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

mammalian immune system as they have been known to contain immunoglobulin like proteins which allow them to stick and hide in mucosal surfaces of the human body (Gorski and Miedzybro 2017). In addition, some bacteria appear to have co-opted genes for the tails of tailed phages and can use these tailocins placed in their outer surface to lyse competing bacteria (Youle 2017; Ghequire and De Mot 2015). It would be interesting to see if microbiome bacteria use these antibacterial weapons. Recent studies have also shown that RBPs can recognize multiprotein complexes which are involved in exchange of antibiotic resistance genes by bacterial conjugation (Huiskonen, J. 2007) and prevent the development of antibiotic resistance. These RPBs could be used as “novel bactericides against antiobiotic-restistant bacteria” as noted by Huiskonen 2017. 5. Design features of the mammalian innate immune system allow for discrimination between infectious pathogenic animal viruses and phages We predict that phages cloak the mammalian bacteriome, but how do the cloaking phages themselves escape immune system detection of the mammalian host? Recent studies of phages being used to treat infections has shown mixed results regarding the recognition of phages by the human immune system (Navarro 2017). Fascinatingly, phages are largely ignored by the innate immune system by an elegant design feature which involves recognition of primarily internalized viruses. For instance, the TLR receptors which are the primary first-responder receptors to viruses are found on internal membranes of innate immune cells and not on the plasma membrane (Owen et al. 2013). Thus, viruses which engage and infect mammalian cells elicit an anti-viral immune response and because phages do not infect eukaryotic cells and are not typically internalized by them they are largely ignored by the immune system. This supports the idea that phages are meant to be long term agents which associate with the mammalian host and mammalian microbiome. CONCLUSION We propose here for the first time thatmammalian associated phages, the most abundant organism associated with mammals, protect the mammalian microbiome from attack by the mammalian immune system, minimize mutational decay of the microbiome, and protect both the mammalian host and its microbiome from pathogens. We base our theory on published facts about the association of phages with the microbiome. Our theory also flows from the biomatrix theory, a creation model concept (Francis 2003) which predicts that microbes including phages form a life supporting network on earth and among organisms. Here is a summary of the data and hypotheses which support the new theory presented in this paper. Here is a summary of the data which support the new theory presented in this paper. • The lytic lifestyle of phages is uniquely capable of controlling fast-growing microbiome populations. • There seems to be one or more phage species specific to each microbiome species which promote the survival of multiple species of microbiome bacteria and prevent any one species from displacing others by overpopulating. • The lysogenic lifecycle of phages promotes long term association of phages with the microbiome at the genome level and cell surface level. • Phages can quickly adapt to the rapidly changing genomes and populations of the microbiome. • Phage and microbiome symbionts adapt over time and the same mechanisms which promote recognition of microbiome bacteria also promote phage recognition of pathogenic bacteria. • Phages possess exquisitely designed systems to protect the mammalian host including the ability to directly neutralize pathogenic invaders and possession of proteins which help them localize to mammalian tissues to effectively accomplish this task. • Phages possess receptor binding proteins which allow them to engage microbiome bacterial MAMPs. MAMPs can activate the immune system. Binding of phages to MAMPs protects the microbiome from attack by the host immune system and also protects the host from an overwhelming life-threatening immune response. • Tailed phages possess designs which may allow them to efficiently cover the bacterial surface. For instance, phage species differ in tail length allowing for the potential formation of layers of phage on the bacterial surface. • The surface of bacteria contain different kinds of MAMPs. Some promote injection of DNA from the phage and some primarily promote binding of phage to the surface. The MAMPs which primarily promote surface binding are in the majority on many bacteria, allowing coating of the bacteria without immediate lysis supporting the hypothesis that phages are designed to block MAMPs. • Phages are also known to bind to soluble MAMPs supporting the hypothesis that phages are designed to block MAMPs from activating the immune system. • Phages are, in general, protected from the mammalian immune system because the immune system’s viral detection mechanisms are geared toward animal viruses and not phages. We propose that the cloaking of the microbiome by phage be considered a new theory known as phage cloaking theory and is a part of the larger theory presented here which proposes that phages can protect the microbiome and mammalian host in general. Perhaps the most interesting aspect of our observation is that the same mechanisms which lead to pathogen elimination by phages can be used to preserve the mammalian microbiome. It appears that it is the context of the relationship, i.e. the long term relationship of phage with microbiome bacteria, which helps determine whether the phage helps to preserve bacteria or eliminate them. Few research groups have been working on these intriguing discoveries as being part of a mechanism to foster the health of the mammalian microbiome. We believe that this is an example of how the creation model can lead to novel insights into biological phenomenon. Those groups who are working in this area have begun to see the Francis et al. ◀ Bacteriophages as beneficial regulators ▶ 2018 ICC 155