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• W2465254510 abstract "Recent research indicates that chronic inflammatory diseases, including allergies and autoimmune and neuropsychiatric diseases, share common pathways of cellular and molecular dysregulation. It was the aim of the International von-Behring-Röntgen Symposium (October 16-18, 2014, in Marburg, Germany) to discuss recent developments in this field. These include a concept of biodiversity; the contribution of urbanization, lifestyle factors, and nutrition (eg, vitamin D); and new mechanisms of metabolic and immune dysregulation, such as extracellular and intracellular RNAs and cellular and mitochondrial stress. Epigenetic mechanisms contribute further to altered gene expression and therefore to the development of chronic inflammation. These novel findings provide the foundation for further development of preventive and therapeutic strategies. Recent research indicates that chronic inflammatory diseases, including allergies and autoimmune and neuropsychiatric diseases, share common pathways of cellular and molecular dysregulation. It was the aim of the International von-Behring-Röntgen Symposium (October 16-18, 2014, in Marburg, Germany) to discuss recent developments in this field. These include a concept of biodiversity; the contribution of urbanization, lifestyle factors, and nutrition (eg, vitamin D); and new mechanisms of metabolic and immune dysregulation, such as extracellular and intracellular RNAs and cellular and mitochondrial stress. Epigenetic mechanisms contribute further to altered gene expression and therefore to the development of chronic inflammation. These novel findings provide the foundation for further development of preventive and therapeutic strategies. Discuss this article on the JACI Journal Club blog: www.jaci-online.blogspot.com. Chronic inflammatory diseases, including allergies and autoimmune and neuropsychiatric diseases, have common pathogenic features of dysregulation of the host immune response. There is increasing experimental evidence that chronic inflammatory diseases are induced and maintained by combinations of host factors and changing environmental influences. In this regard it is well accepted that a variety of anthropogenic factors related to urbanization and adherence to a modern lifestyle, including air pollution, smoking, nutrition, and obesity, represent essential aspects of an altered environment related to the development of chronic inflammatory disease conditions. The effect of these factors has been thoroughly discussed recently.1Kelly F.J. Fussell J.C. Linking ambient particulate matter pollution effects with oxidative biology and immune responses.Ann N Y Acad Sci. 2015; 1340: 84-94Crossref PubMed Scopus (91) Google Scholar, 2Thiering E. Heinrich J. Epidemiology of air pollution and diabetes.Trends Endocrinol Metab. 2015; 26: 384-394Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar, 3Cosselman K.E. Navas-Acien A. Kaufman J.D. Environmental factors in cardiovascular disease.Nat Rev Cardiol. 2015; 12: 627-642Crossref PubMed Scopus (308) Google Scholar, 4Verdile G. Keane K.N. Cruzat V.F. Medic S. Sabale M. Rowles J. et al.Inflammation and oxidative stress: the molecular connectivity between insulin resistance, obesity, and Alzheimer's disease.Mediators Inflamm. 2015; 2015: 105828Crossref PubMed Scopus (242) Google Scholar, 5Andersen C.J. Murphy K.E. Fernandez M.L. Impact of obesity and metabolic syndrome on immunity.Adv Nutr. 2016; 7: 66-75Crossref PubMed Scopus (337) Google Scholar, 6Perez M.K. Piedimonte G. Metabolic asthma: is there a link between obesity, diabetes, and asthma?.Immunol Allergy Clin North Am. 2014; 34: 777-784Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar Special focus of this review, which summarizes the proceedings of the International von-Behring-Röntgen-Symposium (October 16-18, 2014, in Marburg, Germany) is given to the role of microbes combining both environmental and body surface–associated microbes. New findings in this field were discussed in the symposium, with an emphasis on new aspects of cell metabolism, cellular and mitochondrial stress, and the role of intracellular RNAs and extracellular RNAs (eRNAs) as mediators of inflammatory signals, and