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Victor Apanius Assistant Professor Department of Biological Sciences Florida International University |
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Victor Apanius Assistant Professor Department of Biological Sciences Florida International University |
Evolutionary Ecology of Vertebrate Immunity
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| Guest Lecture for
Fall 1999 Graduate Seminar: Hormones, Behavior & Endocrine Discrupting Chemicals in the Environment |
ABSTRACT:
The vertebrate immune system integrates the antigenic stimuli
from and responds to a myriad of infectious agents. Immune
function is tightly regulated with other organismal functions,
such as behavior, growth and reproduction, through local
(cytokine) and systemic (endocrine) regulators. Regulation of
immunity appears to be linked to life history evolution.
Growing birds appear to insulate immunity from extrinsic perturbations. In precocial quail (Coturnix coturnix), nutritional limitation stunted somatic growth of chicks but not antibody responsiveness. In semialtricial kestrels (Falco tinnunculus), experimental increase of sibling competition slowed growth of nestlings but not antibody responsiveness. In semiprecocial black-headed gulls (Larus rudibundus), testosterone implants increased sibling rivalry of nestlings and also enhanced antibody responsiveness. After the age of first reproduction, immunity appears to be downregulated as reproductive effort is increased. In captive zebra finches, manipulation of the number of offspring in the nest was negatively related to antibody responsiveness of the parents. In wild kestrels, manipulation of the number of offspring was positively related to daily energy expenditure and negatively related to antibody responsiveness of the parents. In wild American kestrels (Falco sparverius), the number of offspring was negatively related to leukocyte levels and serum IgG levels and positively related to the intensity of blood parasitism. A study of wild common terns (Sterna hirundo) has been initiated in collaboration with Ian Nesbitt. This population will provide information on regulation of immunity in young, middle-aged and old breeding birds to test the hypothesis that immune function is a function of residual reproductive value, that is the likelihood of contributing to the next generation. |
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| SEMINAR TALK: Bidirectional Communication Between the Endocrine and Immune Systems: Who Said What, When, Where and Why? |
SEMINAR TALK ABSTRACT:
Vertebrate immunity against parasites involves three tiers of molecular, cellular and physiological mechanisms:
1. Circulating cytolytic proteins (complement), circulating phagocytic cells (neutrophils), and ciliated mucosal surfaces (bronchial passages) exemplify molecular, cellular and physiological components of "innate" or "natural" immune mechanisms. These mechanisms operate effectively without prior exposure to or memory of parasite-derived molecular markers (antigens). 2. Antigen-binding proteins, (antibodies/immunoglobulins), antigen-presenting (macrophages) and antibody secreting cells (B- lymphocytes), and competively proliferating lymphoid tissues (germinal centers) represent components of the "humoral" or TH-2-mediated mechanisms of "acquired" immunity. These mechanisms are invoked by antigenic exposure, discrimate between host and parasite markers and can retain memory of previous encounters with specific antigens. 3. Cytotoxic regulatory proteins (interferon-gamma), cytotoxic cells (T-lymphocytes), and lymph nodes are components of "cellular" or TH-1-mediated mechanisms of "acquired" immunity. Like humoral immunity, these mechanisms show antigen- specific induction and memory. These complementary, and sometimes redundant, mechanism are regulated by the complex interplay of these factors: 1. Antigenic stimulation of immunity depends on the chemical nature, dose and route of the antigenic exposure. Some antigenic signals elicit strong responses from all three tiers while others are barely detectable for any single mechanism. The antigenic signals become more potent when accompanied by molecular signals of host tissue damage and inflammation. 2. Cytokines which are released by cells of the immune system and coordinate responses at the site of infection. Particular cytokines (interleukin-1 and tumor necrosis factor) have systemic effects and coordinate intermediate metabolism, thermoregulation and behavior with immunological mechanisms. 3. Hormones that regulate energy metabolism (corticosteroids, growth hormone, thyroid hormone), reproductive function (gonadal steroids, prolactin) and circadian cycles (melatonin) also regulate the activity of the immune system. The complexity of immunological regulation poses serious challenges to the study of anthropogenic chemicals that show endocrine activity in vertebrates. The traditional approach is to use in vivo and in-vitro models to test the effect of suspect chemicals or effluents on innate, humoral and cellular responses. Although the results of these tests are robust, the extrapolation to fitness effects in natural populations remains problematic. At present, we lack information on:
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| RELATED READING: Marsh, James and Marion Kendall (eds.) The Physiology of Immunity. CRC Press, 1996. Section I. An Overview of the Immune System 
ONLINE RESOURCES:Dr. Apanius's Departmental Page |
| OTHER FALL 1999 SPEAKERS: David Crews . Theo Colborn . Lou Guillette . Fred vom Saal |
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