Queue for brain

PART - 3

Consider how unwell certain people with cystic fibrosis can be. CF results from mutations in the gene encoding the Cystic Fibrosis Transmembrane Regulator (CFTR) protein product. CFTR controls the concentration of certain ions, such as chloride Cl- ions, in the layer of fluid that sits atop the air-facing airway lining cells, collectively called the respiratory epithelium. Mutations can occur anywhere in the gene & there is remarkable diversity in the specific mutations that a child with CF has. Some mutations result in severe disease, affecting not only the airways, but also the gastrointestinal tract. Other mutations produce much more subtle changes to phenotype.
What this establishes, to my mind anyway, is that quite modest changes in the dynamic equilibrium of airway surface liquid and protecting the airway from malfunction, are plausibly capable of yielding symptoms of the illnesses we call colds and “flu”. Such changes might plausibly occur in many but by no means all people in response to event’s & environments which we routinely encounter.
As seasons & weather oscillate between high and low atmospheric pressure, humidity, temperature, dusts, pollen, pollution with such as nitrogen oxides at sea level, a person who is unable to briskly alter their composition of airway surface liquid might plausibly develop rapid-onset symptoms of respiratory disorder.
Depending upon where in the airway “tree” the acute failure of homeostasis occurs, so a person might display mostly upper airway symptoms which we call a cold. In other anatomical locations, such failures of homeopathy in central or lower airways could result in symptoms which are far more severe & we call that “flu”.
In this model of “endogenous” illness, timeline to recovery could vary tremendously from an all but overnight event to something that persists for weeks, leaving person somewhat breathless, even at rest. In the case of a hypothetical episode of flu, the functions of your epithelial cells could become further deranged and cause quite worrisome symptoms. These cells are very large in number (note it’s said that the surface area of your gas-exchanging lungs are large enough to more or less cover a tennis court. It doesn’t take much by way of cytokine / chemokine / inflammatory mediators response of those epithelial cells in order to produce systemic symptoms, such as muscle & joint pain, tremendous fatigue, reduced efficiency gas-exchange etc. on top of this, your healthy epithelial cells normally secrete anti-microbial compounds such as trefoil peptides, which make it difficult for microorganisms such as bacteria and fungi to infect you. When damaged, however, I think it very likely that overgrowth of usually benign bacterial infections could occur and be the aetiological explanation for pneumonias, requiring antibiotics to prevent a spiralling down to death, especially in elderly, already chronically unwell individuals. Even without invoking bacterial infection, the release from airway epithelium of pro-inflammatory chemicals will result in recruitment to the lungs & into the luminal compartment of the lungs of very large numbers of several kinds of inflammatory cells, such as neutrophils, eosinophils and macrophages (the latter themselves are normally found as the dominant surveillance cell type in airway washings, obtained using an unpleasant technique called endoscopic pulmonary lavage). These cells, in large enough numbers, are the cause of production of purulent secretions, coughed up as phlegm.
I’m not pretending that this is all correct & explains every facet of the acute respiratory illnesses called colds and influenza, but it’s a better model than the contagious respiratory virus narrative.

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