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1. Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study

Author

Yu Zhang, Li Hua, Quan-Hua Liu, Shu-Yuan Chu, Yue-Xin Gan, Min Wu, Yi-Xiao Bao, Qian Chen, and Jun Zhang

Subjects
Mold, Additive interaction, Rs7216389, Single nucleotide polymorphisms, Childhood asthma, Diseases of the respiratory system, RC705-779
Abstract

Abstract Background A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. Methods A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. Results After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. Conclusions In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma.

Published
2021
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2. WAO International Scientific Conference (WISC 2016) Abstracts

Author

Jun Bao, Yi-Hui Wang, Quan-Hua Liu, Yi-Xiao Bao, Nurit Azouz, Julie Caldwell, Leanne Ray, Mark Rochman, Melissa Mingler, Matthew Eilerman, Ting Wen, Jocelyn Biagini Myers, Gurjit Khurana Hershey, Leah Kottyan, Lisa Martin, Rothenberg Marc, Victor Gonzalez-Uribe, Jaime Del Rio-Chivardi, Blanca Del Rio-Navarro, Hongfei Lou, Siyuan Ma, Yan Zhao, Feifei Cao, Fei He, Zhongyan Liu, Chengshuo Wang, Claus Bachert, Luo Zhang, Elissa Abrams, Allan Becker, Amit Kandhare, Subhash Bodhankar, Nicole Grossman, Gheorghe Doros, Francine Laden, Anne Fuhlbrigge, Michael Wechsler, Wilson Pace, Barbara Yawn, Elliot Israel, Junehyuk Lee, Frederick Adler, Peter Kim, Yung Feng Huang, Ying Yao Chen, Chiun Yen Pan, Herng Sheng Lee, Michael Khalemsky, David G. Schwartz, Pavel Kolkhir, Dmitry Pogorelov, Nikolay Kochergin, Hirsh Komarow, Michael Young, Robin Eisch, Linda Scott, Dean Metcalfe, Alexander Singer, Andrew Wakeman, Thomas Gerstner, Woo-Jung Song, Ji-Su Shim, Ha-Kyeong Won, Sung-Yoon Kang, Kyoung-Hee Sohn, Byung-Keun Kim, Eun-Jung Jo, Min-Hye Kim, Sang-Heon Kim, Heung-Woo Park, Sun-Sin Kim, Yoon-Seok Chang, Alyn H. Morice, Byung-Jae Lee, Sang-Heon Cho, Kyung-Up Min, Maria Assunta Boscolo, Giulio Brivio, Sergio Bosisio, Nicoletta Manzocchi, Edoardo Pulixi, Giulia Grignani, Eloisia D’Andrea, Massimo Ricci, Elena Passini, Maurizio Italia, Marilyn Urrutia-Pereira, Stefani Fagundes, Vinicius Jardim Oliano, Dirceu Solé, Sadia Benzaquen, Alejandro Aragaki, Ricardo Balestra, Dawn Harden, Danielle Caudell-Stamper, Gilbert Glady, Mark Holbreich, Nataliya Lyakhovska, Igor Kaidashev, Jaromir Bystron, Beata Hutyrova, Galina Balakirski, Luk Vanstreels, Gerda Wurpts, Hans F. Merk, Jens Malte Baron, Johanna Plange, Hans-Peter Rihs, Monika Raulf, Stefani Roeseler, Alberto Tolcachier, Armando Chamorro, Ruth Otero, Joel Brooks, Michael Hess, Jared Benz, Joseph MacDonald, Usma Chatha, Dale Lent, Şükran Köse, Bengü Gireniz Tatar, Gülgün Akkoçlu, İbrahim Çukurova, İlker Ödemiş, Ayşin Kılınç Toker, Abdullahi Hasssan, Abdulrazaq Abdullahi