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      Depressive symptoms are not associated with inflammation in younger and older adults in the Philippines

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          Abstract

          Depression is not associated with inflammation among adults in the Philippines, in contrast to prior research in the US. These results suggest that higher levels of microbial exposure in the Philippines may promote the development of immuno-regulatory pathways that prevent the emergence of a relationship between depression and inflammation.

          Abstract

          Depression is positively associated with chronic inflammation in industrialized settings with low burdens of infectious disease, but the pattern of association in environments with higher levels of microbial exposure is not known. We measured C-reactive protein (CRP) and interleukin 6 (IL6) in community-based samples of young adults (20–22 years) and older women (35–69 years) in the Philippines. Concentrations of CRP and IL6 were low, and bivariate and multivariate regression analyses indicated no associations between depressive symptoms and inflammation in either sample. Results are interpreted in light of prior research indicating that higher levels of microbial exposure in infancy have lasting effects on the regulation of inflammation, and may prevent the emergence of a relationship between depression and inflammation in adulthood.

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          Mycobacteria and other environmental organisms as immunomodulators for immunoregulatory disorders.

          In the rich, developed parts of the world there has been a steady and simultaneous increase in at least three groups of disease: (1) allergies, (2) inflammatory bowel diseases (IBD; e.g. Crohn's disease and ulcerative colitis) and (3) autoimmunity (e.g. type 1 diabetes and multiple sclerosis). Because the medical world is so compartmentalised it was some time before the connection between these increases was noticed and understood. There is now evidence that the simultaneous increase in these diseases of immunodysregulation is at least partly attributable to malfunction of regulatory T cells (Treg). This paper provides an overview of relevant work in each of these fields of medicine (though with emphasis on the allergic disorders), and concludes that the increasing failure of Treg is a consequence of diminished exposure to certain micro-organisms that are "old friends", because of their continuous presence throughout mammalian evolution. These organisms, which include saprophytic mycobacteria, helminths and lactobacilli, are recognised by the innate immune system as harmless, and as adjuvants for Treg induction. Polymorphisms of components of the innate immune system such as TLR2 and NOD2 appear to define subsets of the population that will develop immunoregulatory disorders when living in the modern environment. A further role of the "old friends" and of the Treg that they induce might be to maintain the levels of regulatory IL-10 secreting macrophages and antigen-presenting cells, which are depleted in asthma and Crohn's disease. These concepts are leading to novel therapies based on harmless organisms or their components. Phase I/II clinical trials have yielded some statistically significant results, and phase II trials are in progress.
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            Inflammation, sanitation, and consternation: loss of contact with coevolved, tolerogenic microorganisms and the pathophysiology and treatment of major depression.

            Inflammation is increasingly recognized as contributing to the pathogenesis of major depressive disorder (MDD), even in individuals who are otherwise medically healthy. Most studies in search of sources for this increased inflammation have focused on factors such as psychosocial stress and obesity that are known to activate inflammatory processes and increase the risk for depression. However, MDD may be so prevalent in the modern world not just because proinflammatory factors are widespread, but also because we have lost contact with previously available sources of anti-inflammatory, immunoregulatory signaling. To examine evidence that disruptions in coevolved relationships with a variety of tolerogenic microorganisms that were previously ubiquitous in soil, food, and the gut, but that are largely missing from industrialized societies, may contribute to increasing rates of MDD in the modern world. Relevant studies were identified using PubMed and Ovid MEDLINE. Included were laboratory animal and human studies relevant to immune functioning, the hygiene hypothesis, and major depressive disorder identified via PubMed and Ovid MEDLINE searches. Studies were reviewed by all authors, and data considered to be potentially relevant to the contribution of hygiene-related immune variables to major depressive disorder were extracted. Significant data suggest that a variety of microorganisms (frequently referred to as the "old friends") were tasked by coevolutionary processes with training the human immune system to tolerate a wide array of non-threatening but potentially proinflammatory stimuli. Lacking such immune training, vulnerable individuals in the modern world are at significantly increased risk of mounting inappropriate inflammatory attacks on harmless environmental antigens (leading to asthma), benign food contents and commensals in the gut (leading to inflammatory bowel disease), or self-antigens (leading to any of a host of autoimmune diseases). Loss of exposure to the old friends may promote MDD by increasing background levels of depressogenic cytokines and may predispose vulnerable individuals in industrialized societies to mount inappropriately aggressive inflammatory responses to psychosocial stressors, again leading to increased rates of depression. Measured exposure to the old friends or their antigens may offer promise for the prevention and treatment of MDD in modern industrialized societies.
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              Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood.

              Ecological factors are important determinants of the development and function of anti-pathogen defences. Inflammation is a central part of innate immunity, but the developmental factors that shape the regulation of inflammation are not known. We test the hypothesis that microbial exposures in infancy are associated with high sensitivity C-reactive protein (CRP) in adulthood using prospective data from a birth cohort in the Philippines (n = 1461). Lower birth weight was associated with increased CRP, consistent with a role for inflammation in the widely documented inverse relationship between birth weight and adult cardiovascular diseases. In addition, higher levels of microbial exposure in infancy were associated with lower CRP. These associations were independent of socioeconomic status, measures of current body fat and other health behaviours. We conclude that measures of microbial exposure and nutrition during the pre-natal and early post-natal periods are important predictors of CRP concentration in young adulthood. We speculate that the development of anti-inflammatory regulatory networks in response to early microbial exposure represents plasticity in the development of anti-pathogen defences, and that this process may help explain the low CRP concentrations in this population.
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                Author and article information

                Journal
                Evol Med Public Health
                Evol Med Public Health
                emph
                emph
                Evolution, Medicine, and Public Health
                Oxford University Press
                2050-6201
                24 December 2012
                2013
                : 2013
                : 1
                : 18-23
                Affiliations
                1Department of Anthropology, Northwestern University, Evanston, IL 60208, USA; 2Cells to Society (C2S): The Center on Social Disparities and Health, Institute for Policy Research, Northwestern University, Evanston, IL 60208, USA; 3USC-Office of Population Studies Foundation, Inc., University of San Carlos, Cebu City, Philippines; 4Carolina Population Center and Department of Nutrition, University of North Carolina, Chapel Hill, NC, USA.
                Author notes
                *Corresponding author. Department of Anthropology, Northwestern University, 1810 Hinman Avenue, Evanston, IL 60208, USA. Tel: +1-847/467-4304; Fax: +1-847/467-1778; Email: t-mcdade@ 123456northwestern.edu .
                Article
                eos004
                10.1093/emph/eos004
                4183951
                24481182
                8149c8eb-99f7-4337-a1ab-118a8804ae33
                © The Author(s) 2012. Published by Oxford University Press on behalf of the Foundation for Evolution, Medicine, and Public Health 2012.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 7 September 2012
                : 10 October 2012
                : 22 October 2012
                Page count
                Pages: 6
                Categories
                Brevia

                psychoneuroimmunology,infectious disease,cardiovascular disease,developmental origins of adult disease,human ecological immunology

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