The Proceedings of the Eighth International Conference on Creationism (2018)

to their release from the cell to effectively shield them from PRRs preventing immune system activation. It may be argued that this coating only occurs for a short time as phage binding to the bacterial surface typically results in cell lysis . However, it has been demonstrated in several studies that lysogeny instead of the lytic lifestyle is the preferred lifestyle in the mammalian microbiome (Kim and Bae 2018). This is intriguing because lysogeny promotes the long term survival of bacteria by preventing phage invasion of the intracellular environment, and therefore would complement the protective effect of cell surface phage binding. B. Multiple phage bind to microbiome bacteria and may collaborate in phage cloaking and protection of the microbiome and host Several hundred phage are now known to infect E.coli and single E.coli strains can be simultaneously infected with multiple phage species. It ’ s striking that each phage species which infects E.coli has different length tails. This could in theory allow for the packing of multiple icosahedral and other shaped heads to fit in layers on the bacterial surface effectively blocking the access of PRRs to the MAMPs on the surface of the cells. Currently, there is no known evolutionary explanation for phage tail length (Youle 2017). Cloaking theory would predict that tail length would be important for effective phage packing of multiple phage species and phage blocking of PRR receptor engagement. For instance, the extracellular component of the Toll-like-receptors (TLR) immune receptors, which are the primary receptors of the immune system that bind to MAMPs, are arranged in a horseshoe like shape with a 9 nm diameter suggesting that they project at least 9 nm from the surface of the immune cell (Francis 2007; Owen et al. 2013; Yong 2005). Phage tails of some of the well known T-phages range from 90-230 nm and thus we predict that they can effectively block TLRs from binding to microbiome bacteria MAMPs (Rowher 2014). In addition, in support of the idea that phages possess design features which promote their effective collaborative binding on the bacterial surface, T3 phages are known to plug leaking holes in the membrane/cell wall of bacteria which are simultaneously infected by T7 (Villarreal 2009). 3. Phage lysis of mammalian associated bacteria promotes a stable population of microbiome bacteria How then do we reconcile the idea that phages may protect the microbiome with the fact that phages lyse bacteria? We postulate, based on published evidence, that the microbiome bacteria and phage populations achieve a dynamic equilibrium such that each can exist long term in the mammalian host (Youle 2017). The population equilibrium between bacteria and phage involves several defense mechanisms employed by both (Youle 2017). Bacteria possess mechanisms to control phage infection including changing their surface antigens, use of restriction enzymes, and the presence of an immune system known as Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR). CRISPR is a system which involves obtaining small segments of nucleic acid from infecting viruses (Rowher 2014). These small snippets of DNA or RNA can then be used to identify invading viruses during subsequent infection of the same viral species. In turn, phages can adapt to bacterial MAMP alteration by changing their RBPs. RBPs are known as the fastest evolving genes in a phage genome (Youle 2017). In addition, phages can modify their nucleic acids or delay the entry of their DNA into the cell while making defensive proteins from the initial inserted DNA to defend against the anti- nucleic acid bacterial host defense mechanisms. The end result of this back and forth defensive posturing results in the modulation of both bacterial and phage growth and maintenance of populations of both (Youle 2017). Furthermore, the ability of RBP to bind to MAMPs can inhibit immune activation even after cells lysis, because there is evidence that RBPs can bind to soluble MAMPs (Gorski et al. 2012). 4. Mammalian associated phage possess specific mechanisms to protect both of its hosts from pathogenic bacterial invaders How then do the protective mammalian associated phage recognize and lyse foreign pathogenic bacteria if they have become less able to cause lysis in their host bacteria? We speculate that the pathogen invader may not be immune to the phages which have been diversifying and becoming more resistant to bacterial defense mechanisms within the mammalian microbiome so the pathogen invader in fact may be initially more susceptible to the mammalian microbiome phage. We would also speculate that the invading pathogen would be present in small populations and be susceptible to complete lysis before establishing resistance to the phages. Phages also possess design features to complement the Francis et al. ◀ Bacteriophages as beneficial regulators ▶ 2018 ICC 154 Figure 1. Tailed phages bind to the surface of bacteria. In some photos, the phages appear to saturate the bacterial surface. Some phages also bind to pili and flagellum which extend from the bacteria surface. We propose that this evidence supports the theory that phages can coat MAMPS on normal flora bacteria protecting them from the mammalian immune system. Courtesy of Graham Beards, WikiCommons. Retrieved from the web https://commons.wikimedia.org/wiki/File :Phage.jpg, Feb 13, 2018.