Does Inflammation after Injury Traumatize the Case for Intelligent Design?

Nobody likes it when insult is added to injury. But when injury is compounded by inflammation, it is often fatal.

Researchers recently made progress in their understanding of the causes of life-threatening inflammation. It is hoped that this new insight might improve treatment for trauma patients.1 Others see this advance in a different light; it seemingly provides potent evidence for the evolutionary framework. They claim that the cause of inflammation is yet another example of a design flaw in nature—something unexpected if life stems from a Designer’s hand. But does this new discovery really cause injury to the case for a Creator?

Inflammation and Trauma

Physical trauma is a major cause of death. In many instances, the patient survives the injury because of medical intervention only to die from a post-traumatic complication known as systemic inflammatory response syndrome (SIRS). The symptoms of SIRS, including fever and shock (increased heart rate and low blood pressure), are highly similar to those caused by a severe bacterial infection.

Systemic inflammation caused by bacteria stems from the body’s response to biomolecules from a microbial agent. The materials generated by the body’s response are known as pathogen-associated molecular patterns (PAMPs). Biomedical scientists note that when patients suffer from traumatic injury, their bodies generate compounds that elicit the immune system in a way similar to the reaction caused by PAMPs. These compounds are referred to as DAMPs (damage-associated molecular patterns). Presumably, severe tissue injury causes DAMPs to be released into the blood, exposing them to the immune system.

The Source of the Inflammatory Response

Researchers from the United States and Great Britain, speculated that the source of DAMPs may be the mitochondria, organelles in the body’s cells. They reasoned—from an evolutionary standpoint—that these organelles, which are thought to have evolved from bacteria a billion years ago, should possess molecules that cause inflammation in the same way bacterial molecules cause sepsis-induced inflammation.

The researchers discovered that DNA and proteins from mitochondria form part of the repertoire of molecules that comprise the DAMPs. Presumably, these biocompounds are released when cells are damaged as a result of severe injury. For example, the researchers

  1. measured increased levels of the mitochondrial biomolecules in human patients suffering from trauma;
  2. demonstrated that these compounds attract white blood cells; and
  3. showed that these materials cause severe inflammation when injected into rats.

Of course, the hope is that this new discovery will stimulate advances that will improve trauma care.

Trauma, Inflammation, and the Case for Biological Evolution

According to the prevailing paradigm in evolutionary biology, mitochondria arose when a bacterial cell was ingested by a burgeoning eukaryotic cell and evolved to be a permanent internal symbiont. If this is the case, then it is reasonable to expect that mitochondrial compounds would, indeed, make up at least part of DAMPs.

It is impressive the evolutionary paradigm would make a prediction that successfully guided research efforts. But just because this prediction has been satisfied doesn’t mean that the similarity between PAMPs and mitochondrial DAMPs has to be understood exclusively from an evolutionary standpoint. This similarity can be readily accommodated as part of a creation model. The shared features of these molecules (which just happen to cause an immune response) could simply reflect the work of a Creator who designed the molecules in mitochondria with the same structural elements as those from bacteria.

It is tempting to view the existence of SIRS-causing materials within the mitochondria as a bad design—a flaw that would be expected only if evolution generated life. It is not a feature that one would anticipate if an all-knowing, all-powerful, all-good Creator made life. (For example, listen to the March 4, 2010 edition of the Nature Podcast, in which this work is described. The interviewer, Natasha Gilbert, states that the body’s response to mitochondrial DMAPs “seems like a bit of a design flaw.”)

In response to this challenge, however, Carl J. Hauser, who helped lead the investigation, disagrees. He argues that the immune response to mitochondria is a well-designed system, because SIRS doesn’t happen all the time, only when severe injury occurs. The SIRS response is avoided because the immune system doesn’t monitor activities inside cells.

In reality, the secondary inflammation that occurs after a severe injury should be inconsequential. It is only a concern because we now have the medical capabilities to keep people alive after trauma occurs. For much of human history this type of medical intervention simply wasn’t available. Even just a few decades ago, nearly everyone who experienced severe injury died. But the hope is that the number of deaths that result from traumatic injury will dramatically decrease now that we know the source of DAMPs.

And as we learn more about biological systems, I hope that the challenges to the design argument diminish as presumed design flaws in biological systems turn out to be elegant constructs.


1. Qin Zhang et al., “Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury,” Nature 464 (2010): 104–7.


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