Discussion in 'Other health news and research' started by Guest 2176, Nov 11, 2019.
Airborne fungal pathogens, predominantly Aspergillus fumigatus, can cause severe respiratory tract diseases. Here we show that in environments, fungal spores can already be decorated with nanoparticles. Using representative controlled nanoparticle models, we demonstrate that various nanoparticles, but not microparticles, rapidly and stably associate with spores, without specific functionalization. Nanoparticle-spore complex formation was enhanced by small nanoparticle size rather than by material, charge, or “stealth” modifications and was concentration-dependently reduced by the formation of environmental or physiological biomolecule coronas. Assembly of nanoparticle-spore surface hybrid structures affected their pathobiology, including reduced sensitivity against defensins, uptake into phagocytes, lung cell toxicity, and TLR/cytokine-mediated inflammatory responses. Following infection of mice, nanoparticle-spore complexes were detectable in the lung and less efficiently eliminated by the pulmonary immune defense, thereby enhancing A. fumigatus infections in immunocompromised animals. Collectively, self-assembly of nanoparticle-fungal complexes affects their (patho)biological identity, which may impact human health and ecology.
Other important excerpts:
Inhalation is also considered the most relevant exposure route for NPs (4, 15). In addition to adverse effects of fine particulates, the potential toxicologic relevance of NPs is under intense investigation, particularly for individuals with preexisting respiratory diseases (2, 6, 7, 16).
Surprisingly little is known on the direct crosstalk of NPs with spores and its pathobiological consequences even though simultaneous exposure of humans and ecosystems to both occurs. Studies to date have examined sequential exposure scenarios, in which lung disease models were first treated with NPs and then subsequently challenged with bacteria or other pathogens, resulting in increased cytokine responses (17, 18).
Consequently, we here performed a comprehensive tiered analysis of the self-assembly of nanomaterial-fungal hybrid structures and its pathobiological relevance from in situ to in vitro and in vivo"
NPs Adsorb Rapidly and Stably to Fungal Conidia.
Electron microscopy studies demonstrated that conidia harvested from a construction site with fungal contamination in the clinic or outdoors were already partially covered with nanosized particles (Fig. 1A). Energy-dispersive X-ray spectroscopy (EDX) analysis detected silica and other elements on the surface of these specimens, as was expected from the collection from realistic although complex environments (SI Appendix, Fig. S1A and Table S1). As the number of variables during sampling and the complexity of the environments do not allow analysis of the underlying mechanisms and pathobiological relevance of NP-conidia complexes, we next used tiered complementary analytical approaches under standardized conditions.
NP physicochemical properties affect their assembly on spores. (A) SEM images of NP-covered conidia harvested from a construction site. Arrows indicate NPs. (Scale bar: 2 µm.) (B) A. fumigatusGFP conidia incubated with fluorescent silica (SiOR) or polymer NPs (OSiRN or OSiRPEG). Negatively charged SiOR or PEGylated OSiRPEG efficiently adsorbed to conidia in situ, whereas positively charged OSiRN bound less efficiently. (Scale bar: 2 µm.) (C) TEM indicates better fitting of small (∅ ∼30 nm; Left) compared with larger (∅ ∼140 nm; Right) SiO NPs into groove structures on the conidia surface. (Scale bars: 50 nm.) (D) SEM showing assembly of SiO (∅ ∼30/140 nm) and ZnO. (Scale bars: 200 nm.) (E) Kinetic analysis of complex formation demonstrating rapid NP binding (within <30>F and G) NP size, but not charge, is critical for binding. (F) Fluorescence microscopy of vital conidia demonstrating that increasing NP size reduced conidia binding. (Scale bar: 2 µm.) (G) Quantification of NP-conidia interaction by automated microscopy. Compared with small SiOR NPs (∅ ∼30 nm), larger silica SiO140R NPs (∅ ∼140 nm) exhibited reduced binding (Left). Reduced binding was also observed for positively charged (OSiRN; ζ = +24 mV) vs. negatively charged (OSiRC; ζ = −32 mV) polymer NPs. Surface modification with steric molecules (OSiRPEG/OSiRPEtO) did not affect binding. *P = 0.05; **P = 0.01.
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"In healthy individuals, inhaled conidia are cleared mainly by alveolar macrophages and neutrophils (3, 8⇓–10), cells also known to play a major role in the body’s response to NPs (2, 4, 6); however, effective strategies to improve the outcomes for patients with mycoses present an enormous medical challenge. Besides antimycotic drugs, natural antifungal peptides, such as human defensins, have been considered as future therapeutics (14)"
I still think this is a very important paper that deserves more attention.
One impressive aspect is it doesn't just show this can theoretically happen in the lab but that it shows that it happens "in the wild"
It also seems to explain the environmental sensitivity patterns in me/cfs better than a simple reaction to all molds would.
I expound on that here:
It shows that microbes have a massive arsenal of tricks to fool our immune system so they can invade and hijack our biology. We find more and more as technology gets better.
This fact alone discredits MUS as it is used as a disease category and refutes the idea that psychological processes are the most likely cause of disease.
Medicine rejecting the germ theory of disease: part deux
Some classics are best left to history books or drama. It isn't just Hollywood that is obsessed with reruns and reboots. The BPS model is basically the Cats movie of medicine: expensive and completely unnecessary. Although as much as the movie looks bad, I don't think anyone died as a result of it.
I think the germ theory supplanting the "miasma" theory was only half the story... bad air can create risk factors for disease that involves pathogens, by suppressing immunity
That is not the way it works. I understand what you are saying and don't disagree with what you mean but it is a way of saying things that is used against us. "Our unconscious mind does exist so Freud's theories of hysteria are partially true"
The miasma theory of disease was completely wrong as the theories of conversion and hysteria are wrong. Our brain only focuses on certain things consciously at any given time, but this is no Freudian unconscious with id and gratification problems. Making out they are the same lets them ignore the true cause of our disease by conflating them
Similarly, environmental pollutants, lack of oxygen, dangerous gases can make us sick but that is not the miasma theory.
Only organisms with chloroplasts can use the energy of the sun to live (a mind boggling thought) everything else must get it from another living thing. This has been happening for billions of years. The organisms which parasitize us are very, very good at it. They can also evolve at a rapid rate compared to us so the idea that our immune system can be finely tuned and can deal with them unless we are doing something wrong (like thinking in the wrong way) is dangerously wrong.
The surprise is that anything survives. We only survive because it is in the interest of many organisms to let us often by helping us survive. They are all in competition with each other as well.
It is staggering to think that the germ theory of disease was not fully accepted in the 20th century. For a while infections were seen as the primary cause of disease by medicine but then vaccination and antibiotics let it forget what microbes really are so here we are with BPS theories taking over.
Environmental disease is hushed up because it is a threat to profits so that is quashed too and the myths are propagated unchallenged.
I thought the "miasma theory" was simply the idea that "bad air" could cause disease. If it refers to something other than that, maybe I'm mistaken.
Either way I believe environmental factors are under looked in health.
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