Fig 1. Uptake of T4 phage by mammalian cells does not trigger a pro-inflammatory immune response [modified].
(A) A549 cells and (B) MDCK-I cells incubated with T4 phages for 2 hours. Images were taken with a confocal microscope; the plasma membrane is shown in magenta, T4 phage DNA in green, and the cell nucleus in blue.
(A) A549 cells and (B) MDCK-I cells incubated with T4 phages for 2 hours. Images were taken with a confocal microscope; the plasma membrane is shown in magenta, T4 phage DNA in green, and the cell nucleus in blue.
Imagine you're a designer charged with designing a mammalian cell so it grows and multiplies efficiently. You've already designed DNA and genes to make the right proteins to stimulate cell growth, but it isn't working as well as it should.
What do you do?
An intelligent designer, especially an omnipotent, omniscient designer, wouldn't have designed it sub-optimally in the first place, but if it had, it would simply redesign it and make sure all the right genes were provided because, being omnipotent, nothing would be impossible.
But whatever designed the mammalian cell didn't do the intelligent thing.
Instead it opted for an unnecessarily complex solution - it used the bacteriophage viruses that it had designed to infect and kill the bacteria it had designed earlier, to infect mammalian cells and give them the missing genes to correct its mistake. It then modified the process it had designed to protect the cells from infection, so these viruses don't trigger an immune response and get destroyed.
No going for the simple solution like a normal intelligent designer would, when a much more complex solution is available, eh?
This is what you need to believe to be an intelligent [sic] design creationist, to explain the findings of a group of researchers led by Jeremy J. Barr of the School of Biological Sciences, Monash University, Clayton, Australia. They have discovered that phage viruses, which proliferate in our gut where they normally parasitise and kill bacteria, are taken in by mammalian cells where they accumulate and activate metabolic pathways that promote cell metabolism and growth and prolong the cell cycle.
The findings of the team are published open access in PLOS Biology:
AbstractThis degree of unnecessary complexity is typical of evolved systems but gives the lie to any claims of an intelligence being involved in the process, especially an omniscient, omnipotent intelligence like creationists imagine designed all living things.
There is a growing appreciation that the direct interaction between bacteriophages and the mammalian host can facilitate diverse and unexplored symbioses. Yet the impact these bacteriophages may have on mammalian cellular and immunological processes is poorly understood. Here, we applied highly purified phage T4, free from bacterial by-products and endotoxins to mammalian cells and analyzed the cellular responses using luciferase reporter and antibody microarray assays. Phage preparations were applied in vitro to either A549 lung epithelial cells, MDCK-I kidney cells, or primary mouse bone marrow derived macrophages with the phage-free supernatant serving as a comparative control. Highly purified T4 phages were rapidly internalized by mammalian cells and accumulated within macropinosomes but did not activate the inflammatory DNA response TLR9 or cGAS-STING pathways. Following 8 hours of incubation with T4 phage, whole cell lysates were analyzed via antibody microarray that detected expression and phosphorylation levels of human signaling proteins. T4 phage application led to the activation of AKT-dependent pathways, resulting in an increase in cell metabolism, survival, and actin reorganization, the last being critical for macropinocytosis and potentially regulating a positive feedback loop to drive further phage internalization. T4 phages additionally down-regulated CDK1 and its downstream effectors, leading to an inhibition of cell cycle progression and an increase in cellular growth through a prolonged G1 phase. These interactions demonstrate that highly purified T4 phages do not activate DNA-mediated inflammatory pathways but do trigger protein phosphorylation cascades that promote cellular growth and survival. We conclude that mammalian cells are internalizing bacteriophages as a resource to promote cellular growth and metabolism.
Fig 4. Overview of the effect of exogenous phages on cellular pathways.
(A) Innate immune pathways in BMDM and A549 cells. Phage DNA is protected by the phage capsid and is not detected by the TLR9 or cGAS-STING. (B) The effect of phages on MDCK-I and A549 cells after 8 hours. The AKT pathway on the left and the CDK1 pathway on the right show the major cellular changes detected in response to T4 phage.Bichet MC, Adderley J, Avellaneda-Franco L, Magnin-Bougma I, Torriero-Smith N, Gearing LJ, et al. (2023)
Mammalian cells internalize bacteriophages and use them as a resource to enhance cellular growth and survival.
PLoS Biol 21(10): e3002341. https://doi.org/10.1371/journal.pbio.3002341
Copyright: © 2023 The authors.
Published by PLoS. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Typical of an evolved system, where mammalian cells evolved in an environment in which there were already ubiquitous phage viruses, viruses and cells formed a symbiotic association which provided the genetic material the cells needed, and so there was no selection pressure to evolve a more intelligent, less complex solution, and evolution went with the utilitarian option because, regardless of how complex it was, the result was an improvement on what went before it.
For some inexplicable reason, creationists would rather we thought of their putative designer as an incompetent fool who shouldn't be in charge of designing something as complicated as a knitting needle, than accept that biological systems are the result of an unintelligent, utilitarian natural process working without a plan or ultimate goal.
Unlike evolved systems, intelligent design is minimally complex. Complexity is not an argument for intelligent design; it’s an argument against it.
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