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      Maternal exposure to air pollution before and during pregnancy related to changes in newborn's cord blood lymphocyte subpopulations. The EDEN study cohort

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          Abstract

          Background

          Toxicants can cross the placenta and expose the developing fetus to chemical contamination leading to possible adverse health effects, by potentially inducing alterations in immune competence. Our aim was to investigate the impacts of maternal exposure to air pollution before and during pregnancy on newborn's immune system.

          Methods

          Exposure to background particulate matter less than 10 μm in diameter (PM 10) and nitrogen dioxide (NO 2) was assessed in 370 women three months before and during pregnancy using monitoring stations. Personal exposure to four volatile organic compounds (VOCs) was measured in a subsample of 56 non-smoking women with a diffusive air sampler during the second trimester of pregnancy. Cord blood was analyzed at birth by multi-parameter flow cytometry to determine lymphocyte subsets.

          Results

          Among other immunophenotypic changes in cord blood, decreases in the CD4+CD25+ T-cell percentage of 0.82% (p = 0.01), 0.71% (p = 0.04), 0.88% (p = 0.02), and 0.59% (p = 0.04) for a 10 μg/m 3 increase in PM 10 levels three months before and during the first, second and third trimester of pregnancy, respectively, were observed after adjusting for confounders. A similar decrease in CD4+CD25+ T-cell percentage was observed in association with personal exposure to benzene. A similar trend was observed between NO 2 exposure and CD4+CD25+ T-cell percentage; however the association was stronger between NO 2 exposure and an increased percentage of CD8+ T-cells.

          Conclusions

          These data suggest that maternal exposure to air pollution before and during pregnancy may alter the immune competence in offspring thus increasing the child's risk of developing health conditions later in life, including asthma and allergies.

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          CD4+CD25high regulatory cells in human peripheral blood.

          Andrew Allan, David A. Hafler, Emery Brown … (2001)
          Thymectomy in mice on neonatal day 3 leads to the development of multiorgan autoimmune disease due to loss of a CD(+)CD25(+) T cell regulatory population in their peripheral lymphoid tissues. Here, we report the identification of a CD4(+) population of regulatory T cells in the circulation of humans expressing high levels of CD25 that exhibit in vitro characteristics identical with those of the CD4(+)CD25(+) regulatory cells isolated in mice. With TCR cross-linking, CD4(+)CD25(high) cells did not proliferate but instead totally inhibited proliferation and cytokine secretion by activated CD4(+)CD25(-) responder T cells in a contact-dependent manner. The CD4(+)CD25(high) regulatory T cells expressed high levels of CD45RO but not CD45RA, akin to the expression of CD45RB(low) on murine CD4(+)CD25(+) regulatory cells. Increasing the strength of signal by providing either costimulation with CD28 cross-linking or the addition of IL-2 to a maximal anti-CD3 stimulus resulted in a modest induction of proliferation and the loss of observable suppression in cocultures of CD4(+)CD25(high) regulatory cells and CD4(+)CD25(-) responder cells. Whereas higher ratios of CD4(+)CD25(high) T cells are required to suppress proliferation if the PD-L1 receptor is blocked, regulatory cell function is shown to persist in the absence of the PD-1/PD-L1 or CTLA-4/B7 pathway. Thus, regulatory CD4 T cells expressing high levels of the IL-2 receptor are present in humans, providing the opportunity to determine whether alterations of these populations of T cells are involved in the induction of human autoimmune disorders.
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            Immune Responses in Healthy and Allergic Individuals Are Characterized by a Fine Balance between Allergen-specific T Regulatory 1 and T Helper 2 Cells

