Research

Maternal exposure to combustion generated PM inhibits pulmonary Th1 maturation and concomitantly enhances postnatal asthma development in offspring

Pingli Wang, Dahui You, Jordy Saravia, Huahao Shen and Stephania Cormier

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Particle and Fibre Toxicology 2013, 10:29 doi:10.1186/1743-8977-10-29

Published: 16 July 2013

Abstract (provisional)

Background

Epidemiological studies suggest that maternal exposure to environmental hazards, such as particulate matter, is associated with increased incidence of asthma in childhood. We hypothesized that maternal exposure to combustion derived ultrafine particles containing persistent free radicals (MCP230) disrupts the development of the infant immune system and results in aberrant immune responses to allergens and enhances asthma severity.

Methods

Pregnant C57/BL6 mice received MCP230 or saline by oropharyngeal aspiration on gestational days 10 and 17. Three days after the second administration, blood was collected from MCP230 or saline treated dams and 8-isoprostanes in the serum were measured to assess maternal oxidative stress. Pulmonary T cell populations were assayed in the infant mice at six days, three and six weeks of postnatal age. When the infant mice matured to adults (i.e. six weeks of age), an asthma model was established with ovalbumin (OVA). Airway inflammation, mucus production and airway hyperresponsiveness were then examined.

Results

Maternal exposure to MCP230 induced systemic oxidative stress. The development of pulmonary T helper (Th1/Th2/Th17) and T regulatory (Treg) cells were inhibited in the infant offspring from MCP230-exposed dams. As the offspring matured, the development of Th2 and Treg cells recovered and eventually became equivalent to that of offspring from non-exposed dams. However, Th1 and Th17 cells remained attenuated through 6 weeks of age. Following OVA sensitization and challenge, mice from MCP230-exposed dams exhibited greater airway hyperresponsiveness, eosinophilia and pulmonary Th2 responses compared to offspring from non-exposed dams.

Conclusions

Our data suggest that maternal exposure to MCP230 enhances postnatal asthma development in mice, which might be related to the inhibition of pulmonary Th1 maturation and systemic oxidative stress in the dams.

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Prevention and Control of Noncommunicable Diseases - Guidelines for Primary Health Care in Low Resource Settings

Bookshelf ID: NBK148622PMID: 23844451

Prevention and Control of Noncommunicable Diseases

Guidelines for Primary Health Care in Low Resource Settings

Geneva: World Health Organization; 2012.

ISBN-13: 978-92-4-154839-7

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Overview

These guidelines provide recommendations on the diagnosis and management of type 2 diabetes and the management of asthma and chronic obstructive pulmonary disease in primary health care in low-resource settings. The target users are health care professionals responsible for developing the protocols which will be used by health care staff in primary care units in low-resource settings.

Contents

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• Acknowledgments
• Why do we need these guidelines?
• I. Diagnosis and management of type 2 diabetes in primary health care in low-resource settings
  • Abbreviations
  • 1. Executive Summary
  • 2. Background
  • 3. Objectives and target audience
  • 4. Funding and declarations of interest
  • 5. Methodology and process
    • Scope of the guideline
  • 6. Adaptation and implementation
  • 7. Update
  • 8. Format and dissemination
  • 9. Impact and quality of the guideline
  • 10. Recommendations and evidence
    • A Diagnosing diabetes
    • B Glycaemic control
    • C Reducing the risk of cardiovascular disease and diabetic nephropathy
    • D Prevention of lower limb amputations
    • E Prevention of blindness
    • F Severe hypoglycaemia
    • G Hyperglycaemic emergencies
  • Reference List
  • Annex 1 Systematic reviews and GRADE tables
  • Annex 2 Benefits and harms of recommendations
  • Members of the guideline development group
• II. Management of Asthma and Chronic Obstructive Pulmonary Disease in primary health care in low-resource settings
  • Abbreviations
  • 1. Executive summary
  • 2. Recommendations
    • Management of stable asthma
    • Management of exacerbation of asthma
    • Management of stable COPD
    • Management of exacerbation of COPD
  • 3. Methodology used to prepare the guideline
    • Identification of important outcomes
    • Search strategy, selection criteria, data collection and judgement
  • Annex 3 PICOT questions
  • Annex 4 Grade tables
  • Annex 5 Search strategies
  • Annex 6 References (systematic reviews)
  • Annex 7 Summary of recommendations
  • Members of the Guideline Development Committee
• Simplified tools for implementation of the guidelines
• Other WHO documents on Prevention and Control of Noncommunicable Diseases

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The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.

The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.

All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either expressed or implied. The responsibility for the interpretation and use of the material lies with the reader. In no event shall the World Health Organization be liable for damages arising from its use.

Copyright © 2012, World Health Organization.

All rights reserved. Publications of the World Health Organization are available on the WHO web site (www.who.int) or can be purchased from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: bookorders@who.int).

Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press through the WHO web site (http://www.who.int/about/licensing/copyright_form/en/index.html).

