Friday 23 December 2011

Does the Immune Response in Sea Fans Provide Hope for the Survival of Corals during Climate Change?

Climate change is resulting in higher sea temperatures, influencing coral health which leads to an increase in disease. Sea fans become infected with what seem to be opportunistic pathogens such as Aspergillus fumigatuus and A. sydowii, the latter is investigated here. The sea fan speciesGorgonia ventalina is experiencing a prolonged and widespread outbreak of A. sydowii and so is the species of choice in this paper. Immunity to pathogens which take advantage of warmer sea temperatures is seen in many corals but the mechanisms used are not well known. Therefore immune responses, including increase density of ameobocytes and melanization via the prophenoloxidase cascade, are reviewed with particular emphasis on the link between the cellular response and natural warming events (the 2005 Caribbean Bleaching Event).

A. Sydowii is a deep tissue infection which causes darkened lesions on Sea Fans caused by pigmented calcium carbonate. However amoebocytes have been shown to play a role in wound repair, not only in corals but sea anemones also, with influxes becoming known as inflammatory responses because their increase due to infection is so dramatic. Histological images of the mesoglea (connective tissue) allow calculations to be made referring to increased density of amoebocytes here. On average in a healthy coral amoebocytes occupy 15.2% of the mesoglea, in an infected coral this number rose to 24.5%. However in lab experiments this increase is localized to within 1mm of the infection with no difference between corals in amoebocyte density outside of this zone (resulting in the conclusion that there was no systemic increase with regards to fungal exposure). Staining with hematoxylin and eosin revealed that melanin is produced by the host and is found surrounding the infected areas of infected corals. Melanin is a dark pigment that is known to be involved in coral protection, with theories suggesting it keeps UV light away from important symbiotic bacteria. Some amoebocytes also contained black stained granules when used with the Fontana – Masson procedure but this was not consistent for all suggesting differences in immune response function between groups of amoebocytes. Melanin in the form of melanosomes was also noted as present and their synthesis was down to a prophenoloxidase cascade event, an immune response seen only before, in invertebrates.

Interestingly, the sea fans that had been affected by the 2005 bleaching event, caused by the biggest flux of sea temperature in 100 years, showed an increase in amoebocyte density throughout the entirety of the coral tissue, not just in damaged tissue. Different to the results found in corals exposed to the fungus at ambient sea temperature. Replication experiments completed in the lab further supported these findings as keeping corals at a temperature of 31.5˚C for 8 days, compared to those kept at ambient sea temperature, resulted in increased amoebocyte density that was found to be consistent throughout the coral tissue (from 16.9% to 29.2%). This is the first piece of evidence producing results that allow us to see a systemic reaction to elevated temperature.

Amoebocytes, the prophenoloxidase cascade events and the production of melanin have all been observed in Gorgonia ventlina as immune response and resistance to temperature induced fungal infection. The amoebocyte increase is correlated with anti fungal metabolites, immune reactive enzymes and the production of melanin which could provide this coral with an advantage over its scleractinian relatives, which show no amoebocyte increase when faced with fungal infection. The melanin provides a barrier which stops the spread of the damaging A. sydowii fungus. However no long term experiments were reported in this paper with no suggestion as to what would happen if temperature increase was prolonged for longer than what was seen in 2005. Also no systemic system was observed and so the mechanism for the production of amoebocytes located at the points of fungal infection are unknwn and further experiments need to be undertaken.

A review of: Mydlarz LD, Holthouse SF, Peters EC, Harvell CD (2008) Cellular Responses in Sea Fan Corals: Granular Amoebocytes React to Pathogen and Climate Stressors. PLoS ONE

3 comments:

Mario Lewis said...

Hi Sarah,

Interesting review. Anthozoan species apparently have an innate immune system but do not have an adaptive one, unlike higher eukaryotes. The amoebocytes described in your review seem to function like macrophages. Could it be that amoebocytes are an ancestral lineage to the adaptive immune system?

The melanosomes mentioned are also intriguing. I wonder if their photoprotective function is in conjunction with fluorescent proteins, or whether they are part of the fluorescent protein superfamily but diverged in the past or more recently.

Colin Munn said...

In response to Mario's interesting comment - the malanosomescare structures that produce melanin. Melanin KIS a simple organic compound built from amino acid tyrosine and so is very different to the fluorescent proteins.

Mario Lewis said...

Hi Colin,

Thanks for the information. I find it interesting that tyrosine is intrinsic to melanin synthesis. Tyrosine seems to be in all sorts of pigmentation. Im doing a paper on fluorescent proteins and it is a key amino acid in the FP chromophore, highly conserved in all natural FPs identified to date. Could it be because of the phenolic side chain that has a key role in light absorption/reflection?