 100 Km of Kuwait), zone 2 (within 100-190 Km) & zone 3 (within 200-300 km). The study questionnaires include different types of Allergy and the participants was asked to answer yes or no for the following allergies: (1) pre-asthma symptoms (2) rhinitis (3) skin allergy (4) eye allergy (5) chemical sensitivity allergy and (6) other allergy (could be food, drug etc.). For Ch exposures, participants were asked if during the GW they had direct contact with certain exposures: E.g. petrochemical fuel. For NCh exposures the questions included: E.g. missiles exploding. Different statistical tests were used through SPS version 22.

Results: Study results showed a significant difference in the prevalence of allergies (combined or separated) except for eye allergy by different zones (higher in war zone). Regarding type of allergies, the highest rate was rhinitis (36.2%) and the lowest was chemical sensitivities (2.4%). There was difference in the prevalence rate of allergy when testing their demographic variables at different war zones (higher at war zones). The results identified the predictor risk factors for each type of allergy, in which some of them were related to Ch or NCh. 22.1% of the study population who lived in war zones reported their current health was fair to poor, compared to 8.6% among those who were in zone 3.

Conclusion: There were significant differences between the location of participants during the GW-1991 in relation to different types of allergies. Those who reported excellent heath were: younger age, less years in army, hold high school or above, labor work, never smoke, have low scale of allergy and did not exposed to Ch or NCh.

Biography:

Anil Mishra is a Professor of Medicine. He is also the Director of Tulane Eosinophilic Disorder Center in the Section of Pulmonary Diseases at Tulane University School of Medicine. His research established that eosinophils are the resident cells of the gastrointestinal tract that home prenatally. He showed that eosinophil active chemokine eotaxin-1 constitutively expressed and has significant role for eosinophils homing into the gastrointestinal tract. He developed the first murine model of eosinophilic esophagitis (EoE). His findings implicated aeroallergen in the etiology of EoE and suggested that esophageal eosinophilic inflammation is mechanistically associated with pulmonary inflammation. Recently, he reported that rIL-15 is a therapeutic molecule for the allergen-induced airway hyperactivity and fibrosis for chronic asthma and other pulmonary functional impairment. He is an elected fellow of American Academy of Allergy Asthma Immunology (FAAAAI) and American Gastrointestinal Association (FAGA). He has published over 72 articles, book chapters and reviews on molecular mechanisms of pulmonary and gastrointestinal allergic responses in high impact factor journals. His research is supported by National Institutes of Health via NIDDK and NIAID institutes. He is also a member of several NIH study sections and serving as Editor and Editorial Board Member in a number of international journals.

Abstract:

Allergen-induced airway obstruction is a physiologic feature of asthma and IL-15 deficiency is reported in asthmatic patients. Therefore, we tested the hypothesis that regulation of IL-15 is critical for the preservation of allergen-induced airway hyper responsiveness (AHR), airway resistance and compliance. Accordingly, airway inflammation, AHR, resistance and compliance were assessed in IL-15- gene deficient mice and IL-15 overexpressing mice in an allergen-induced murine model of asthma. Herein, we report that IL-15 deficiency promotes baseline airway resistance in naïve mice. Moreover, rIL-15 delivery to the lung down regulates expression of proinflammatory cytokines, and improves allergen-induced AHR, resistance and compliance. These observations were further validated in DOX-inducible CC-10-IL-15 transgenic mice. DOX exposed Aspergillus extract challenged CC-10-IL-15 bi-transgenic mice exhibited significantly reduced levels of pro inflammatory cytokines (IL-4, IL-5, IL-13) and decreased goblet cell hyperplasia. Airway obstruction including AHR and resistance was diminished in allergen challenged DOX exposed mice compared to non-DOX exposed CC-10-IL-15 bi-transgenic mice. Mechanistically, we observed that IL-15-mediated protection of airway obstruction is associated with induced IL-10-producing regulatory CD4⁺CD25⁺Foxp3⁺ T cells. Additionally, we found that a human IL-15 agonist (ALT-803) improved airway resistance and compliance in an experimental asthma model. Taken together, our studies conclude that IL-15 has a potent inhibitory effect on the airway obstruction that occurs in response to environmental allergens.