• PLoS One
• v.8(7); 2013
• PMC3700929

PLoS One. 2013; 8(7): e68473.

Published online 2013 July 3. doi:  10.1371/journal.pone.0068473

PMCID: PMC3700929

A Twin Study of Early-Childhood Asthma in Puerto Ricans

Supinda Bunyavanich,#1,2,3,4,5,* Judy L. Silberg,#6 Jessica Lasky-Su,4,5 Nathan A. Gillespie,7,8 Nancy E. Lange,4,5Glorisa Canino,9 and Juan C. Celedόn10,11,12

Andrew Dewan, Editor

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Abstract

Background

The relative contributions of genetics and environment to asthma in Hispanics or to asthma in children younger than 3 years are not well understood.

Objective

To examine the relative contributions of genetics and environment to early-childhood asthma by performing a longitudinal twin study of asthma in Puerto Rican children ≤3 years old.

Methods

678 twin infants from the Puerto Rico Neo-Natal Twin Registry were assessed for asthma at age 1 year, with follow-up data obtained for 624 twins at age 3 years. Zygosity was determined by DNA microsatellite profiling. Structural equation modeling was performed for three phenotypes at ages 1 and 3 years: physician-diagnosed asthma, asthma medication use in the past year, and ≥1 hospitalization for asthma in the past year. Models were additionally adjusted for early-life environmental tobacco smoke exposure, sex, and age.

Results

The prevalences of physician-diagnosed asthma, asthma medication use, and hospitalization for asthma were 11.6%, 10.8%, 4.9% at age 1 year, and 34.1%, 40.1%, and 8.5% at 3 years, respectively. Shared environmental effects contributed to the majority of variance in susceptibility to physician-diagnosed asthma and asthma medication use in the first year of life (84%–86%), while genetic effects drove variance in all phenotypes (45%–65%) at age 3 years. Early-life environmental tobacco smoke, sex, and age contributed to variance in susceptibility.

Conclusion

Our longitudinal study in Puerto Rican twins demonstrates a changing contribution of shared environmental effects to liability for physician-diagnosed asthma and asthma medication use between ages 1 and 3 years. Early-life environmental tobacco smoke reduction could markedly reduce asthma morbidity in young Puerto Rican children.

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Pivotal Roles of T-Helper 17-Related Cytokines, IL-17, IL-22, and IL-23, in Inflammatory Diseases

Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 968549, 13 pages
http://dx.doi.org/10.1155/2013/968549

Review Article

Pivotal Roles of T-Helper 17-Related Cytokines, IL-17, IL-22, and IL-23, in Inflammatory Diseases

Ning Qu,¹ Mingli Xu,² Izuru Mizoguchi,³ Jun-ichi Furusawa,³ Kotaro Kaneko,³ Kazunori Watanabe,³ Junichiro Mizuguchi,⁴ Masahiro Itoh,¹Yutaka Kawakami,² and Takayuki Yoshimoto³

¹Department of Anatomy, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402, Japan
²Division of Cellular Signaling, Institute for Advanced Medical Research School of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
³Department of Immunoregulation, Institute of Medical Science, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo160-8402, Japan
⁴Department of Immunology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402, Japan

Received 12 April 2013; Accepted 25 June 2013

Academic Editor: William O’Connor Jr.

Copyright © 2013 Ning Qu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

T-helper 17 (Th17) cells are characterized by producing interleukin-17 (IL-17, also called IL-17A), IL-17F, IL-21, and IL-22 and potentially TNF-α and IL-6 upon certain stimulation. IL-23, which promotes Th17 cell development, as well as IL-17 and IL-22 produced by the Th17 cells plays essential roles in various inflammatory diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, colitis, and Concanavalin A-induced hepatitis. In this review, we summarize the characteristics of the functional role of Th17 cells, with particular focus on the Th17 cell-related cytokines such as IL-17, IL-22, and IL-23, in mouse models and human inflammatory diseases.

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The Interplay between the Bone and the Immune System

Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 720504, 16 pages
http://dx.doi.org/10.1155/2013/720504

Review Article

The Interplay between the Bone and the Immune System

Giorgio Mori,¹ Patrizia D'Amelio,² Roberta Faccio,³ and Giacomina Brunetti⁴

¹Department of Clinical and Experimental Medicine, University of Foggia, 71100 Foggia, Italy
²Department of Medical Sciences, University of Torino, 10126 Torino, Italy
³Department of Orthopedics, Washington University School of Medicine, St. Louis, MO 63110, USA
⁴Department of Basic Medical Sciences, Neurosciences and Sense Organs, Section of Human Anatomy and Histology, University of Bari, Piazza Giulio Cesare, 11, 70124 Bari, Italy

Received 1 March 2013; Accepted 7 June 2013

Academic Editor: Enrico Maggi

Copyright © 2013 Giorgio Mori et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In the last two decades, numerous scientists have highlighted the interactions between bone and immune cells as well as their overlapping regulatory mechanisms. For example, osteoclasts, the bone-resorbing cells, are derived from the same myeloid precursor cells that give rise to macrophages and myeloid dendritic cells. On the other hand, osteoblasts, the bone-forming cells, regulate hematopoietic stem cell niches from which all blood and immune cells are derived. Furthermore, many of the soluble mediators of immune cells, including cytokines and growth factors, regulate the activities of osteoblasts and osteoclasts. This increased recognition of the complex interactions between the immune system and bone led to the development of the interdisciplinary osteoimmunology field. Research in this field has great potential to provide a better understanding of the pathogenesis of several diseases affecting both the bone and immune systems, thus providing the molecular basis for novel therapeutic strategies. In these review, we reported the latest findings about the reciprocal regulation of bone and immune cells.

