Legionnaires Bacteria Travel Long Distances in the Air in Victoria

Aerosol transport of Legionella has killed people in recent weeks in my home state. Let's look at how their Endotoxin hits our TLRs.

Here is the Victorian Chief Health Officer, clearly worried about the latest Legionnaires Disease outbreak.¹ It kills about one of every ten afflicted individuals.

I wish she understood Mandatory Jabbing produces the same effects.

The Legionella pneumophila bacteria traveled many kilometers from a site in Laverton, as was confirmed by genetic sequencing.

Found a nice free paper from 2021 which explains much of the damage done by the Endotoxin (LPS) from this particular species² and links in nicely with my recent article on cGAS/STING³ and plans to hit your TLRs by Qu Biologics⁴ ⁵and Moderna with Flagellin.⁶⁷

The authors emphasize that prior work using Mice could not be extrapolated to Humans, so they looked at the impact on our Macrophages.

Here is their Figure 11A

The caption reads:

The TLR3 and TLR4 signaling axes. TLR4 recognizes L. pneumophila (Lpn) LPS (Endotoxin) at both the macrophage surface and the endosomal / Legionella-containing vacuole (LCV) compartment. TLR4 at the surface signals via MyD88, whereas endosomal-localized TLR4 requires the TRIF/TRAM adaptors. TLR3 recognizes dsRNA presumably originating from the LCV and then utilizes the TRIF adaptor to begin signal transduction. TLR4/MyD88, TLR4/TRAM/TRIF, and TLR3/TRIF all engage downstream TBK1 and finally TRAF6 leading to transcription factor (e.g., NF-κΒ {shown}, AP-1) activation, which induces cytokine gene transcription (e.g., TNFα and IL-6) and its associated protein synthesis and secretion (dashed line arrows). In this study, we confirmed the TLR4- and TLR3-dependency of IL-6 and TNFα as well as IL-1β and IL-10.

Here is their Figure 11B

The caption reads:

Human PRRs (Pathogen Recogntion Receptors) that recognize and respond to L. pneumophila (Lpn) infection, based on the results from the current study as well as past work (see main text for references). At the macrophage surface, TLR4 and its co-receptor CD14 work to recognize LPS (Endotoxin), TLR2 likely senses a lipoprotein(s) and/or a component of outer membrane vesicles, and TLR5 detects flagellin. At the level of the endosome / LCV, TLR3 recognizes dsRNA, while TLR4 recognizes LPS. Within the macrophage cytosol, DNA-PK and cGAS/STING sense DNA, while RIG-I/MAVS recognizes dsRNA species, including those generated by the action of Pol III on released DNA, and NLR’s NOD1 and/or NOD2 recognize peptidoglycan. Finally, cytoplasmic inflammasomes, both AIM2 and hNAIP-dependent ones, recognize DNA, peptidoglycan, LPS (Endotoxin), and flagellin. Regardless of the PRR or its location, signal transduction leads to the upregulation of cytokine gene transcription (solid black arrows). Cytokines that are known to be produced and secreted by human macrophages upon L. pneumophila infection include IL-1β, IL-6, IL-8, IL-10, and TNFα (dashed line arrows). PPRs that have been examined by KO (knockout) analysis but were found not to be required for the production of cytokines (as measured by IL-6 and TNFα levels) include TLR9, MCL, and the Malt1-dependent CLRs.

Watch out for cooling towers that have not been properly maintained.

1. William Ton. 30 July 2024. CHO warns of ‘nasty pneumonia’ risk after legionnaires’ disease outbreak. https://www.theage.com.au/national/victoria/cho-warns-of-nasty-pneumonia-risk-after-legionnaires-disease-outbreak-20240730-p5jxmu.html

2. Lubov S. Grigoryeva, Nicholas P. Cianciotto. 2021. Human macrophages utilize a wide range of pathogen recognition receptors to recognize Legionella pneumophila, including Toll-Like Receptor 4 engaging Legionella lipopolysaccharide and the Toll-like Receptor 3 nucleic-acid sensor. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009781

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