Try this exercise
Charlie Janeway's group are/were central to the development of the PAMP (pathogen associated molecular pattern) theories of immune activation. Essentially, they see/saw the innate immune system as being responsible for identifying the presence of "pathogens" and alerting the anamnestic (cognate) immune system of their presence so that they mount an aggressive response to them on any re-encounter. The excellent textbook on immunology, instituted by Janeway and others, is "Immunobiology 5" (several newer versions are now available).
Take the first two chapters in Part I and highlight every occurrence of the word "pathogen". Now ask yourself two things.
- Would "micro-organism" (or even "bacterium") have been an adequate and sufficient replacement for the word "pathogen"? I contend that in the vast majority of its appearances this replacement would be perfectly appropriate and much more precise.
- Where the authors have used the word "pathogen", are they referring specifically and exclusively to the property that this organism (for so they define a "pathogen" on page 36) is an agent that has damaged tissues? Or is it a loose and careless abbreviation for a "potentially pathogenic micro-organism"? I contend that you ought to conclude, in the vast majority of instances, that it is the latter and that this careless abbreviation has led to much conceptual confusion. Immunologists have, in effect, hijacked this highly generic term to represent a much more general and imprecise meaning (sometimes just "micro-organism" and sometimes a "potentially pathogenic micro-organism"). Any agent that has damaged tissues (in a particular host) can claim the title "pathogen" (but only in that host and on that occasion). Non living agents frequently earn "pathogen" status (eg, asbestos).
Remember, an organism that can act in a pathogenic way is dedicating genes, and so nucleic acid resources, to the "purpose" of damaging tissues (to generate a "food" substrate). In so doing, it is almost certainly reducing its capacity to act as a simple saprophyte. Genes dedicated to pathogenesis are likely to be targeted at potential Achilles heels in the host's defence (of homeostasis) repertoire. It strikes me as unlikely that the innate immune system has a generic way of recognising the phenotypic products of these pathogenesis genes. Plants do counteract pathogenesis and in these instances each pathogenesis gene is countered by the evolution of a specific (not generic) host resistance gene.
An invading organism may well have genes that are dedicated to damaging its host. Nevertheless, if that chosen host – by courtesy of some resistance mechanism – is not damaged by it, it fails to achieve pathogen status on this encounter. Pathogen status is a post hoc property.