Gobir, Cheol-Woo Kim, Young Hwa Choi, Jeong Hye Lee, Rae Jeong Cho, Yu Ran Nam, Joo Hyun Nam, Woo Kyung Kim, Ivana Filipovic, Zorica Zivkovic, Djordje Filipovic, Dana Shik, Andrew Smith, Wang Yui Hsi, Stuart Friedman, Yonatan Gizaw, Rima Bakhda, Kumail Mohammed, Richard Wasserman, Angela Hague, Deanna Pence, Joanna Rolen, Robert Sugerman, Stacy Silvers, Qurat Kamili, Nadezhda Knauer, Alexandr Zazernyi, Elena Blinova, Daria Demina, Vladimir Kozlov, Komal Agrawal, Sagar Kale, Naveen Arora, Volha Vasilkova, Tatiana Mokhort, William Silvers, Rachel Eisenberg, Rushita Mehta, Arye Rubinstein, Antony Aston, Paul Turner, Monica Ruiz-Garcia, Robert Boyle, Simon Brown, Yael Dinur Schejter, Adi Ovadia, Vy Kim, Brenda Reid, Chaim Roifman, Lana Rosenfield, Ernie Avilla, Laurie Harada, Marilyn Allen, Susan Waserman, Ho Joo Yoon, Gun Woo Koo, Suk-Il Chang, Hye-Ran Yoon, Dong Won Park, Tai Sun Park, Ji-Yong Moon, Tae Hyung Kim, Jang Won Sohn, Dong Ho Shin, Tsici Jorjoliani, Lia Jorjoliani, Nino Adamia, Nona katamadze, Deepika Ramachandra, Liana Jorjoliani, Rusudan Karseladze, Lali Saginadze, Natalia Chkuaseli, Anna Dolgova, Olga Stukolova, Anna Sudina, Anna Cherkashina, German Shipulin, Richard Rosenthal, Harvey Howe, Paul Knause, Rony Greemberg, Jean Jacques De Bruycker, Isabel Fernandez, Françoise Le Deist, Elie Haddad, Yeong Ho Rha, Kyung Suk Lee, Sun Hee Choi, Herman Tam, Estelle Simons, Elinor Simons, Maria Golebiowska-Wawrzyniak, Katarzyna Markiewicz, Yoram Faitelson, Miguel Stein, Avigdor Mandelberg, Ilan Dalal, Michael Levin, Lelani Hobane, Wisdom Basera, Maresa Botha, Claudia Gray, Heather Zar, Biserka Jovkovska Kjaeva, Zoran Arsovski, Vesna Grivcheva-Panovska, Adeyinka Odebode, Adedotun Adekunle, Peter Adeonipekun, Ebenezer Farombi, Nadezhda Camacho-Ordoñez, Alejandrina Josefina Martinez-Vázquez, María de la Luz H. García-Cruz, Qi Tan, Rui Min, Guan-qun Dai, Wei-Ping Xie, Huang Mao, Hong Wang, Rakesh Yadav, Sneha Singh, Divya Yadav, Ekaterina Khaleva, Henry T. Bahnson, Amber Franz, Lene Heise Garvey, Nicola Jay, Rubaiyat Haque, Adam Fox, Gideon Lack, George du Toit, Snezana Radic, Branislava Milenkovic, Ana Neskovic, Ljiljana Danojevic, Liat Nachshon, Michael Goldberg, Michael Levy, Yitzhak Katz, Arnon Elizur, Cristine Rosario, Juliana Kasper, Herbeto Chong-Neto, Carlos Riedi, Nelson Rosario, Michael B. Levy, Ronly Har-Even, Mor Carmel, Michael R. Goldberg, Maia Kherkheulidze, Nani Kavlashvili, Eka Kandelaki, Nino Adamai, Irma Ubiria, Andrea Burke, Monika Kastner, Denica Zheleva, Razvigor Darlenski, Konstantinos Bozinakis, Anastasios Kriebardis, Sofia Styliara, Aikaterini Karastathi, Nikolaos Farmakas, Maria Luiza Kraft Kohler Ribeiro, Ana Carolina Barcellos, Hannah Gabriele Ferreira Silva, Luís Henrique Mattei Carletto, Marcela Carolina Bet, Nathalia Zorze Rossetto, Nelson Augusto Rosario, Herberto Jose