Sea Star Wasting: Does environmental stress lead to an autoimmune response?
By Dr. Brian Livingston, California State University, Long Beach
Sea star populations of multiple species in western North America have been degrading and dying from an outbreak of an epidemic Sea Star Wasting Syndrome. These outbreaks have occurred periodically along the Pacific coast, but appear more extensive and involve more species in recent years. Infected individuals develop white skin lesions which spread until the whole body decays. The loss of sea stars has had trophic effects on intertidal ecosystems. The Sea Star-associated Densovirus (SSaDV) discovered in symptomatic individuals of some species was implicated as a potential initiator of the disease, but recent studies suggest this does not hold true for all species. Currently the mechanisms of tissue disintegration are unknown. Echinoderm innate immune reactions include an organismic response (increasing numbers of coelomocytes (immune cells)), and a cellular response (e.g. increasing phagocytic activity, clumping cells, and the expression of defensive proteins).
We examined the bat star coelomic fluid before and throughout disease progression to determine differences in the coelomocytes of healthy and wasting bat stars, and after exposure to isolated virus. We identified several coelomocyte types and increases in the concentration, aggregation, and phagocytic activity of coelomocytes throughout disease progression. The increase in phagocytosis and cell death before the symptoms appear suggests the beginnings of an immune response before the appearance of wasting symptoms. Our analysis of the coelomic fluid proteome shows an increase in signaling, adhesion, and immune response proteins before and after symptoms appear. The increase in cell signaling, phagocytosis, and death is suggests the bat stars have an elevated immune response prior to the wasting syndrome, and sugggest an autoimmune response may be associated with the epidemic.
Dr. Livingston received his Bachelor’s degree in Biology with an emphasis on aquatic biology from the University of California, Santa Barbara. He then transitioned to a graduate program in Molecular Biology and Biochemistry at the same institution where he studied the formation of the nervous system during embryonic development of amphibians. He received his PhD from UCSB in 1987. From there Dr. Livingston went on to a postdoctoral research fellowship at the University of California, Berkeley where he began studies on formation of the skeleton in echinoderm embryos. He has continued research in that area in faculty positions at the University of Missouri and University of South Florida before taking a position as Chair of the Department of Biological Sciences at California State University, Long Beach. While at CSULB Dr. Livingston initiated studies on the role of the immune system in sea star wasting syndrome. Dr. Livingston’s research spans the fields of embryology, cell biology, genomics and proteomics.
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