future research directions for chronic inflammatory diseases were defined. Both internal and external microbiota play a role in the development and regulation of our immune system and, subsequently, the development of chronic inflammatory diseases (Fig 1). The hygiene hypothesis, which was first proposed in 1989 after the observation that having older siblings provided some protection from allergic disorders,7Strachan D.P. Hay fever, hygiene, and household size.BMJ. 1989; 299: 1259-1260Crossref PubMed Scopus (3844) Google Scholar states that a lack of exposure to microbes in early life increases susceptibility to allergic diseases, indicating that altered immune regulation is linked to chronic inflammatory diseases (Graham Rook, London, United Kingdom). Human subjects, like all vertebrates, coevolved with a symbiotic microbiota, particularly in the gut, which plays a pivotal role in the development and function of all organ systems, including the brain.8McFall-Ngai M. Hadfield M.G. Bosch T.C. Carey H.V. Domazet-Loso T. Douglas A.E. et al.Animals in a bacterial world, a new imperative for the life sciences.Proc Natl Acad Sci U S A. 2013; 110: 3229-3236Crossref PubMed Scopus (1553) Google Scholar The microbiota also has an essential effect on immune system regulation,9Round J.L. Mazmanian S.K. The gut microbiota shapes intestinal immune responses during health and disease.Nat Rev Immunol. 2009; 9: 313-323Crossref PubMed Scopus (3250) Google Scholar and many aspects of modern life, such as cesarean delivery, lack of breast-feeding, use of antibiotics, and untargeted hygiene, tend to disrupt transmission of the microbiota to the infant. There are probably specific windows of opportunity for this transmission during infancy, and animal data suggest that if these are missed, immunoregulatory, metabolic,10Cox L.M. Yamanishi S. Sohn J. Alekseyenko A.V. Leung J.M. Cho I. et al.Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.Cell. 2014; 158: 705-721Abstract Full Text Full Text PDF PubMed Scopus (1181) Google Scholar and central nervous system11Diaz H.R. Wang S. Anuar F. Qian Y. Bjorkholm B. Samuelsson A. et al.Normal gut microbiota modulates brain development and behavior.Proc Natl Acad Sci U S A. 2011; 108: 3047-3052Crossref PubMed Scopus (178) Google Scholar dysfunctions can result. Additionally, human subjects evolved as small hunter-gatherer groups and coevolved with the “old infections,” which did not kill the host and persisted for life. These organisms limited immunopathology and evolved to drive immunoregulatory responses. This resulted in selection of mutations within the human immune system that partially compensated for these immunoregulatory activities. However, in the absence of these infections, in the era of modern medicine, these proinflammatory mutations lead to “inflammatory overshoot” and have become risk factors for chronic inflammatory diseases. Some studies suggest that the exchange of organisms and genes (by means of horizontal gene transfer) from the microbiota of the natural environment is also important.12Rook G.A. Regulation of the immune system by biodiversity from the natural environment: an ecosystem service essential to health.Proc Natl Acad Sci U S A. 2013; 110: 18360-18367Crossref PubMed Scopus (395) Google Scholar Together, these observations highlight immunoregulatory links between commensal and environmental microbiota and their connections to health and disease. Studies are required to merge these different lines of research and characterize the balance among these factors that maintains health. The biodiversity hypothesis states that reduced biodiversity leads to alterations in human microbiomes, which contribute to inflammatory diseases (Tari Haahtela, Helsinki, Finland). Biodiversity is defined as the variety of life on Earth. It includes the genes found in living things of all species and the ecosystems these species comprise. In 1850, the world population was somewhere between 630 and 930 million, and 160 years later, it is more than 7 billion. The exponential population growth and rapidly escalating urbanization has led to biodiversity loss. This loss and climate change secondary to human activity are now being associated with various adverse health effects. Immune tolerance