Maternal antibodies reduce costs of an immune response during development.
Young vertebrates are dependent primarily on innate immunity and maternally derived antibodies for immune defense. This reliance on innate immunity and the associated inflammatory response often leads to reduced growth rates after antigenic challenge. However, if offspring have maternal antibodies that recognize an antigen, these antibodies should block stimulation of the inflammatory response and reduce growth suppression. To determine whether maternal and/or offspring antigen exposure affect antibody transmission and offspring growth, female Japanese quail (Coturnix japonica) and their newly hatched chicks were immunized. Mothers were immunized with lipopolysaccharide (LPS), killed avian reovirus vaccine (AR), or were given a control, phosphate-buffered saline, injection. Within each family, one-third of offspring were immunized with LPS, one-third were immunized with AR, and one-third were given the control treatment. Maternal immunization significantly affected the specific types of antibodies that were transmitted. In general, immunization depressed offspring growth. However, offspring immunized with the same antigen as their mother exhibited elevated growth in comparison to siblings immunized with a different antigen. This suggests that the growth suppressive effects of antigen exposure during development can be partially ameliorated by the presence of maternal antibodies, but in the absence of specific maternal antibodies, offspring are dependent on more costly innate immune defenses. Together, the results suggest that the local disease environment of mothers prior to reproduction significantly affects maternal antibody transmission and these maternal antibodies may allow offspring to partially maintain growth during infection in addition to providing passive humoral immune defense.
Grindstaff
Jennifer L
JL
Indiana University, Department of Biology and Center for the Integrative Study of Animal Behavior, 1001 E. Third Street, Bloomington, IN 47405, USA. jen.grindstaff@okstate.edu
D000818:Animals; D000906:Antibodies / Q000097:blood* / Q000276:immunology; D003370:Coturnix / Q000254:growth & development* / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D007112:Immunity, Maternally-Acquired / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D030101:Orthoreovirus, Avian / Q000276:immunology; D010063:Ovum / Q000166:cytology
D000906:Antibodies; D007074:Immunoglobulin G; D008070:Lipopolysaccharides