Chong-Neto, Fernanda Valença, Marina Novaes, Mariana Gomes, Carla Seifert, Alfredo Neto, Flavia Loyola, José Rios, Tatiana Silva, Aline Neves, Oznur Abadoglu, Bilun Gemicioglu, Hasan Bayram, Arif Cimrin, Levent Akyildiz, Aykut Cilli, Hakan Gunen, Tevfik Ozlu, Mecit Suerdem, Esra Uzaslan, Zeynep Misirligil, Snezana Ristic-Stojanovic, A. Milicevic, A. Milenkovic, Jelena Cvejic, Jelena Jankovic, Sanja Dimic-Janjic, Natasa Djurdjevic, Vladyslava Barzylovych, Tetiana Umanets, Anastasia Barzylovych, Karyn Winkler, Jessica Margarinos, Dylan Martin, Maja Nowakowski, Rauno Joks, Tsili Zangen, Olga Bernadsky, Mona Boaz, Gratiana Hermann, Rachel Aviv, Olga Kuperboim, Larisa Ramichanov, Efrat Broide, Raanan Shamir, Noam Zevit, Ron Shaoul, Alex Fich, Arie Levine, Isaac Melamed, Roopesh Singh Gangwar, Yael Minai-Fleminger, Mansour Seaf, Amichai Gutgold, Aarti Shikotra, Anoop Chauhan, Stephen Holgate, Peter Bradding, Peter Howarth, Ron Eliashar, Neville Berkman, Francesca Levi-Schaffer, Sung-il Woo, Betul Celik, Tangul Bulut, Arzu Didem Yalcin, Luiz Querino Caldas, Ronit Confino-Cohen, Yossi Rosman, Arnon Goldberg, Oded Breuer, Roopesh Singh, Ahlam Barhoum, Eitan Kerem, Tatiana Slavyanskaya, Revaz Sepiashvili, Elena A. Blinova, Ekaterina A. Pashkina, Marina I. Leonova, Vera M. Nepomnyaschikh, Darya V. Demina, Vladimir A. Kozlov, Revital Shamri, Kristen M. Young, Peter F. Weller, Rodolfo de Paula Vieira, Manoel Carneiro Oliveira-Junior, Nilsa Regina Damasceno-Rodrigues, Fernanda Magalhães Arantes-Costa, Milton Arruda Martins, Ana Paula Ligeiro Oliveira, Alfred Bernard, Antonia Sardella, Catherine Voisin, Simon Royce, Hamish Philpott, Sanjay Nandurkar, Francis Thien, Peter Gibson, Rodolfo Bianchini, Franziska Roth-Walter, Anna Ohradanova-Repic, Gerlinde Hofstetter, Ina Herrmann, Maria Isabel Carvalho, Karin Hufnagl, Erika Bajna, Georg Roth, Hannes Stockinger, Erika Jensen-Jarolim, Meital Almog, Aharon Kessel, Larisa Apov, Carlos Sanchez Salguero, Alvaro Sanchez Chacon, Abbos Nazarov, Shaxbos Ergashev, Irina Nesterova, Svetlana Kovaleva, Galina Chudilova, Ludmila Lomtatidze, Sarah De Schryver, Alizee Dery, Ann Clarke, Kari Nadeau, Kimberly Weatherall, Celia Greenwood, Denise Daley, Yuka Asai, Moshe Ben-Shoshan, Irina Balmasova, Elena Malova, Stefanie Wagner, Luis F. Pacios, Michael Wallner, Markus Wiederstein, Anna E. Tevs, Nataly Tataurshchikova, Baigalmaa Sangidorj, Anna Ronzhina, Manana Chikhladze, Oliver F. Wirz, Willem van de Veen, David Mirer, Hideaki Morita, Can Altunbulakli, Sebastian L. Johnston, Nicholas Glanville, Nikolaos G. Papadopoulos, Cezmi A. Akdis, Mübeccel Akdis, Avner Reshef, Marc Riedl, Vesna Grivcheva Panovska, Dumitru Moldovan, James Baker, William H. Yang, Sladjana Andrejevic, Richard F. Lockey, Roman Hakl, Shmuel Kivity, Luca Bellizzi, Joseph R. Harper, Anurag Relan, and Marco Cicardi

