Robert L. Buckingham, United States
Title: Particulates, Inhaled Toxins and Breathlessness-Harbingers to broken Capillaries
Buckingham,MD, FACP, practising internist for 39 years, author, and patient advocate, has dedicated a lifetime to the understanding of how chronic inflammation is evoked within interstitial spaces. Through his recently published books, he exposes the chronic inflammatory underworld and how it does its dirty business to transform end organ interstitial spaces into a sea of diseases. These books dissect what is currently known about inflammation to clarify how chronic inflammation disables the signalling apparatus of the protective capillary cells and then proceeds to dismantle all of the cells within the interstitial space that capillaries are allied with. In the end, after mission accomplished, the interstitial space footprint now belongs to chronic inflammation and the anti-organ. In this final apocalypse, capillary cells have long since stopped dancing, and their feedback loop signals to the allied partners have been replaced by rogue influences. White blood cells, cytokines, platelets, and immunoglobulins within the darkened corners of end-organ interstitial spaces now belong to chronic inflammation. The interstitial spaces become barren and lifeless as we know it. A perfect backdrop for cancer, pain, fatigue and ageing.
Unfortunately, with chronic particulate/smoke inhalation, the immune arsenal sequencing with lung alveoli breaks down as the capillary cell dance is nullified and its infrastructure, outer membrane receptors and mitochondrial mass decline. As capillary cell choreography fails and their outer membranes enable the leaking of additional hostile influences into the interstitial space, proinflammatory chain reactions develop. Capillary (and endothelial) cell mitochondria overheat, as they get stuck in energy combustion. This increases production of superoxide free radicals (or reactive oxygen species or ROS), which subsequently drain antioxidants used to neutralize them and then damages DNA in its path. This disrupts protein synthesis coding utilized for repair/replacement of anything worn out within the capillary cell.
Capillary cell infrastructure cracks feed proinflammatory momentum as they perpetuate more and more rogue immune arsenal entrance into the interstitial space thereby punctuating an even greater disparity of useful cytokines signaling. Eventually these devious signals become so prominent that when coupled by a crippled capillary cell feedback loop signalling system, they overrun the interstitial space with their own hostile brand of rogue signalling. This welcomes the chronic inflammatory matrix into the interstitial space.
In the lung alveolus, persistently inhaled hydrocarbon particulates, gases or allergens from dirty air serve as vascular inflammatory free radical fuel. In aggregate, they fester within interstitial spaces to trigger the eventual takeover by hostile white blood cells of interstitial space feedback loops, while they hijack disabled capillary cell outer membranes. Together, the particulate/hydrocarbon fuel, the rebel white blood cells, and the feedback loops signalling system they elicit become the tools of a chronic inflammatory agenda. As chronic inflammation within lung alveolar surfaces unfolds, cough, bronchitis and wheezing eventually breed scarring (COPD), cancer, and serious infections (pneumonia).