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      The influence of pregnancy on systemic immunity

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          Abstract

          Adaptations in maternal systemic immunity are presumed to be responsible for observed alterations in disease susceptibility and severity as pregnancy progresses. Epidemiological evidence as well as animal studies have shown that influenza infections are more severe during the second and third trimesters of pregnancy, resulting in greater morbidity and mortality, although the reason for this is still unclear. Our laboratory has taken advantage of 20 years of experience studying the murine immune response to respiratory viruses to address questions of altered immunity during pregnancy. With clinical studies and unique animal model systems, we are working to define the mechanisms responsible for altered immune responses to influenza infection during pregnancy and what roles hormones such as estrogen or progesterone play in these alterations.

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          Most cited references52

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          The complex role of estrogens in inflammation.

          There is still an unresolved paradox with respect to the immunomodulating role of estrogens. On one side, we recognize inhibition of bone resorption and suppression of inflammation in several animal models of chronic inflammatory diseases. On the other hand, we realize the immunosupportive role of estrogens in trauma/sepsis and the proinflammatory effects in some chronic autoimmune diseases in humans. This review examines possible causes for this paradox. This review delineates how the effects of estrogens are dependent on criteria such as: 1) the immune stimulus (foreign antigens or autoantigens) and subsequent antigen-specific immune responses (e.g., T cell inhibited by estrogens vs. activation of B cell); 2) the cell types involved during different phases of the disease; 3) the target organ with its specific microenvironment; 4) timing of 17beta-estradiol administration in relation to the disease course (and the reproductive status of a woman); 5) the concentration of estrogens; 6) the variability in expression of estrogen receptor alpha and beta depending on the microenvironment and the cell type; and 7) intracellular metabolism of estrogens leading to important biologically active metabolites with quite different anti- and proinflammatory function. Also mentioned are systemic supersystems such as the hypothalamic-pituitary-adrenal axis, the sensory nervous system, and the sympathetic nervous system and how they are influenced by estrogens. This review reinforces the concept that estrogens have antiinflammatory but also proinflammatory roles depending on above-mentioned criteria. It also explains that a uniform concept as to the action of estrogens cannot be found for all inflammatory diseases due to the enormous variable responses of immune and repair systems.
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            Is Open Access

            1918 Influenza: the Mother of All Pandemics

            The "Spanish" influenza pandemic of 1918–1919, which caused ≈50 million deaths worldwide, remains an ominous warning to public health. Many questions about its origins, its unusual epidemiologic features, and the basis of its pathogenicity remain unanswered. The public health implications of the pandemic therefore remain in doubt even as we now grapple with the feared emergence of a pandemic caused by H5N1 or other virus. However, new information about the 1918 virus is emerging, for example, sequencing of the entire genome from archival autopsy tissues. But, the viral genome alone is unlikely to provide answers to some critical questions. Understanding the 1918 pandemic and its implications for future pandemics requires careful experimentation and in-depth historical analysis.
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              Impact of influenza on acute cardiopulmonary hospitalizations in pregnant women.

              This study sought to quantify influenza-related serious morbidity in pregnant women, as measured by hospitalizations for or death from selected acute cardiopulmonary conditions during predefined influenza seasons. The study population included women aged 15-44 years who were enrolled in the Tennessee Medicaid program for at least 180 days between 1974 and 1993. In a nested case-control study, 4,369 women with a first study event during influenza season were compared with 21,845 population controls. The odds ratios associated with study events increased from 1.44 (95% confidence interval (CI) 0.97-2.15) for women at 14-20 weeks' gestation to 4.67 (95% CI 3.42-6.39) for those at 37-42 weeks in comparison with postpartum women. A retrospective cohort analysis, which controlled for risk factors identified in the case-control study, identified 22,824 study events during 1,393,166 women-years of follow-up. Women in their third trimester without other identified risk factors for influenza morbidity had an event rate of 21.7 per 10,000 women-months during influenza season. Approximately half of this morbidity, 10.5 (95% CI 6.7-14.3) events per 10,000 women-months, was attributable to influenza. Influenza-attributable risks in comparable nonpregnant and postpartum women were 1.91 (95% CI 1.51-2.31) and 1.16 (95% CI -0.09 to 2.42) per 10,000 women-months, respectively. The data suggest that, out of every 10,000 women in their third trimester without other identified risk factors who experience an average influenza season of 2.5 months, 25 will be hospitalized with influenza-related morbidity.
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                Author and article information

                Contributors
                +1212-241-6927 , Thomas.Moran@mssm.edu
                Journal
                Immunol Res
                Immunol. Res
                Immunologic Research
                Springer-Verlag (New York )
                0257-277X
                1559-0755
                24 March 2012
                2012
                : 54
                : 1
                : 254-261
                Affiliations
                [1 ]GRID grid.59734.3c, ISNI 0000000106702351, Department of Microbiology, , Mount Sinai School of Medicine, ; 1 Gustave L. Levy Place, Box 1124, New York, NY 10029 USA
                [2 ]GRID grid.59734.3c, ISNI 0000000106702351, Department of Obstetrics, Gynecology, and Reproductive Sciences, , Mount Sinai School of Medicine, ; New York, NY 10029 USA
                Article
                8303
                10.1007/s12026-012-8303-9
                7091327
                22447351
                2e15a8ea-d1e4-4657-992e-3f58a232f101
                © Springer Science+Business Media, LLC 2012

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Categories
                Immunology at Mount Sinai
                Custom metadata
                © Springer Science+Business Media New York 2012

                gestation,immunology,th2,fetus,placenta,pregnancy,inflammation,immunosuppression

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