ovalbumin and Protein-Energy-Malnutrition

While severe protein energy malnutrition (PEM) has been known to depress several immune functions, allergies are suppressed by decreasing IgE and impairing vascular permeability and mast cell functions. To address the effect of moderate protein malnutrition without growth arrest and protein hypernutrition on type I allergy, we examined the effect of various levels of protein nutrition on allergy at humoral immunity and the regulation of Th cell function levels. Mice fed 100 g/kg (moderate protein malnutrition; MPM), 200 g/kg (normal protein nutrition; PN) and 400 g/kg (protein hypernutrition; PH) protein diets were intraperitoneally sensitized to ovalbumin (OVA) in aluminum hydroxide. Higher elevations of OVA-specific IgE and total IgE in the serum were observed in the PH group as compared to the PN group. However, OVA-specific IgE in the MPM group was not significantly different from that in the PN group, although the former appeared higher than the latter. While CD3, CD4, CD8 and B220 expressions in the splenic lymphocytes were decreased in the MPM group, B220 expressions were increased in the PH group. Splenic lymphocyte proliferative responses to OVA were augmented in the PH group and depressed in the MPM group. IFN-gamma production from splenic lymphocytes was significantly decreased; however, IL-4 production was not affected significantly in the MPM group, and increased in the PH group. These findings suggest that immune functions to specific antigens in the MPM state are depressed at the cytokine level but not in terms of IgE responses. They also suggest that immune functions become Th2-predominant in the PH state, resulting in an increased risk of type I allergy.

Topics: Animals; Animals, Newborn; Antibody Formation; Diet, Protein-Restricted; Dietary Proteins; Dose-Response Relationship, Immunologic; Female; Immunity, Cellular; Immunoglobulin E; Injections, Intraperitoneal; Mice; Mice, Inbred BALB C; Ovalbumin; Protein-Energy Malnutrition

The role of the sympathetic nervous system in the immune deficiency developed in protein-energy malnutrition (PEM) was investigated by assessing the effects of sympathectomy on the intestinal immune response of rats subject to prenatal or postnatal malnutrition. Chemical sympathectomy increased the number of IgA+ cells migrating into the intestinal lamina propria of control animals, but this effect was abrogated in rats malnourished during their perinatal stage. The method by which perinatal malnutrition was achieved influenced the magnitude of the effect on serum IgA levels with malnutrition during lactation having a more pronounced depressive effect on IgA than malnutrition during gestation. In experiments in which animals were intestinally immunised with ovalbumin (OVA) the mucosal immune response was reduced in non-sympathectomised malnourished (MN) animals and a lower level of anti-OVA IgA was detected in serum. However, in sympathectomised animals, there was no difference between MN animals and controls in the intestinal and humoral immune responses. The preliminary evidence presented in this paper strongly supports a role for the noradrenergic neurotransmitter system in the immunodeficiency developed during PEM.

Topics: Animals; Female; Immunoglobulin A; Immunologic Deficiency Syndromes; Injections, Intraperitoneal; Intestinal Mucosa; Jejunum; Lactation; Models, Immunological; Neuroimmunomodulation; Ovalbumin; Oxidopamine; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Protein-Energy Malnutrition; Rats; Sympathectomy, Chemical; Sympathetic Nervous System

Immunodeficiency syndromes associated with protein-energy malnutrition (PEM) have been documented extensively, although to date the mechanism underlying these defects remains uncharacterized. In this study, we have evaluated T, B, and antigen-presenting cell functions of malnourished mice fed a 4% protein diet compared with litter-mate controls fed a 20% protein diet. Spleen cells from malnourished mice presented both soluble foreign protein and allogeneic MHC antigens less efficiently than control mice. However, T cells from malnourished animals demonstrated effective or enhanced specific T-cell activation when stimulated with allogeneic cells, while B cells from protein-deprived animals responded normally in proliferative responses to T-cell driven cognate and non-cognate, as well as mitogen, stimulation. To assess further antigen-presenting cell function, three requirements for successful antigen presentation were evaluated. First, the proliferation of the IL-1-dependent cloned T-cell line D10 demonstrated a slight deficiency in IL-1 production by malnourished splenic antigen-presenting cells, and the addition of saturating amounts of IL-1 to the assay could partially reconstitute function. Second, quantitative cell-sorter analysis revealed minimal deficiencies of spleen-cell Ia expression. Third, antigen-processing function was assayed in vitro by using processed antigen fragments; no improvement in protein-deprived antigen-presenting function resulted. Together, these findings suggest that either decreased Ia glycoprotein expression on a critical subset of antigen-presenting cells (APCs) or a quantitative deficiency in such a subset of cells, or both, underlie the defective antigen-presenting cell function observed in chronic protein deprivation (CPD).

Topics: Animals; Antigen-Presenting Cells; B-Lymphocytes; Chronic Disease; Histocompatibility Antigens Class II; Interleukin-1; Lymphocyte Activation; Mice; Mice, Inbred Strains; Ovalbumin; Protein-Energy Malnutrition; Spleen; T-Lymphocytes

Mice maintained on a low protein diet (4% casein initiated at weaning) produced IgE antibody responses to both ovalbumin and Ascaris body fluid proteins. The titres in young mice were comparable to those of mice maintained on a normal (20% protein) diet particularly at high doses of immunogen. However, following immunization with low doses of immunogen the initiation of antibody response in malnourished mice was delayed and the levels finally obtained were significantly suppressed below normal levels. This effect was more apparent in animals maintained for prolonged periods on diet. Possible mechanisms for this suppression are presented.

Topics: Animals; Antigens; Ascaris; Dietary Proteins; Dose-Response Relationship, Immunologic; Female; Immunoglobulin E; Immunosuppression Therapy; Male; Mice; Mice, Inbred BALB C; Ovalbumin; Protein-Energy Malnutrition; Time Factors