is an active process throughout life; however, early events are the most important for building connections to beneficial commensals that are prerequisite to health. Naturally biodiverse environments include ancient microorganisms, which modulate the human microbiota and keep immune processes alert. The interplay between the environmental metagenome, human microbial genome, and human cell genome determines health and disease.13Hanski I. von H.L. Fyhrquist N. Koskinen K. Torppa K. Laatikainen T. et al.Environmental biodiversity, human microbiota, and allergy are interrelated.Proc Natl Acad Sci U S A. 2012; 109: 8334-8339Crossref PubMed Scopus (667) Google Scholar The modern epidemics of chronic inflammatory diseases, including allergy and asthma, are largely a result of reduced exposure to natural environments, changed diet, and sedentary lifestyle. Biodiversity loss (poor macrobiota/microbiota) leads to poor human microbiota (dysbiosis), immune dysfunction (poor tolerance), inappropriate inflammatory responses, and finally symptoms and diseases.13Hanski I. von H.L. Fyhrquist N. Koskinen K. Torppa K. Laatikainen T. et al.Environmental biodiversity, human microbiota, and allergy are interrelated.Proc Natl Acad Sci U S A. 2012; 109: 8334-8339Crossref PubMed Scopus (667) Google Scholar, 14von Hertzen L. Hanski I. Haahtela T. Natural immunity. Biodiversity loss and inflammatory diseases are two global megatrends that might be related.EMBO Rep. 2011; 12: 1089-1093Crossref PubMed Scopus (176) Google Scholar, 15Haahtela T. Holgate S. Pawankar R. Akdis C.A. Benjaponpitak S. Caraballo L. et al.The biodiversity hypothesis and allergic disease: World Allergy Organization position statement.World Allergy Organ J. 2013; 6: 3Abstract Full Text Full Text PDF PubMed Scopus (247) Google Scholar, 16Ruokolainen L. von H.L. Fyhrquist N. Laatikainen T. Lehtomaki J. Auvinen P. et al.Green areas around homes reduce atopic sensitization in children.Allergy. 2015; 70: 195-202Crossref PubMed Scopus (163) Google Scholar, 17Fyhrquist N. Ruokolainen L. Suomalainen A. Lehtimaki S. Veckman V. Vendelin J. et al.Acinetobacter species in the skin microbiota protect against allergic sensitization and inflammation.J Allergy Clin Immunol. 2014; 134: 1301-1309Abstract Full Text Full Text PDF PubMed Scopus (123) Google Scholar Research is needed to characterize connections between the environmental microbiota and the human microbiota, to characterize how interactions between these and the immune system create and maintain immunologic competence and tolerance, and to guide the development of novel therapeutics that are useful and safe interventions for maintaining the balance between environmental and human microbiota. In addition to external and internal microbiomes, host cell structures are factors that contribute to immune regulation. Epithelial surfaces play a regulatory role in innate immune responses (Thaddeus Stappenbeck, St Louis, Mo). The innate immune system is responsible for initial recognition of infection and damage and quickly triggers a range of host responses. Epithelial surfaces rapidly react to environmental insults to maintain barrier function and prevent further injury. However, some interactions between epithelial barriers and innate immune responses are still unknown. Chronic viral infection can stimulate epithelial turnover and repair in part through type I interferons that signal through myeloid cells. These events link together the responses of the innate immune and epithelial systems to damage and infection.18Sun L. Miyoshi H. Origanti S. Nice T.J. Barger A.C. Manieri N.A. et al.Type I interferons link viral infection to enhanced epithelial turnover and repair.Cell Host Microbe. 2015; 17: 85-97Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar The human virome is a relatively unexplored component of the microbiome and is the complex collection of chronic viruses within a given host.19Virgin H.W. The virome in mammalian physiology and disease.Cell. 2014; 157: 142-150Abstract Full Text Full Text PDF PubMed Scopus (395) Google Scholar Most human subjects are chronically infected with multiple viruses, and the long-term consequences of repeated cycles of epithelial inflammation, damage, and repair are not yet fully characterized. Other environmental factors that guide host immune responses are food antigens. The mechanisms by which dietary antigens stimulate intestinal T cells and the fate of these lymphocytes are unknown.20Pabst O. Mowat A.M. Oral tolerance to food protein.Mucosal Immunol. 