Subjects
Immunologic diseases. Allergy, RC581-607
Published
2017
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3. IL-13R130Q modulates human airway smooth muscle cell phenotype to contribute to severe asthma

Author

Yafang He, Qin Pan, Luanluan Li, Quanhua Liu, Yi-xiao Bao, and Jianhua Zhang

Abstract

Background A small percentage of asthma patients experience severe and refractory asthma that responds poorly to standard therapy. However, this percentage is increasing and better treatment options are therefore needed. Our previous study showed that cultured human airway smooth muscle cells treated with IL-13 R130Q, a naturally occurring IL-13 variant, displayed enhanced functional activities compared to wild-type (WT) IL-13. The present study aims to determine whether IL-13 R130Q could modulate the ASMC phenotype to further contribute to severe asthma. Methods Human bronchial smooth muscle cells (hBSMCs) were treated with increasing concentrations of IL-13R130Q or WT IL-13 for 24 h. Endogenous expressions of IL-5 and IL-4 were characterized with Enzyme-linked immunosorbent assay analysis. Acetylcholine-induced changes in intracellular calcium concentration were analyzed with the fluorescent probe Fluo-3/AM with flow-cytometric analysis. Cell proliferation was quantified using the CCK-8 kit and cell migration using the Boyden chamber assay. Results IL-13 R130Q induced significantly higher levels of proliferation, migration, and contraction, as well as secretion of IL-4 and IL-5 in hBSMCs compared to WT IL-13. Conclusions Taken all together, our data indicate that IL-13R130Q may contribute to severe asthma through phenotypic modulation of hBSMCs.

Published
2022
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6. Identification of IL13 C1923T as a Single Nucleotide Polymorphism for Asthma in Children from Mauritius

Author

Li Hua, Quan Hua Liu, Yi Xiao Bao, Ding Zhu Fang, Jing Yang Li, Kamleshun Ramphul, and Ruo Xu Ji

Subjects
Pulmonary and Respiratory Medicine, Genetics, education.field_of_study, business.industry, Population, Single-nucleotide polymorphism, Bioinformatics, medicine.disease, CHI3L1, respiratory tract diseases, Pediatrics, Perinatology and Child Health, Genotype, medicine, MS4A2, Immunology and Allergy, Population study, SNP, business, education, Original Research, Asthma
Abstract

Background: Research increasingly suggests that asthma is a familial and hereditary disorder and that genetic and environmental factors play a key role in its pathogenesis. Objective: The aim of this study was to investigate the associations between 10 single nucleotide polymorphism (SNP) loci in the development of asthma in children from the Mauritian population. Methods: The study population consisted of 193 children with asthma and 189 healthy controls from the Mauritian population. Asthma was diagnosed in accordance with the American Thoracic Society criteria. TaqMan real-time quantitative polymerase chain reaction was used to detect the genotypes of the SNP loci. Results: No statistically significant differences (p>0.05) were found between the experimental and control group in genotype distribution among nine of the loci (MS4A2 E237G, MS4A2 C-109T, ADRB2 R16G, IL4RA Q551R, IL4RA I75V, IL4 C-590T, IL13 A2044G, IL13 C-1112T, and CHI3L1 C-131G). However, the frequency of IL13 C1923T TT in the asthma gro...

