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      Inflammatory Long Pentraxin 3 is Associated with Leukocyte Telomere Length in Night-Shift Workers

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          Abstract

          Aging is an emerging worldwide threat to public health, even in the workplace, as it links with risk of illness and death. Bewildered inflammatory responses and stressful conditions associate with age-related disorders. Additionally, circadian rhythm disruption, a critical health issue in night-shift workers, correlates with premature aging. We investigated the hypothesis of a link between altered inflammatory response, detected by plasmatic long pentraxin 3 (PTX3), and biological aging, measured by leukocyte telomere length (LTL), attrition, and possibly induced by night-shift work. Within the framework of a cross-sectional study, such possible relationships were appraised by simultaneous equation model (SEM) technique among day and night-shift hospital workers. PTX3 levels, modulated by several aging conditions [i.e., body mass index (BMI) (beta = −0.22; p = 0.022), C-reactive protein (CRP) (beta = −0.07; p = 0.000), and cardiovascular diseases with hypertension included (CVD) (beta = −0.12; p = 0.000)], positively associate with LTL (coefficient = 0.15; p = 0.033). LTL, in turn is reduced by CVD (beta = −0.15; p = 0.000), binge drinking (beta = −0.10; p = 0.004), and CRP (beta = −0.05; p = 0.026). On the other hand, night-shift work, found to be remarkably free from aging risk factors [i.e., age (beta = −0.13; p = 0.017), BMI (beta = −0.17; p = 0.030), CVD (beta = −0.14; p = 0.000), and binge drinking (beta = −0.13; p = 0.000)], does associate almost significantly with reversed PTX3 (coefficient = −0.09; p = 0.089) and even with CRP (beta = 0.17; p = 0.000). In conclusion, the SEM analysis indicates that PTX3 is positively linked to LTL. The finding suggests a possible new role of this long pentraxin that, by orchestrating an efficient governance of inflammatory processes, may protect telomere from attrition, ensuring therefore the genetic stability of cells. The higher CRP levels among night-shift workers suggest that night-shift work is associated with increased systemic inflammation. This would make nocturnal workers more susceptible to premature aging.

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          Most cited references39

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          Oxidative stress shortens telomeres.

          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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            Telomere diseases.

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              Modeling the rate of senescence: can estimated biological age predict mortality more accurately than chronological age?

              Biological age (BA) is useful for examining differences in aging rates. Nevertheless, little consensus exists regarding optimal methods for calculating BA. The aim of this study is to compare the predictive ability of five BA algorithms. The sample included 9,389 persons, aged 30-75 years, from National Health and Nutrition Examination Survey III. During the 18-year follow-up, 1,843 deaths were counted. Each BA algorithm was compared with chronological age on the basis of predictive sensitivity and strength of association with mortality. Results found that the Klemera and Doubal method was the most reliable predictor of mortality and performed significantly better than chronological age. Furthermore, when included with chronological age in a model, Klemera and Doubal method had more robust predictive ability and caused chronological age to no longer be significantly associated with mortality. Given the potential of BA to highlight heterogeneity, the Klemera and Doubal method algorithm may be useful for studying a number of questions regarding the biology of aging.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                09 May 2017
                2017
                : 8
                : 516
                Affiliations
                [1] 1Occupational Medicine, Department of Cardiac, Thoracic and Vascular Sciences, University of Padova , Padova, Italy
                [2] 2Department of Medical Sciences, University of Ferrara , Ferrara, Italy
                [3] 3Laboratory of Research in Immunology and Inflammation, Humanitas Clinical and Research Center , Rozzano, Milan, Italy
                [4] 4Department of Prevention and Protection, University-Hospital and Public Health Service of Ferrara , Ferrara, Italy
                [5] 5Humanitas University , Rozzano, Milan, Italy
                Author notes

                Edited by: Heiko Mühl, Goethe University Frankfurt, Germany

                Reviewed by: Bartosz Hudzik, Silesian Center for Heart Disease, Poland; Concettina Fenga, University of Messina, Italy

                *Correspondence: Sofia Pavanello, sofia.pavanello@ 123456unipd.it

                Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Article
                10.3389/fimmu.2017.00516
                5422482
                28536575
                a73a4ce1-1192-4fb2-bb95-b4fd8b8dee23
                Copyright © 2017 Pavanello, Stendardo, Mastrangelo, Bonci, Bottazzi, Campisi, Nardini, Leone, Mantovani and Boschetto.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 17 February 2017
                : 18 April 2017
                Page count
                Figures: 1, Tables: 3, Equations: 0, References: 50, Pages: 9, Words: 7209
                Funding
                Funded by: Fondazione Cariplo 10.13039/501100002803
                Award ID: 2015-0564
                Categories
                Immunology
                Original Research

                Immunology
                inflammation,aging,premature,telomere,pentraxin 3,circadian rhythm,genetic instability,night-shift work

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