Further notes about the morphostasis concept – split files

(30) Injury and infection

Nature Immunology, this month (Oct 2013), has a series on tissue resident leukocytes. In the introductory article they say "Immune cells are found in diverse nonlymphoid tissues where they patrol against infection and injury and help to maintain homeostasis." because pathogenic organisms require injury to conjure up their repast, the statement can be contracted to "Immune cells are found in diverse nonlymphoid tissues where they patrol against injury and help to maintain homeostasis." When pathogenic organisms are recognised by adaptive immune cells it is because they have, in the past, been closely associated with some injury (damage). The big question is this: Is it now time to ditch this conviction that the adaptive immune system is primarily interested in infection? Are all such apparent "pathogen specific adaptive immune responses" just a manifestation of remembering the pattern of debris associated with damage?

Here's another: "Inflammation is an innate immune response to infection or tissue damage." Micro–organisms have nothing to "eat" unless there is damage and debris. "Inflammation is an innate immune response to tissue damage [full stop]." We don't need more.

A great number of different cells can (very likely) recognise, ingest, digest and assimilate micro–organisms. If they don't, then they have suppressed this ancient capacity for some "loss of old function"/"gain of new function" strategy. They may not do it as aggressively as phagocytes but they, quite likely, retain some amateur capacity to do this. Phagocytes do it more aggressively and efficiently: and with the vast proportion of microbes they do it without any need to go on to aggravate adaptive immune memory. Indeed, this would be metabolically wasteful. The ones that do aggravate adaptive immunity are the "damagers": these have strategies to macerate host cells in order to provide a repast (or they capitalise on coincident damage). This is the big point. Current perceptions, at least until recently, regard the response to microbial presence as an inevitable provoker of aggressive adaptive immunity. But, I propose, it is damage that is the inevitable provoker of aggressive adaptive immunity.