Immune response to a pathogen in corals Claudia Patricia Ruiz-Diaz a,n , Carlos Toledo-Hernández b , Alberto M. Sabat b , Mariano Marcano c a Department of Environmental Sciences, University of Puerto Rico, Río Piedras Campus, PO Box 70377 San Juan, PR 00936-8377, United States b Department of Biology, University of Puerto Rico, Río Piedras Campus, PO Box 23360, San Juan, PR 00931-3360, United States c Department of Computer Science, University of Puerto Rico, Río Piedras Campus, PO Box 70377 San Juan, PR 00936-8377, United States AUTHOR-HIGHLIGHTS  The model analyzed the sea fan immune capacity to eradicate pathogen.  The model also analyzed the capacity of sea fan to reach maximal growth.  Healthy host eradicated the pathogen and reach maximal growth.  Chronically diseased host, coexist with pathogen and fail to reach maximal growth.  Terminal diseased host succumbed by the pathogen. article info Article history: Received 4 November 2012 Received in revised form 6 April 2013 Accepted 25 April 2013 Available online 6 May 2013 Keywords: Immune response Sea fans Health condition Coral diseases abstract The sea fan coral (Gorgonia ventalina), one of the most abundant gorgonians in the tropical and subtropical Atlantic waters, have suffered several diseases that have diminished its abundance throughout their range. In this study, we present a model that analyzes the capacity of G. ventalina to eradicate a micro-pathogen under three immune responses: strong, moderate, and very weak. The model assumes that: (1) polyps are the main unit of the coral; (2) the population of polyps is homogeneously distributed; and (3) the immune system is activated by a signal. When an endosymbiont exceeds a density threshold, it becomes pathogenic, increasing polyp mortality. As a consequence, the colony emits a signal to its stem cells to differentiate into phagocytic and humoral cells, both of which combat the pathogen. Given a strong immune response, the pathogen is rapidly eradicated by the immune cells, and the coral polyp population returns to an equilibrium state. With a moderate immune response, polyps and pathogen coexist, but the maximum capacity of polyp density is never reached. An immunologically compromised colony offering a weak immune response is unable to stop pathogen growth, and the colony dies. This analysis suggests an alternative explanation for the spatial and temporal variability in disease incidence and mortality, which is based on the strength of the immune system of hosts rather than the virulence of the pathogen. & 2013 Elsevier Ltd. All rights reserved. 1. Introduction Sea fans (Gorgonia spp.) are among the most conspicuous members of the tropical and subtropical Atalntic shallow-water fauna (Toledo-Hernández et al., 2007). An increasing number of afflictions have been reported in sea fans: protozoan infection (Morse et al., 1981; Goldberg et al., 1984), red band disease (Williams and Bunkley-Williams, 2000; Weill and Hooten, 2008) and aspergillosis infections (Nagelkerken et al., 1997). These diseases can cause partial tissue mortality and under severe infection, entire colony mortality (Nagelkerken et al., 1997; Toledo-Hernández et al., 2009). However, field observations have also documented full colony recovery (Toledo-Hernández et al., 2009), presumably due to strong immune responses. The immune response of corals involves a chain of reactions that start with recognition of self from non-self (Mydlarz and Harvell, 2007). Once a foreign entity has been detected, a signal is produced for the amoebocytes to stream into the invaded area to initiate phagocytosis (Meszaros and Bigger, 1999). Amoebocytes are the putative immunocytes of anthozoans and are scattered throughout the mesoglea in gorgonians (Hildemann et al., 1977; Mullen et al., 2004). When the invader is large enough to be engulfed by a single phagocyte i.e., protozoan or fungi, they may be Contents lists available at SciVerse ScienceDirect journal homepage: www.elsevier.com/locate/yjtbi Journal of Theoretical Biology 0022-5193/$ - see front matter & 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jtbi.2013.04.028 n Corresponding author. Tel.: +1 787 764 0000x7244; fax:+1 787 773 1717. E-mail addresses: claudiapatriciaruiz@gmail.com (C.P. Ruiz-Diaz), c_toledo_hernandez@yahoo.com (C. Toledo-Hernández), amsabat@gmail.com (A.M. Sabat), mariano.marcano@upr.edu (M. Marcano). Journal of Theoretical Biology 332 (2013) 141–148