2012; 5: 232-239Crossref PubMed Scopus (471) Google Scholar Ulrich Steinhoff et al (Marburg, Germany) demonstrated that the oral uptake of food antigens resulted in the expansion and accumulation of food antigen–specific CD4+ T-cell populations and subsequent anergy and apoptosis in Peyer patches. The activation and death of food-reactive CD4 T cells is a default program required for normal development of the small intestine. Furthermore, removal of apoptotic cells by macrophages leads to increased production of anti-inflammatory IL-10, which suppresses inflammatory lesions in the small intestine. The mechanisms of immune stimulation by food antigens under physiologic conditions are still unknown and might be important in understanding chronic intestinal inflammation. Characterizing the immunologic and structural effects of food antigen recognition might reveal patterns in food tolerance, inflammation, and intestinal structure/barrier function that are disturbed in disease states. Immuno-ontogeny, or the developmental stage and conditions during antigen exposure, is another host factor that plays a role in influencing the outcomes of immune responses. Differences are observed in preterm versus term neonates with or without exposure to extrauterine microbiota (Michael Zemlin, Marburg, Germany). Current thinking is that the origin of allergies and autoimmunity occurs within the fetal and neonatal periods of development. Thus changes in the immune system can be influenced by exogenous factors or those that occur because of endogenous triggers in an age-dependent manner. Preterm birth prematurely elicits humoral immune responses.21Zemlin M. Hoersch G. Zemlin C. Pohl-Schickinger A. Hummel M. Berek C. et al.The postnatal maturation of the immunoglobulin heavy chain IgG repertoire in human preterm neonates is slower than in term neonates.J Immunol. 2007; 178: 1180-1188Crossref PubMed Scopus (36) Google Scholar However, the expressed secondary antibody repertoires are unique in neonates. This could contribute to the increased risk of infection observed in neonates but might also influence the ability to induce immune responses against self-antigens or allergens.22Rogosch T. Kerzel S. Hoss K. Hoersch G. Zemlin C. Heckmann M. et al.IgA response in preterm neonates shows little evidence of antigen-driven selection.J Immunol. 2012; 189: 5449-5456Crossref PubMed Scopus (39) Google Scholar Future research is needed to determine why preterm compared with full-term neonates have a reduced risk of atopic dermatitis and an increased risk of bronchial asthma. Ongoing research into the pathogenesis of chronic inflammatory diseases continues to reveal host cell functions that can trigger or exacerbate disease states (Table I). Leukocyte recruitment is a central process in inflammation and immunity (Triantafyllos Chavakis, Dresden, Germany). Although several adhesion receptors and chemokines/chemokine receptors have been identified that promote leukocyte infiltration into an inflamed tissue, little is known about endogenous inhibitors of the leukocyte adhesion cascade. Developmental endothelial locus 1 (Del-1) is a secreted molecule that interferes with β2-integrin–dependent neutrophil adhesion to the endothelium and subsequent recruitment of inflammatory cells.23Choi E.Y. Chavakis E. Czabanka M.A. Langer H.F. Fraemohs L. Economopoulou M. et al.Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment.Science. 2008; 322: 1101-1104Crossref PubMed Scopus (218) Google Scholar, 24Mitroulis I. Kang Y.Y. Gahmberg C.G. Siegert G. Hajishengallis G. Chavakis T. et al.Developmental endothelial locus-1 attenuates complement-dependent phagocytosis through inhibition of Mac-1-integrin.Thromb Haemost. 2014; 111: 1004-1006Crossref PubMed Scopus (33) Google Scholar In addition, these authors observed that downregulation of Del-1 expression predisposes experimental animals to IL-17–dependent inflammation and inflammatory bone loss.25Eskan M.A. Jotwani R. Abe T. Chmelar J. Lim J.H. Liang S. et al.The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss.Nat Immunol. 