Bacteria We Can Live With

You may be aware that a number of strains of bacteria live in mutual coexistence within us and are fed and nurtured by us in exchange for work they do on our behalf. Indeed, these commensal microbial cells, representing many hundreds of distinct bacterial species, may actually outnumber the human cells that make up our bodies! (Since they're less than a millionth of our cells in individual size, they're hard to notice.) They live mostly in the large intestine, or colon, and help us break down food that would otherwise pass through unused, and they also make and secrete a few things that we need, such as certain fats and vitamin K1. Because they are in the gut in such high density, they make it difficult for other, potentially pathogenic (disease-causing) bacteria to gain a foothold.

How did these bacteria get there, and why doesn't our immune system kick them out? We are not born with these helpful bacteria, but must take them in from our environment. Some come in with food; many come in from kids just playing in dirt. We know from experiments in mice that failure to take in such bacteria can cause major nutritional problems, and it is thought that living in an increasingly germ-free (in relative terms) environment may also cause problems for humans including, aside from digestive difficulties, things like allergies and autoimmune disease.

But still, how does the immune system know these bacteria are "good guys"? Why doesn't it deal with them in the same way it does other microbes? Do immune cells that encounter commensal bacteria in the gut not have TLRs or other PRRs, or do the bacteria lack PAMPs? Do they not see these bacteria, or do they see them and just ignore them? The answer may be a combination of both, but the bottom line is that we don't really know.

We do know that if bacteria commensal in the gut enter into the general tissue spaces of the body, they are rapidly destroyed by the immune system. On the other hand, there are potent immune elements present in the gut itself that can act on and destroy noncommensal bacteria, largely through the antibodies of subclass IgA (Figure 2.1). This tells us two things: commensal bacteria are not immunologically invisible and can trigger immune responses outside the gut, and the immune elements in the gut have what it takes to spot potentially harmful bacteria.

There is in fact good evidence that the immune system within the gut does react to intestinal bacteria and can kill them, but mostly it keeps them from entering the general circulation, where they would be rapidly and completely destroyed. The immune system and commensal bacteria seem to have developed a delicate balance, whereby the bacteria survive sufficiently well to provide needed functions but do not expand to a point where they would threaten their host (us).

The exact basis upon which this balance is achieved is still obscure but may involve modulating PRRs on host immune elements and PAMPs on the bacteria. It seems likely that commensal bacteria may also release moderately immunosuppressive molecules of various sorts, which slow the immune response mounted against them. Trying to unravel the intricacies of the dance between our gut and its commensals has occupied immunologists for nearly a century, and it is not clear we know much more now than we did when we started.

The immune system takes microbial invasion very seriously. The mechanisms it employs are far more extensive and complex than could ever have been imagined at the dawn of the age of immunology. Still, inflammation—one of the first manifestations noted by humans of the power underlying immunity to infection—remains the ultimate weapon in our antimicrobial armamentarium. It is a violent response, and as we will see in coming chapters, the collateral damage it causes to healthy tissues can be deadly, even fatal—but it works. The fact that we are still here is mute testimony to its effectiveness.

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