The University of Southampton
University of Southampton Institutional Repository

Early nutrition and immunity - progress and perspectives

Early nutrition and immunity - progress and perspectives
Early nutrition and immunity - progress and perspectives
The immune system exists to protect the host against pathogenic organisms and highly complex pathways of recognition, response, elimination and memory have evolved in order to fulfil this role. The immune system also acts to ensure tolerance to 'self', to food and other environmental components, and to commensal bacteria. A breakdown in the tolerogenic pathways can also lead to inflammatory diseases. The prevalence of inflammatory diseases, including atopic disorders, has increased over the last 60 years. The development of tolerance is the result of active immune mechanisms and both development and maintenance of tolerance are lifelong processes which start very early in life, even prenatally. Profound immunologic changes occur during pregnancy, involving a polarization of T helper (Th) cells towards a dominance of Th2 and regulatory T cell effector responses in both mother and fetus. This situation is important to maintain pregnancy through avoidance of the rejection of the immunologically incompatible fetus. During the third trimester of human pregnancy, fetal T cells are able to mount antigen-specific responses to environmental and food-derived antigens and antigen-specific T cells are detectable in cord blood in virtually all newborns indicating in utero sensitization. If the neonatal immune system is not able to down-regulate the pre-existing Th2 dominance effectively then an allergic phenotype may develop. Changes occur at, and soon after, birth in order that the immune system of the neonate becomes competent and functional and that the gut becomes colonized with bacteria. Exposure to bacteria during birth and from the mother's skin and the provision of immunologic factors in breast milk are amongst the key events that promote maturation of the infant's gut and gut-associated and systemic immune systems. The introduction of formula and of solid foods exposes the infant to novel food antigens and also affects the gut flora. Nutrition may be the source of antigens to which the immune system must become tolerant, provide factors, including nutrients, that themselves might modulate immune maturation and responses, and provide factors that influence intestinal flora, which in turn will affect antigen exposure, immune maturation and immune responses. Through these mechanisms it is possible that nutrition early in life might affect later immune competence, the ability to mount an appropriate immune response upon infection, the ability to develop a tolerogenic response to 'self' and to benign environmental antigens, and the development of immunologic disorders. A Workshop held in February 2006 considered recent findings in the areas of oral tolerance, routes of sensitization to allergens and factors affecting the development of atopic disease; factors influencing the maturation of dendritic cells and the development of regulatory T cells; the influence of gut microflora on immunity, allergic sensitization and infectious disease; the role of nutrition in preventing necrotizing enterocolitis in an animal model of preterm birth; and the role of PUFA of different classes in influencing immune responses and in shaping the development of atopic disease. This report summarizes the content of the lectures and the subsequent discussions
unsaturated, acid, exposure, pregnancy, infant, fetal, pufa, nutrition, research, models, animal, responses, birth, in-utero, immune tolerance, fatty acids, blood, immediate, infection, hypersensitivity, phenotype, dendritic cells, fetus, fatty acid, immunology, animals, microbiology, premature, human, infant nutrition physiology, development, newborn, milk, humans, cells, immune system, gastrointestinal tract, disease, allergens, preterm, report, environmental, prevalence, tolerance
0007-1145
774-790
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Krauss-Etschmann, S.
60f8dbe2-6dcc-4f03-a33d-9338adc378cc
De Jong, E.C.
e39fa6ac-7e6c-4c31-98bc-b99055813fee
Dupont, C.
857a3e96-7ca0-4c13-868d-8dd65d2c8ba7
Frick, J.S.
ca63f2da-fd33-4208-80ad-87d2e9014eef
Frokiaer, H.
13e4d97d-9100-465f-9a80-34fd53aee6a8
Heinrich, J.
aa9af3c9-be31-428c-8238-96a7c186a779
Garn, H.
8592c861-ddb1-485c-b843-f2edaa81ad70
Koletzko, S.
cc9ed7bf-af6b-49a6-8824-e33c3124456f
Lack, G.
27fa8c20-ab77-4037-96f6-1e9298d71f68
Mattelio, G.
7a355212-c3c3-4953-9004-41825b3f4256
Renz, H.
998439e3-882e-42c7-adc7-b8973a3b0b0a
Sangild, P.T.
db73b95f-b123-4b89-ad2a-657707efdd93
Schrezenmeir, J.
61a7a30a-7080-482f-99f3-38a10fba8f42
Stulnig, T.M.
30cadd0d-b14f-4205-b777-a55daea4943e
Thymann, T.
283d5785-8209-4c8d-9021-68142ae5479e
Wold, A.E.
df97f16f-c492-4fe9-971d-69e3884e4823
Koletzko, B.
1d600e42-8989-4634-848b-203029211ffc
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Krauss-Etschmann, S.
60f8dbe2-6dcc-4f03-a33d-9338adc378cc
De Jong, E.C.
e39fa6ac-7e6c-4c31-98bc-b99055813fee
Dupont, C.
857a3e96-7ca0-4c13-868d-8dd65d2c8ba7
Frick, J.S.
ca63f2da-fd33-4208-80ad-87d2e9014eef
Frokiaer, H.
13e4d97d-9100-465f-9a80-34fd53aee6a8
Heinrich, J.
aa9af3c9-be31-428c-8238-96a7c186a779
Garn, H.
8592c861-ddb1-485c-b843-f2edaa81ad70
Koletzko, S.
cc9ed7bf-af6b-49a6-8824-e33c3124456f
Lack, G.
27fa8c20-ab77-4037-96f6-1e9298d71f68
Mattelio, G.
7a355212-c3c3-4953-9004-41825b3f4256
Renz, H.
998439e3-882e-42c7-adc7-b8973a3b0b0a
Sangild, P.T.
db73b95f-b123-4b89-ad2a-657707efdd93
Schrezenmeir, J.
61a7a30a-7080-482f-99f3-38a10fba8f42
Stulnig, T.M.
30cadd0d-b14f-4205-b777-a55daea4943e
Thymann, T.
283d5785-8209-4c8d-9021-68142ae5479e
Wold, A.E.
df97f16f-c492-4fe9-971d-69e3884e4823
Koletzko, B.
1d600e42-8989-4634-848b-203029211ffc