2012; 13: 465-473Crossref PubMed Scopus (300) Google Scholar Thus Del-1 is an endogenous tissue homeostatic factor that modulates the inflammatory response.26Hajishengallis G. Chavakis T. Endogenous modulators of inflammatory cell recruitment.Trends Immunol. 2013; 34: 1-6Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar It remains to be investigated whether Del-1 expression modulates the outcome of chronic inflammatory diseases as well.Table INovel subcellular and intercellular mechanisms•eRNA•Noncoding RNA•Long noncoding RNA•miRNA•Exosomal cell-cell communication•Cellular stress•Mitochondrial dysfunction•Epigenetic regulation Open table in a new tab A novel role for endogenous eRNA functioning as a proinflammatory signal has been described (Klaus T. Preissner, Giessen, Germany). Previous studies from this group have shown that eRNA is released under conditions of tissue stress or injury or during pathological conditions, such as ischemia or tumor growth, and acts as a prothrombotic, permeability-increasing, and proinflammatory factor.27Cabrera-Fuentes H.A. Ruiz-Meana M. Simsekyilmaz S. Kostin S. Inserte J. Saffarzadeh M. et al.RNase1 prevents the damaging interplay between extracellular RNA and tumour necrosis factor-alpha in cardiac ischaemia/reperfusion injury.Thromb Haemost. 2014; 112: 1110-1119Crossref PubMed Scopus (72) Google Scholar, 28Fischer S. Cabrera-Fuentes H.A. Noll T. Preissner K.T. Impact of extracellular RNA on endothelial barrier function.Cell Tissue Res. 2014; 355: 635-645Crossref PubMed Scopus (32) Google Scholar, 29Simsekyilmaz S. Cabrera-Fuentes H.A. Meiler S. Kostin S. Baumer Y. Liehn E.A. et al.Role of extracellular RNA in atherosclerotic plaque formation in mice.Circulation. 2014; 129: 598-606Crossref PubMed Scopus (66) Google Scholar eRNA released from activated mast cells provides a newly recognized alarm signal that triggers an endogenous inflammatory cascade, which appears to be essential for the release of cytokines in health and disease. Additional research is needed to determine whether the eRNA-triggered inflammatory cascade also plays a role in allergic diseases. Such experiments can be done in established mouse models and by using biomarker analysis in patients. Exosomal cell-to-cell transfer has been described as another way to transmit extracellular signaling and communication with a potential role in regulating inflammatory responses (Bernd T. Schmeck, Marburg, Germany). It has been shown that microbes can interfere with host immune regulation (ie, by injecting specific histone modifying enzymes).30Rolando M. Sanulli S. Rusniok C. Gomez-Valero L. Bertholet C. Sahr T. et al.Legionella pneumophila effector RomA uniquely modifies host chromatin to repress gene expression and promote intracellular bacterial replication.Cell Host Microbe. 2013; 13: 395-405Abstract Full Text Full Text PDF PubMed Scopus (164) Google Scholar These changes can then be propagated to other cell types by cytokines or their antagonists.31Herold S. Tabar T.S. Janssen H. Hoegner K. Cabanski M. Lewe-Schlosser P. et al.Exudate macrophages attenuate lung injury by the release of IL-1 receptor antagonist in gram-negative pneumonia.Am J Respir Crit Care Med. 2011; 183: 1380-1390Crossref PubMed Scopus (86) Google Scholar Recent findings show that cell-to-cell communication can also take place through exosomal transfer of noncoding RNAs that act specifically on the gene expression of a recipient cell.32Hergenreider E. Heydt S. Treguer K. Boettger T. Horrevoets A.J. Zeiher A.M. et al.Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs.Nat Cell Biol. 2012; 14: 249-256Crossref PubMed Scopus (1026) Google Scholar Schmeck et al found that microbial exposure of human macrophages impaired the pro-inflammatory reactivity of neighboring epithelial cells. Interactions took place partly by cytokines but also by exosomes that were able to transfer microRNAs (miRNA) to the “target cells.” Bacteria-exposed macrophages change the inflammatory phenotype of bystander cells by soluble mediators and exosomes. Research is needed to determine the function of RNA, protein, and lipid components of exosomes in immune regulation; whether microbes participate or interfere in this vesicle transfer; and which differences exist between the effect of a beneficial microbiome and the detrimental effects of pathogens. The microbiome also plays a role in host structural components that can be involved in disease (Christoph Reinhardt, Mainz, Germany). Indigenous microbiota affects tissue remodeling and formation of intricate capillary networks in small intestinal villus structures through mechanisms involving Paneth cell function and coagulation factor signaling.33Stappenbeck T.S. Hooper L.V. Gordon J.I. Developmental regulation of intestinal angiogenesis by indigenous microbes via Paneth cells.Proc Natl Acad Sci U S A. 2002; 99: 15451-15455Crossref PubMed Scopus (813) Google Scholar, 34Reinhardt C. Bergentall M. Greiner T.U. Schaffner F. Ostergren-Lunden G. Petersen L.C. et al.Tissue factor and PAR1 promote microbiota-induced intestinal vascular remodelling.Nature. 2012; 483: 627-631Crossref PubMed Scopus (179) Google Scholar The gut microbiota and its metabolic functions have been identified as risk factors for the development of cardiovascular disease.35Koeth R.A. Wang Z. Levison B.S. Buffa J.A. Org E. Sheehy B.T. et al.Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis.Nat Med. 2013; 19: 576-585Crossref PubMed Scopus (2706) Google Scholar Moreover, symptomatic atherosclerosis is associated with an altered gut metagenome.36Karlsson F.H. Fak F. Nookaew I. Tremaroli V. Fagerberg B. Petranovic D. et al.Symptomatic atherosclerosis is associated with an altered gut metagenome.Nat Commun. 2012; 3: 1245Crossref PubMed Scopus (776) Google Scholar Data are still lacking that provide a causal link between colonization of the gut by microbial communities and the pathomechanisms that trigger atherosclerotic plaque rupture and thrombotic disease states. Experiments in germ-free mice showed that microbiota colonization of the gut affected its epithelial Toll-like receptor expression and downstream signaling to induce experimental thrombus formation through Toll-like receptors.37Hormann N. Brandao I. Jackel S. Ens N. Lillich M. Walter U. et al.Gut microbial colonization orchestrates TLR2 expression, signaling and epithelial proliferation in the small intestinal mucosa.PLoS One. 2014; 9: e113080Crossref PubMed Scopus (75) Google Scholar, 38Brandao I. Hormann N. Jackel S. Reinhardt C. TLR5 expression in the small intestine depends on the adaptors MyD88 and TRIF, but is independent of the enteric microbiota.Gut Microbes. 2015; 6: 202-206Crossref PubMed Scopus (13) Google Scholar Future work with germ-free mouse models combined with bacterial mutant strains will show how constituents of the microbiota might affect host metabolism, will provide a mechanistic link to coagulation factor signaling, and could influence the development of cardiovascular disease and the sequelae of thrombotic events. Interactions between the external environment (eg, allergens and environmental microbes) and internal host factors (eg, commensal microbiomes, diet, genetics, and developmental stages) affect the health but also the disease states of host organisms (Fig 1). Allergy and asthma are 2 medically important chronic inflammatory diseases in which these interactions are out of balance. Here the human microbiome plays an important role in allergic asthma (Hans Bisgaard, Copenhagen, Denmark) because a link between the type of human microbiomes and the risk for asthma was proposed in several studies.39Bisgaard H. Bonnelykke K. Stokholm J. Immune-mediated diseases and microbial exposure in early life.Clin Exp Allergy. 2014; 44: 475-481Crossref PubMed Scopus (22) Google Scholar For example, maternal use of antibiotics is associated with increased risk of childhood asthma in a dose-related fashion independently of pregnancy periods and antibiotic type.40Stensballe L.G. Simonsen J. Jensen S.M. Bonnelykke K. Bisgaard H. Use of antibiotics during pregnancy increases the risk of asthma in early childhood.J Pediatr. 2013; 162: 832-838Abstract Full Text Full Text PDF PubMed Scopus (187) Google Scholar Also, delivery by means of cesarean section is associated with changes in the neonatal gut flora and an increased risk of asthma in the child.41Sevelsted A. Stokholm J. Bonnelykke K. Bisgaard H. Cesarean section and chronic immune disorders.Pediatrics. 