What Do Age-Related Inflammatory Disease Syndromes Have in Common With AIDS?
We do need to be aware of what happens when the inflammatory signalling mechanism has gone awry.
Age-related inflammatory disease syndromes appear to sound milder than Acquired Immunodeficiency Syndrome (AIDS), to be honest.
While most AIDS patients have been treated as social pariahs because of the connotations that AIDS brings about with regards to promiscuity or illicit drug use, nobody gives that same stigma to a heart disease patient or a diabetic.
But yet, both kinds of problems do indicate that there is something going wrong with the body somewhere:
Isn’t it so? We feel sensations of pain in our bodies when we take a hard bump. We feel the runny nose and the phlegm buildup when we get infected by a flu virus.
We know that one who has AIDS has acquired an “immunodeficiency”. With this immunodeficiency, the immune system of an AIDS patient would face additional difficulties in trying to defend themselves from infections and/or disease.
In fact, a scientific study did show that in the absence of highly active antiretroviral therapy (HAART),
adults aged 25–54 years with AIDS experience a substantially elevated risk of influenza-associated death, 150–200-fold higher than that in the general population of the same age and 2–4-fold higher than that in adults aged ≥65 years.
The study is perhaps suggesting that an AIDS patient would not even be able to defend themselves from an influenza infection — because any AIDS-infected defender cells (or macrophages/white blood cells) are simply unable to do what they ought to be doing in getting rid of the virus.
But the problem is that while the defensive activity of the macrophages has been reduced, it is also the case that:
acute HIV infection is marked by an intense surge of cytokines such as interferon-α, interferon-γ, tumor necrosis factor, and IL-6 which leads to immune activation and severe inflammatory reaction.
Which also means that the body is in a state of chronic inflammation.
The problem is that even though the inflammatory signal is chronically elevated, this signal does not, in any way, help to improve the defensive efficiency of the macrophage defenders.
How’s that any different from age-related inflammatory disease syndromes?
While age-related inflammatory disease syndromes don’t directly shut down macrophage activity as it is in the case of AIDS, the problem is that they may cause a change in the population subtypes of these macrophages based on the prevailing inflammatory signals that they are experiencing as a result of having that condition.
Especially when we look at heart disease patients, for instance. They do need more of the M2-type macrophages to clear out dead necrotic cells trapped in those atherosclerotic plaques via this process known as efferocytosis.
However, these dead necrotic cells do give off pro-inflammatory cytokine signals that actually forces new macrophages to differentiate into the pro-inflammatory M1 type.
Which doesn’t help the heart disease patient, because M1-type macrophages have a lower efferocytosis capability than the M2 type.
Which is why a heart disease patient won’t find it easy to naturally reduce the sizes of the atherosclerotic plaques that are causing partial blockages of their arteries. The macrophages that are needed to conduct efferocytosis and reduce plaque sizes from within would be in short supply.
So while immune defensive activity isn’t completely shut down, we’d see that these people would also have impaired immune responses, as it was the case with heart disease patients at the height of the COVID-19 pandemic.
These pro-inflammatory signals aren’t fun to deal with.
They are there for a reason, and that is to signal the defenders to swarm and defuse an infectious situation before it gets out of hand.
However, when the first line of defence is unable to neutralise the threat completely, the immune system would have to call on the higher levels of the defensive system.
It’s like being in the army, really.
Why would a colonel be called upon to mitigate a problem if a private or a corporal can easily do the job? In the corporate world, why would the CEO be called upon to mitigate a problem that a normal employee can handle on their own?
The army corporals know that involving a colonel would require dealing with a gigantic headache. The corporate rank and file know that involving the CEO would have similar consequences. If we can deal with issues at the lower rank without involving upper management, the issue can be resolved more quickly.
But when higher powered members in the hierarchy are involved, we’d expect more consequences. In the same way, that’s what happens in the body when all the high-powered immune cells are galvanised into action, each bringing their own unique blend of cytokines into the mix, and therein bringing about a cytokine storm.
So while heart disease may not be as stigmatised as AIDS is, we ought to bear in mind that immune systems are affected in both cases — and therefore that brings about an impaired healing process and a higher vulnerability to severe overreactions from common infections.
Keeping one’s body physically healthy is a tough balance, especially in today’s modern society, where everyone is overworked and sleep deprived.
But we have to learn how to do it properly, so that our bodies are better able to respond appropriately to threats or infections. Before we even do that, though, we ought to be able to make sense of what our immune system can or cannot do.
The point being that it does not benefit us in any way to live an unbalanced lifestyle. AIDS or other age-related inflammatory disease syndromes will throw our immune system’s regulation of the inflammation signalling mechanism completely off-kilter, and then we’ll end up having to pay the price for it by experiencing a much lower quality of life — which I’m sure none of us would want to!
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