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The Role of the Immune System in Huntington’s Disease

Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 541259, 11 pages
http://dx.doi.org/10.1155/2013/541259

Review Article

The Role of the Immune System in Huntington’s Disease

Gisa Ellrichmann,¹ Christiane Reick,^1,2 Carsten Saft,¹ and Ralf A. Linker³

¹Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany
²International Graduate School of Neuroscience, Ruhr-University Bochum, 44791 Bochum, Germany
³Department of Neurology, Friedrich-Alexander-University Erlangen, 91054 Erlangen, Germany

Received 3 April 2013; Accepted 19 June 2013

Academic Editor: Dan Frenkel

Copyright © 2013 Gisa Ellrichmann et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Huntington’s disease (HD) is characterized by a progressive course of disease until death 15–20 years after the first symptoms occur and is caused by a mutation with expanded CAG repeats in the huntingtin (htt) protein. Mutant htt (mhtt) in the striatum is assumed to be the main reason for neurodegeneration. Knowledge about pathophysiology has rapidly improved discussing influences of excitotoxicity, mitochondrial damage, free radicals, and inflammatory mechanisms. Both innate and adaptive immune systems may play an important role in HD. Activation of microglia with expression of proinflammatory cytokines, impaired migration of macrophages, and deposition of complement factors in the striatum indicate an activation of the innate immune system. As part of the adaptive immune system, dendritic cells (DCs) prime T-cell responses secreting inflammatory mediators. In HD, DCs may contain mhtt which brings the adaptive immune system into the focus of interest. These data underline an increasing interest in the peripheral immune system for pathomechanisms of HD. It is still unclear if neuroinflammation is a reactive process or if there is an active influence on disease progression. Further understanding the influence of inflammation in HD using mouse models may open various avenues for promising therapeutic approaches aiming at slowing disease progression or forestalling onset of disease.

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OPEN ACCESS PEER-REVIEWED

RESEARCH ARTICLE

Influenza Vaccination in Adults with Chronic Obstructive Pulmonary Disease: The Impact of a Diagnostic Breathing Test on Vaccination Rates

• Dana S. Mowls,
 
• Vinay K. Cheruvu,
 
• Melissa D. Zullo 

Abstract

Introduction

Influenza vaccination rates are low in adults with chronic obstructive pulmonary disease (COPD). A diagnostic breathing test in adults with COPD may increase vaccination rates; however, research has not demonstrated this relationship. The purpose of this research was to determine if adults with COPD diagnosed by a breathing test were more likely to have had an influenza vaccination during the past 12 months when compared to those with COPD diagnosed without a breathing test.

Methods

This was a cross-sectional study using data from the 2011 Behavioral Risk Factor Surveillance System. Logistic regression examined the relationship between influenza vaccination among adults with COPD diagnosed with a breathing test (n = 13,201) compared to those diagnosed without a breathing test (n = 3,108), after controlling for all potential confounders.

Results

Overall, 49% of respondents with COPD received an influenza vaccination within the past 12 months and 78% reported their COPD was diagnosed by a breathing test. The prevalence of influenza vaccination in the past 12 months was greater in those with COPD diagnosed by a breathing test (53%) compared to those diagnosed without a breathing test (36%). In adjusted analysis, adults with COPD who had a breathing test were 31% (confidence interval 1.1, 1.6) more likely to have received an influenza vaccination in the past 12 months compared to those without a breathing test.

Discussion

A diagnostic breathing test for COPD was associated with increased likelihood of having had an influenza vaccination in the past 12 months. This may be an indicator of the relationship between knowledge of lung function and the need for preventative care, a sign of quality healthcare, or good health-seeking behaviors in patients with COPD. This research is the first to use a nationally representative sample to suggest that spirometry diagnosis of COPD may increase rates of influenza vaccination.

Citation: Mowls DS, Cheruvu VK, Zullo MD (2013) Influenza Vaccination in Adults with Chronic Obstructive Pulmonary Disease: The Impact of a Diagnostic Breathing Test on Vaccination Rates. PLoS ONE 8(6): e67600. doi:10.1371/journal.pone.0067600

Editor: Stephen J. Turner, University of Melbourne, Australia

Received: January 23, 2013; Accepted: May 20, 2013; Published: June 28, 2013

Copyright: © 2013 Mowls et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors have no support or funding to report.

Competing interests: The authors have declared that no competing interests exist.

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