Effect of single or combined climatic and hygienic stress on natural and specific humoral immune competence in four layer lines.

Effects of long-term climatic stress (heat exposure), short-term hygienic stress [lipopolysaccharide (LPS)], or a combination of both challenges on the immune competence of 4 layer lines was investigated. The lines were earlier characterized for natural humoral immune competence and survival rate. Eighty hens per line were randomly divided over 2 identical climate chambers and exposed to a constant high temperature (32 degrees C) or a control temperature (21 degrees C) for 23 d. Half of the hens housed in each chamber were i.v. injected with LPS at d 1 after the start of the heat stress period. Within each of the treatment groups, half of the hens were s.c. immunized with human serum albumin (HuSA) at d 2 after the start of the heat stress period to measure specific antibody (Ab) titers to HuSA. The effect of heat, LPS, or a combined challenge on specific Ab titers to HuSA, natural Ab titers to keyhole limpet hemocyanin or HuSA (in hens that were not immunized with HuSA), and activity of the classical and alternative complement pathways were investigated. Heat stress enhanced specific and natural immune responses. Administration of LPS enhanced natural immune responses but decreased specific immune responses. The lack of interaction between heat stress and LPS administration, except for natural Ab titers to HuSA, suggest that these were 2 independent stressors. The lines had a similar response pattern but differed in the response level. Neither natural humoral immune competence nor survival rate, for which the lines had been characterized, was indicative of the specific and natural immune response to different stressors. Lipopolysaccharide and heat stress initiated sequential responses over time, with an earlier effect of short-term LPS exposure (within the first and second week) and a later effect of long-term heat exposure (within the second and third week). These data suggest that LPS and heat stress affect the natural and specific immune competence of laying hens.