Calder, P.C., Krauss-Etschmann, S., De Jong, E.C., Dupont, C., Frick, J.S., Frokiaer, H., Heinrich, J., Garn, H., Koletzko, S., Lack, G., Mattelio, G., Renz, H., Sangild, P.T., Schrezenmeir, J., Stulnig, T.M., Thymann, T., Wold, A.E. and Koletzko, B. (2006) Early nutrition and immunity - progress and perspectives. British Journal of Nutrition, 96 (4), 774-790. (doi:10.1079/BJN20061917). (PMID:17010239)

Record type: Article

Abstract

The immune system exists to protect the host against pathogenic organisms and highly complex pathways of recognition, response, elimination and memory have evolved in order to fulfil this role. The immune system also acts to ensure tolerance to 'self', to food and other environmental components, and to commensal bacteria. A breakdown in the tolerogenic pathways can also lead to inflammatory diseases. The prevalence of inflammatory diseases, including atopic disorders, has increased over the last 60 years. The development of tolerance is the result of active immune mechanisms and both development and maintenance of tolerance are lifelong processes which start very early in life, even prenatally. Profound immunologic changes occur during pregnancy, involving a polarization of T helper (Th) cells towards a dominance of Th2 and regulatory T cell effector responses in both mother and fetus. This situation is important to maintain pregnancy through avoidance of the rejection of the immunologically incompatible fetus. During the third trimester of human pregnancy, fetal T cells are able to mount antigen-specific responses to environmental and food-derived antigens and antigen-specific T cells are detectable in cord blood in virtually all newborns indicating in utero sensitization. If the neonatal immune system is not able to down-regulate the pre-existing Th2 dominance effectively then an allergic phenotype may develop. Changes occur at, and soon after, birth in order that the immune system of the neonate becomes competent and functional and that the gut becomes colonized with bacteria. Exposure to bacteria during birth and from the mother's skin and the provision of immunologic factors in breast milk are amongst the key events that promote maturation of the infant's gut and gut-associated and systemic immune systems. The introduction of formula and of solid foods exposes the infant to novel food antigens and also affects the gut flora. Nutrition may be the source of antigens to which the immune system must become tolerant, provide factors, including nutrients, that themselves might modulate immune maturation and responses, and provide factors that influence intestinal flora, which in turn will affect antigen exposure, immune maturation and immune responses. Through these mechanisms it is possible that nutrition early in life might affect later immune competence, the ability to mount an appropriate immune response upon infection, the ability to develop a tolerogenic response to 'self' and to benign environmental antigens, and the development of immunologic disorders. A Workshop held in February 2006 considered recent findings in the areas of oral tolerance, routes of sensitization to allergens and factors affecting the development of atopic disease; factors influencing the maturation of dendritic cells and the development of regulatory T cells; the influence of gut microflora on immunity, allergic sensitization and infectious disease; the role of nutrition in preventing necrotizing enterocolitis in an animal model of preterm birth; and the role of PUFA of different classes in influencing immune responses and in shaping the development of atopic disease. This report summarizes the content of the lectures and the subsequent discussions

Full text not available from this repository.

More information

Published date: 2006
Keywords: unsaturated, acid, exposure, pregnancy, infant, fetal, pufa, nutrition, research, models, animal, responses, birth, in-utero, immune tolerance, fatty acids, blood, immediate, infection, hypersensitivity, phenotype, dendritic cells, fetus, fatty acid, immunology, animals, microbiology, premature, human, infant nutrition physiology, development, newborn, milk, humans, cells, immune system, gastrointestinal tract, disease, allergens, preterm, report, environmental, prevalence, tolerance

Identifiers

Local EPrints ID: 60961
URI: https://eprints.soton.ac.uk/id/eprint/60961
ISSN: 0007-1145
PURE UUID: 2367dc2c-5328-435c-aa41-6792d7019ffa

Catalogue record

Date deposited: 04 Sep 2008
Last modified: 13 Mar 2019 20:29

Export record

Altmetrics

Contributors

Author: P.C. Calder
Author: S. Krauss-Etschmann
Author: E.C. De Jong
Author: C. Dupont
Author: J.S. Frick
Author: H. Frokiaer
Author: J. Heinrich
Author: H. Garn
Author: S. Koletzko
Author: G. Lack
Author: G. Mattelio
Author: H. Renz
Author: P.T. Sangild
Author: J. Schrezenmeir
Author: T.M. Stulnig
Author: T. Thymann
Author: A.E. Wold
Author: B. Koletzko

University divisions

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of https://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×