Published
2015
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7. Clinical immunology Recombinant human interleukin receptor antagonist influences serum chemokines in patients with rheumatoid arthritis

Author

Jun Bao, Yi-Xiao Bao, and Wei Liu

Subjects
medicine.medical_specialty, medicine.drug_class, business.industry, Immunology, Antagonist, Arthritis, Interleukin, medicine.disease, Placebo, Receptor antagonist, Endocrinology, Interleukin 1 receptor antagonist, Internal medicine, Rheumatoid arthritis, medicine, Immunology and Allergy, Interleukin receptor, business
Abstract

Objective: To investigate the serum expressions of chemokines CCL2 and CCL3 in patients with rheumatoid arthritis (RA) who were treated with recombinant human interleukin 1 (IL-1) receptor antagonist (IL-1Ra). Material and methods: Serum CCL2 and CCL3 were determined using an enzyme-linked immunosorbent assay in 54 active RA patients before and after treatment with IL-1Ra or a placebo, as well as 36 healthy controls. Results: Compared with the healthy controls, all the 54 RA patients exhibited higher serum CCL2 and CCL3 before and after treatment (p < 0.05). However, patients who had a good response to IL-1Ra treatment had significantly lower mean changes in the serum CCL2 and CCL3 levels from baseline to the last injection than IL-1Ra non-responders (p < 0.01). Conclusions: CCL2 and CCL3 may be useful efficacy markers of IL-1Ra treatment.

Published
2014
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8. Atopy: a risk factor of refractory mycoplasma pneumoniae pneumonia?

Author

Yi-Xiao, Bao, Jing, Li, Ye, Tian, Quang-Hua, Liu, and Jun, Bao

Subjects
Hypersensitivity, Immediate, DNA Copy Number Variations, Tumor Necrosis Factor-alpha, Eosinophil Cationic Protein, Interleukin-8, Interferon-alpha, Immunoglobulin E, Bacterial Load, Anti-Bacterial Agents, Mycoplasma pneumoniae, Risk Factors, Child, Preschool, Pneumonia, Mycoplasma, Humans, Female, Interleukin-4, Macrolides, Child, Bronchoalveolar Lavage Fluid
Abstract

To investigate the relationship of pathogen DNA copies with clinic and laboratory features among children with Mycoplasma pneumoniae (MP) pneumonia.A total of 95 enrolled children with MP pneumonia were assigned into the high-MP-load group (10Compared with the low-MP-load group, 72.7% in the high-MP-load group developed refractory MP pneumonia who failed to respond to at least 1-week treatment with macrolides (72.7% vs 41.9%, P = 0.005). More children in the high-load group than those in the low-load group presented with extrapulmonary manifestations, lung consolidation, pleural effusion and atopic conditions including any allergy history, positive findings of aeroallergen test and increased serum IgE and ECP (P 0.05). A significant higher BALF IL-4 level was seen in the high-load group versus the low-load group (23.00 ± 11.24 vs 14.68 ± 7.12; pg/mL; P 0.01). There were no significant differences in BALF levels of IFN-γ, IL-8 and TNF-α between the two groups (P 0.05).Atopy may be a risk factor for the presence and severity of refractory MP pneumonia due to the high pathogen load in airway.

Published
2015

9. IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

Author

Yi Xiao Bao, Yohannes Tesfaigzi, Cynthia L. Rosenberger, Shan Ze Wang, Kevin S. Harrod, and James M. Stark

Subjects
CD3 Complex, medicine.medical_treatment, Immunology, Inflammation, Respiratory Syncytial Virus Infections, Virus, Interferon-gamma, Leukocyte Count, Mice, Th2 Cells, Immune system, Adjuvants, Immunologic, Neutralization Tests, Animals, Bronchiolitis, Viral, Immunology and Allergy, Medicine, Respiratory system, Antibodies, Blocking, Lung, Mice, Knockout, Mice, Inbred BALB C, Interleukin-12 Subunit p40, business.industry, Interleukin-18, Periodic Acid-Schiff Reaction, Viral Load, medicine.disease, Interleukin-12, Lymphocyte Subsets, Respiratory Syncytial Viruses, Up-Regulation, Mucus, Protein Subunits, medicine.anatomical_structure, Cytokine, Bronchiolitis, Cytokines, Alcian Blue, Inflammation Mediators, medicine.symptom, business, Bronchoalveolar Lavage Fluid, Viral load
Abstract

