Oral Tolerance and Regulation of Immunity to Dietary Antigens

We examined whether maternal exposure to food antigens during lactation and maternal allergic status would affect the development of food allergy in offspring. OVA-sensitized or OVA-nonsensitized BALB/c female mice were exposed or unexposed to OVA during lactation. After weaning, their offspring were systemically sensitized twice with OVA and repeatedly given OVA by oral intubation. While 97.1% of the mice breastfed by OVA-nonsensitized and OVA-unexposed mothers developed allergic diarrhea, 59.7% of the mice breastfed by OVA-exposed nonallergic mothers during lactation and 24.6% of the mice breastfed by OVA-exposed allergic mothers during lactation developed food allergy. Furthermore, OVA was detected in breast-milk from OVA-exposed nonallergic mothers during lactation (4.6±0.5 μg/mL). In addition, OVA-specific IgG1 titers were markedly increased in breast milk from allergic mothers (OVA-sensitized and OVA-unexposed mother:11.0±0.5, OVA-sensitized and OVA-exposed mother:12.3±0.3). Our results suggest that oral tolerance induced by breast milk-mediated transfer of dietary antigens along with their specific immunoglobulins to offspring leads to antigen-specific protection from food allergy.

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V. Mechanisms of immunologic sensation of intestinal contents

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2000.278.2.g191 ◽

2000 ◽

Vol 278 (2) ◽

pp. G191-G196 ◽

Cited By ~ 30

Author(s):

Fergus Shanahan

Keyword(s):

Oral Tolerance ◽

Food Hypersensitivity ◽

Mucosal Inflammation ◽

Systemic Autoimmunity ◽

Dietary Nutrients ◽

Dietary Antigens ◽

Intestinal Contents ◽

Mucosal Homeostasis ◽

Mucosal Pathogens ◽

Adaptive Recognition

Immune perception of intestinal contents reflects a functional dualism with systemic hyporesponsiveness to dietary antigens and resident microflora (oral tolerance) and active immune responses to mucosal pathogens. This facilitates optimal absorption of dietary nutrients while conserving immunologic resources for episodic pathogenic challenge. Discrimination between dangerous and harmless antigens within the enteric lumen requires continual sampling of the microenvironment by multiple potential pathways, innate and adaptive recognition mechanisms, bidirectional lymphoepithelial signaling, and rigorous control of effector responses. Errors in these processes disrupt mucosal homeostasis and are associated with food hypersensitivity and mucosal inflammation. Mechanisms of mucosal immune perception and handling of dietary proteins and other antigens have several practical and theoretical implications including vaccine design, therapy of systemic autoimmunity, and alteration of enteric flora with probiotics.

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Management - Disease interactions in pigs 3: Nutrition - disease interactions

Proceedings of the British Society of Animal Production (1972) ◽

10.1017/s0308229600016755 ◽

1988 ◽

Vol 1988 ◽

pp. 34-34

Author(s):

B.G. Miller ◽

M.Bailey ◽

E. Telemo ◽

C.R. Stokes ◽

F.J. Bourne

Keyword(s):

Oral Tolerance ◽

Crypt Cell ◽

Dietary Composition ◽

Bacterial Colonisation ◽

Cell Hyperplasia ◽

E Coli ◽

Type Iv ◽

Dietary Antigens ◽

Weaned Pig ◽

Cell Mitosis

Both level of feeding and dietary composition have been demonstrated to influence bacterial colonisation and diarrhoea in the weaned pig (Smith & Hall 1968, Bertschinger et al 1978, Lecce et al 1983). Kenworthy and Allen 1966 proposed that “the stimulus to bacterial growth derives from the hosts response mechanisms to intestinal irritation” and that the enterotoxigenic E Coli “Acts as an exacerbating agent rather than a primary pathogen” (Kenworthy et al 1967).Several workers have suggested that the primary intestinal response is villus atrophy, an elevation in crypt cell mitosis (by up to x10) and crypt cell hyperplasia, associated with malabsorption, mal-digestion and increased intra-epithelial lymphocytes. Such a response is characteristic of a T cell mediated type IV hypersensitivity (Ferguson 1980). Miller et al (1984) have therefore suggested that one of the factors which may contribute to the aetiology of postweaning diarrhoea is a transient hypersensitivity to dietary antigens prior to the development of oral tolerance.

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