Immune response phenotype induced by controlled immunization of neonatal pigs varies in type 1:type 2 bias.
Immune response (IR) of pigs varies by litter and by individual such that ratios of type-1 and type-2 IR differ. Estimates of heritability for antibody and cell-mediated IR suggest that genotype and the environment contribute approximately 20% and 80% to this variation. It is hypothesized that the IR phenotype of outbred neonatal pigs is immature and variable progressing with age from type-2 bias to a more balanced phenotype. To test this, pigs were IR phenotyped by a standardized protocol using two intramuscular injections of the combined type-1 and type-2 antigens (Ag) Candida albicans (CA) and hen egg white lysozyme (HEWL). Immune response was measured by wheal and flare reaction to HEWL and double skin fold thickness (DSFT) response to each Ag injected intradermally at 35 days of age. Blood was collected at 14 and 35 days of age to measure immunoglobulin IgG(1), IgG(2) and IgE isotype-relatedness of antibody (Ab) to CA and HEWL. Comparison was made between two different groups of pigs (A) and (B), from the same herd tested separately at an interval of two and a half years. An unexpected group difference in IR bias was observed. Bias in IR was not consistently toward type-2. Increase in DSFT to CA, an indicator of type-1 IR, was greater in A while frequency of wheal and flare to injection of HEWL, a type-2 IR correlate, was greater in B. Frequency of individuals with positive serum Ab activity to both Ags was greater in B than A for most isotypes. Ratios of Ab activity by type-1 and 2 isotypes and DSFT to type-1 and 2 Ags indicate diminished type-1 relative to type-2 biased IR response in B. We conclude that in normal neonatal pigs under standard husbandry IR bias is not invariably toward type-2. Phenotype varied between groups in type-1:type-2 bias with implications for protective and immunopathogenic IR. While the etiology was not pursued it is possible that unidentified environmental variables may have induced this change in IR phenotype.
Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, N1G 2W1 Canada.
J
J
Schmied
K
K
Hamilton
P
P
Rupa
S-Y
SY
Oh
B
B
Wilkie
D000818:Animals; D000831:Animals, Newborn; D002176:Candida albicans / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007111:Immunity, Cellular / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology*; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D007132:Immunoglobulin Isotypes / Q000097:blood / Q000276:immunology; D009113:Muramidase / Q000276:immunology; D010641:Phenotype; D013047:Specific Pathogen-Free Organisms; D013552:Swine / Q000276:immunology*
D007074:Immunoglobulin G; D007130:Immunoglobulin Idiotypes; D007132:Immunoglobulin Isotypes; D007073:Immunoglobulin E; C421864:hen egg lysozyme; D009113:Muramidase