Respiratory syncytial virus-induced bronchiolitis has been linked to the development of allergy and atopic asthma. IL-12 and possibly IL-18 are central mediators orchestrating Th1 and/or Th2 immune responses to infection. To determine a possible role for IL-12 in regulating the immune response to acute respiratory syncytial virus infection, IL-12p40 gene-targeted (IL-12p40−/−) and wild-type mice were intratracheally infected with respiratory syncytial virus, and lung inflammatory and immune responses were assessed. Lung inflammation and mucus production were increased in the airways of IL-12p40−/− mice as compared with those of wild-type mice, concurrent with increased levels of the Th2 effector cytokines IL-5 and IL-13. Respiratory syncytial virus clearance and levels of Th1 effector cytokine IFN-γ were not altered. Interestingly, IL-18, another mediator of IFN-γ production, was significantly increased in the lungs of IL-12p40−/− mice early during the course of infection. Abrogation of IL-18-mediated signaling in IL-12p40−/− mice further enhanced Th2 immune response and mucus production in the airways during respiratory syncytial virus infection but failed to modulate IFN-γ production or viral clearance. These findings implicate a role for IL-12 and IL-18 in modulating respiratory syncytial virus-induced airway inflammation distinct from that of viral clearance.

Published
2004
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10. Clara Cell Secretory Protein Modulates Lung Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

Author

Kevin S. Harrod, Cynthia L. Rosenberger, Yi Xiao Bao, James M. Stark, and Shan Ze Wang

Subjects
Gene Expression Regulation, Viral, Lung Diseases, Chemokine, Neutrophils, viruses, Immunology, Inflammation, Respiratory Syncytial Virus Infections, Virus Replication, Virus, Mice, Mucoproteins, Th2 Cells, Immune system, Gene expression, medicine, Animals, Uteroglobin, Immunology and Allergy, Respiratory system, Mice, Knockout, Lung, biology, Airway Resistance, Proteins, Respiratory infection, Periodic Acid-Schiff Reaction, respiratory system, Respiratory Syncytial Viruses, respiratory tract diseases, medicine.anatomical_structure, biology.protein, Cytokines, Alcian Blue, Bronchial Hyperreactivity, Chemokines, medicine.symptom, Gene Deletion
Abstract

Clara cell secretory protein (CCSP) has been shown to have anti-inflammatory and immunomodulatory functions in the lung. Respiratory syncytial virus (RSV) is the most common cause of respiratory infection in infants and young children. RSV usually infects small airways and likely interacts with the Clara cells of bronchioles. To determine a possible role for CCSP during acute RSV infection, CCSP-deficient (CCSP−/−) and wild-type (WT) mice were intratracheally infected with RSV and the lung inflammatory and immune responses to RSV infection were assessed. RSV-F gene expression was increased in the lungs of CCSP−/− mice as compared with WT mice following RSV infection, consistent with increased viral persistence. Lung inflammation was significantly increased in CCSP−/− mice as compared with WT mice after infection. Moreover, although the levels of Th1 cytokines were similar, the levels of Th2 cytokines and neutrophil chemokines were increased in the lungs of CCSP−/− mice following infection. Physiologic endpoints of exacerbated lung disease, specifically airway reactivity and mucus production, were increased in CCSP−/− mice after RSV infection. Importantly, restoration of CCSP in the airways of CCSP−/− mice abrogated the increased viral persistence, lung inflammation, and airway reactivity. These findings suggest a role for CCSP and Clara cells in regulating lung inflammatory and immune responses to RSV infection.

Published
2003
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