Version note Version 1.0 of this record (DOI: 10.5281/zenodo.19423074) proposed a Master Table of twelve candidate bacterium–disease associations as co-initiators of organ-specific autoimmunity, and a secondary pattern-mimicry amplifier based on anti-PEG/PS80 antibody cross-reactivity with cytoskeletal antigens. This Version 2.0 supersedes it. It preserves Version 1.0’s central architectural intuition — that excipient mediated tissue access and microbial specificity may be separable levels of disease initiation — but abandons its broad multi-disease scope: it restricts the framework to the single association — Campylobacter jejuni/Guillain–Barré syndrome — that independently satisfies all four molecular-mimicry validation criteria, drops the pattern mimicry amplifier to a brief discussion note (§5) rather than a load-bearing component, and incorporates the receptor architecture and coexposure formalism subsequently developed elsewhere in this series (the VECT model; Microbial Excipient Synergy), developing the result into a fully specified, falsifiable single-phenotype model. Version 1.0 is retained on Zenodo only for provenance; the body of this paper is written as a self-contained text and cites Version 1.0’s content as prior work 1 rather than referring back to it by version number throughout. Abstract Background A prior framework proposed that aluminum adjuvants, polysorbate 80 (PS80), and gram-negative bacteria act as co-initiators of organ-specific autoimmunity across a Master Table of twelve candidate bacterium–disease associations 1. Most of those associations rested on a single line of evidence — a reported homology between a bacterial protein and a host tissue antigen — without independently established cross-reactivity, epidemiology, and animal reproduction. The original Master Table is therefore best understood retrospectively as a hypothesis-generating screen rather than as a validated disease map. This paper restricts the framework to its one case that satisfies all four validation criteria for molecular mimicry: Guillain–Barré syndrome (GBS) following infection with Campylobacter jejuni. Hypothesis We propose a two-level mechanism specific to this pairing. Level 1 — iatrogenic initiation — operates independently of infection: an aluminum-adjuvanted, PS80-containing vaccine forms a plasma protein corona on the nanometre-scale fraction of aluminum particulate that escapes vascularly, engaging LRP1 (LDL receptor family) at the blood–nerve barrier (BNB) and delivering the complex to a compartment where Schwann cell and axonal antigens are exposed under NLRP3 driven danger signalling. Level 2 — antigenic specification — requires concurrent or recent C. jejuni infection: cross-reactive antibodies against the GM1 ganglioside, generated against the bacterium’s lipooligosaccharide (LOS), convert the innate activation of Level 1 into the specific autoreactive attack on peripheral nerve that defines GBS. Evidence base Campylobacter jejuni/GBS is not an arbitrary entry drawn from that Master Table 1 — it is the association both the VECT model 2 and Microbial Excipient Synergy 3 already cite as a positive control, because it is among the few molecular-mimicry cases in all of autoimmune immunology to satisfy all four Oldstone criteria with independent solidity: structurally characterised GM1 homology, cross-reactivity demonstrated directly in patient sera, a robust and repeatedly replicated epidemiological association, and reproduction in animal models. Of the twelve original rows, it is the one that survives this scrutiny best; most of the other eleven depend on the homology criterion alone — precisely the pattern this series now treats as statistically unreliable given a ~20,000-protein human search space. Level 1’s receptor mechanism requires no new construct: VECT already assigns GBS to its LRP1/LDLR-family receptor axis, one of only two receptors VECT rates at its highest (Level 1) confidence tier and the one specifically mapped to the blood–nerve barrier, rather than the more speculative extension to steroidogenic tissue used elsewhere in the series (e.g., for POI). The aluminum-specific size-dependent partition feeding that route is developed in the companion Microbial Excipient Synergy paper, Section 7.2.1 3. Conclusion Restricting a twelve-association framework to its single best-supported case is a deliberate loss of scope in exchange for testability — and it supplies something Microbial Excipient Synergy explicitly flags as missing from its own limitations: an anchor case worked through to the level of quantitative prediction, rather than one candidate scenario among several equally speculative others 3. If aluminum–PS80 co-initiation and Campylobacter mimicry converge on the same phenotype through independently characterised mechanisms, GBS following concurrent vaccination and campylobacteriosis should be more frequent or severe than either exposure alone — a narrow, falsifiable prediction existing pharmacovigilance and case-control designs could test directly.
Añaños et al. (Sat,) studied this question.