            Mubeccel Akdis, Johan Verhagen, Alison Taylor … (2004)
            The mechanisms by which immune responses to nonpathogenic environmental antigens lead to either allergy or nonharmful immunity are unknown. Single allergen-specific T cells constitute a very small fraction of the whole CD4+ T cell repertoire and can be isolated from the peripheral blood of humans according to their cytokine profile. Freshly purified interferon-γ–, interleukin (IL)-4–, and IL-10–producing allergen-specific CD4+ T cells display characteristics of T helper cell (Th)1-, Th2-, and T regulatory (Tr)1–like cells, respectively. Tr1 cells consistently represent the dominant subset specific for common environmental allergens in healthy individuals; in contrast, there is a high frequency of allergen-specific IL-4–secreting T cells in allergic individuals. Tr1 cells use multiple suppressive mechanisms, IL-10 and TGF-β as secreted cytokines, and cytotoxic T lymphocyte antigen 4 and programmed death 1 as surface molecules. Healthy and allergic individuals exhibit all three allergen-specific subsets in different proportions, indicating that a change in the dominant subset may lead to allergy development or recovery. Accordingly, blocking the suppressor activity of Tr1 cells or increasing Th2 cell frequency enhances allergen-specific Th2 cell activation ex vivo. These results indicate that the balance between allergen-specific Tr1 cells and Th2 cells may be decisive in the development of allergy.
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              Barrier Capacity of Human Placenta for Nanosized Materials

              Peter Wick, Antoine Malek, Pius Manser … (2009)
              Background Humans have been exposed to fine and ultrafine particles throughout their history. Since the Industrial Revolution, sources, doses, and types of nanoparticles have changed dramatically. In the last decade, the rapidly developing field of nanotechnology has led to an increase of engineered nanoparticles with novel physical and chemical properties. Regardless of whether this exposure is unintended or not, a careful assessment of possible adverse effects is needed. A large number of projects have been carried out to assess the consequences of combustion-derived or engineered nanoparticle exposure on human health. In recent years there has been a growing concern about the possible health influence of exposure to air pollutants during pregnancy, hence an implicit concern about potential risk for nanoparticle exposure in utero. Previous work has not addressed the question of whether nanoparticles may cross the placenta. Objective In this study we investigated whether particles can cross the placental barrier and affect the fetus. Methods We used the ex vivo human placental perfusion model to investigate whether nanoparticles can cross this barrier and whether this process is size dependent. Fluorescently labeled polystyrene beads with diameters of 50, 80, 240, and 500 nm were chosen as model particles. Results We showed that fluorescent polystyrene particles with diameter up to 240 nm were taken up by the placenta and were able to cross the placental barrier without affecting the viability of the placental explant. Conclusions The findings suggest that nanomaterials have the potential for transplacental transfer and underscore the need for further nanotoxicologic studies on this important organ system.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMC Pregnancy Childbirth
                Title: BMC Pregnancy and Childbirth
                Publisher: BioMed Central
                ISSN (Electronic): 1471-2393
                Publication date Collection: 2011
                Publication date (Electronic): 2 November 2011
                Volume: 11
                Page: 87
                Affiliations
                [1 ]Inserm, Institut national de la santé et de la recherche médicale, Epidemiology of Allergic and Respiratory (EPAR) Department, UMR-S707, Paris, France
                [2 ]Faculté de Médecine de Saint-Antoine, UPMC Univ6, Paris, France
                [3 ]Inserm, U823, Team "Environmental Epidemiology applied to Reproduction and Respiratory Health", Institut Albert Bonniot, Grenoble, France
                [4 ]Université J. Fourier Grenoble, Grenoble, France
                [5 ]Laboratoire d'Immunologie, CHU de Brabois & Nancy Université, Nancy, France
                [6 ]Institut national de la santé et de la recherche médicale, UMR 780, Villejuif, France
                [7 ]Institut national de la santé et de la recherché médicale, U684, Vandoeuvre les Nancy, France
                [8 ]Institut national de la santé et de la recherche médicale, UMR 915, Institut du Thorax, IRT-UN, Nantes, France
                [9 ]Service de Gynécologie-Obstétrique, Maternité de Nancy, Nancy, France
                Article
                Publisher ID: 1471-2393-11-87
                DOI: 10.1186/1471-2393-11-87
                PMC ID: 3227583
                PubMed ID: 22047167
                SO-VID: 60fdb519-b442-4ed6-9102-e4e3e93b477b
                Copyright © Copyright ©2011 Baïz et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 June 2011
                Date accepted : 2 November 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Obstetrics & Gynecology
                Data availability:
                ScienceOpen disciplines: Obstetrics & Gynecology

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