2015; 135: e92-e98Crossref PubMed Scopus (314) Google Scholar The lung microbiome might also play a role in asthma development because pathogen-affected airways are associated with the risk of asthma in neonates.42Bonnelykke K. Vissing N.H. Sevelsted A. Johnston S.L. Bisgaard H. Association between respiratory infections in early life and later asthma is independent of virus type.J Allergy Clin Immunol. 2015; 136: 81-86Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar Future work is needed to further characterize the associations that might guide the use of therapeutics to alter the gut and lung microbiomes for the prevention or treatment of asthma, respectively. Like host microbiomes, environmental microbiomes also affect the development of allergic diseases. Some environmental bacteria exert protective effects for allergic disease (Holger Garn, Marburg, Germany), and recent observations from epidemiologic studies suggest that a higher environmental microbial diversity is associated with increased protection form allergies and asthma.43Ege M.J. Mayer M. Normand A.C. Genuneit J. Cookson W.O. Braun-Fahrlander C. et al.Exposure to environmental microorganisms and childhood asthma.N Engl J Med. 2011; 364: 701-709Crossref PubMed Scopus (1108) Google Scholar Certain bacterial strains are specifically associated with protective effects of farming environments.44Ege M.J. Mayer M. Schwaiger K. Mattes J. Pershagen G. van Hage M. et al.Environmental bacteria and childhood asthma.Allergy. 2012; 67: 1565-1571PubMed Google Scholar Here insights from studies using ovalbumin- and house dust mite–based murine models of allergic airway inflammation proposed that nonpathogenic environmental bacteria can exert protective effects on allergy involving different effector pathways.45Conrad M.L. Ferstl R. Teich R. Brand S. Blumer N. Yildirim A.O. et al.Maternal TLR signaling is required for prenatal asthma protection by the nonpathogenic microbe Acinetobacter lwoffii F78.J Exp Med. 2009; 206: 2869-2877Crossref PubMed Scopus (270) Google Scholar, 46Hagner S. Harb H. Zhao M. Stein K. Holst O. Ege M.J. et al.Farm-derived gram-positive bacterium Staphylococcus sciuri W620 prevents asthma phenotype in HDM- and OVA-exposed mice.Allergy. 2013; 68: 322-329Crossref PubMed Scopus (57) Google Scholar However, the underlying mechanisms by which higher microbial diversity is associated with increased protection from allergic disorders remain unresolved. Future work can reveal involvement of the following mechanisms: (1) higher microbial diversity increases the probability to provide signals for a single or a few decisive signaling pathway(s); (2) various signals from different microbes recognized by a variety of receptors converge on a common decisive effector pathway; and (3) various signals from different microbes involve multiple distinct effector pathways that synergize to result in optimal allergy protection. The developmental stage during which exposure to environmental allergens occurs can also influence asthma and allergic diseases (James E. Gern, Madison, Wis), whereby early-life environmental exposures modify the risk for allergic diseases and asthma.44Ege M.J. Mayer M. Schwaiger K. Mattes J. Pershagen G. van Hage M. et al.Environmental bacteria and childhood asthma.Allergy. 2012; 67: 1565-1571PubMed Google Scholar A prospective birth cohort study was conducted (Urban Environment and Childhood Asthma [URECA]) involving 560 babies of families residing in urban neighborhoods with high rates of poverty in Baltimore, Boston, New York City, and St Louis.47Gern J.E. Visness C.M. Gergen P.J. Wood R.A. Bloomberg G.R. O'Connor G.T. et al.The Urban Environment and Childhood Asthma (URECA) birth cohort study: design, methods, and study population.BMC Pulm Med. 2009; 9: 17Crossref PubMed Scopus (75) Google Scholar Results from this study provide evidence that in urban environments exposure to allergenic proteins i" @default.
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• W2465254510 title "Current concepts in chronic inflammatory diseases: Interactions between microbes, cellular metabolism, and inflammation" @default.
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