No Man Is an Island We Are the World
Myriads of organisms live in and on our bodies, reminds an article in the Feb. 27 issue of Science,1 and they’re not just freeloaders on a hayride. We need them, and they need us. “We are not alone,” claim the three microbiologist authors, but “we get by with a little help from our (little) friends.” Is this an uneasy truce between enemies, or a loving relationship between friends, promoting health and happiness? Microbiologists have tended to investigate the nasty germs, but does that focus give a distorted picture? “Remarkably,” the authors note, “we know far less about the thousands of species that make up our intrinsic microbiota than we know about the few dozen microbes that cause disease.” We need to start thinking of ourselves as communities, they say:
Genomic and evolutionary analyses show us that we are not the single “individuals” that we think we are. Instead, we and other complex organisms are composed of an interconnected ecosystem of eukaryotic and prokaryotic cells whose interactions can best be understood in the context of community ecology.
The authors feel the community is a result of coevolution, but seem somewhat befuddled at the growing realization that many of our beneficial bacteria share mechanisms with the harmful ones. Friend or foe, they ask:
The historical emphasis on pathogenic bacteria and their diseases has led to an assumption that genes encoding virulence factors are specific to those relationships. However, several of the cellular and molecular mechanisms that underlie interactions between an animal and its beneficial microbiota are remarkably similar to those first found in pathogens. Svanborg described how molecules that enhance persistence at a site where a given microbe is a member of the normal microbiota can be the very factors that promote disease when these bacteria emigrate to other sites of the body…. Thus, the presence of these genes may indicate the potential for host interactions, which may be pathogenic or benign according to how these genes are regulated or the sensitivity of the tissue in which they are expressed.
The Type III secretion systems, for instance, “first described as a mechanism by which animal pathogens hijack their host‘s cell biology, have been implicated in mutualistic associations between nonpathogenic bacteria and their hosts.” The study of these heretofore misunderstood relationships, they say, forms a “wide-open frontier” with big paradigm shifts ahead:
As the depth of host-microbe interactions and the mechanisms underlying them continue to be unraveled, fundamental paradigms of pathogenic microbiology, developmental biology, and immunology will need to be reevaluated. For this reason, a specific recommendation arising from the workshop is that biology be taught in a new way, incorporating our growing knowledge about the importance of beneficial microbial interactions and their evolutionary, ecological, and biochemical impact on both animals and plants.
1Edward Ruby, Brian Henderson, Margaret McFall-Ngai, “Microbiology: We Get By with a Little Help from Our (Little) Friends,” Science.
One of the most frequent and hard-to-answer criticisms of creation science has been the presence of pathogens. Bacteria and viruses, if designed, would seem to be the nefarious products of a malevolent genius rather than of a compassionate Creator. This was one of the main reasons for Darwin’s slide to agnosticism, from youthful admiration of Paley to middle-aged rejection of Christianity, revelation and purpose in nature. While most people can appreciate the abundant evidences of design in nature, creationists have been hard pressed to explain disease-causing bacteria and viruses.
But what if they were beneficial living machines running wild, out of bounds and out of control? The Type III secretion system looks like a weapon, designed to inject poison into a hapless victim. But could it have originally been like a compassionate doctor’s hypodermic needle, intended for good? Instead of weapons, were pathogens originally regulatory devices, meant to act as governors on our engines? Do our metaphors mislead us? After all, too much of a good thing can be bad. We need accelerators, but we need brakes, too.
These authors seem open to the possibility that harmful pathogens may be the exception rather than the rule. They point out that beneficial interactions probably vastly outnumber harmful ones, and at least some of the harmful ones may be beneficial interactions out of kilter. Their chosen belief is that these interactions “coevolved” on the long Darwinian road from bacteria to man, but this fails to explain the intricate design of even the one-celled organisms. There is an alternative explanation that should not be arbitrarily dismissed, because it explains good design gone bad: the curse because of sin.
See also 03/14/2003 and 02/21/2002 entries on this subject, and also the next headline, below.