Idiopathic Pulmonary Fibrosis: helminths or not helminths

Published June 22, 2026 by Jacques Le Marois

Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible lung disease for which three approved agents slow progression without ever halting it. Helminthic therapy raises a legitimate concern in this context: several type 2 cytokines induced by helminths are documented as pro-fibrotic in the lung. This article examines that concern seriously before nuancing it: recent data show that helminths simultaneously exert anti-fibrotic effects via the Th17/Treg axis, a protective remodelling of alveolar macrophages against post-viral hyperinflammation, and a remarkable convergence toward inhibition of the NLRP3 inflammasome. On this basis, a two-arm preclinical programme on living organisms is proposed. The goal is not to demonstrate that helminthic therapy treats IPF, but to produce the data that would make it possible to know.

A second part, devoted to helminth-derived molecules, is published on Substack.

A note before we begin: this article is a synthesis of recent scientific work, written with the assistance of an AI. Please treat this as hypotheses to explore and verify, not established conclusions. All corrections are welcome in the comments.

Introduction

A disease that destroys the lung through substitution

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and irreversible interstitial lung disease. Its central mechanism is the progressive destruction of the alveolar parenchyma and its replacement by fibrous scar tissue composed primarily of collagen. This rigid, non-functional tissue literally smothers the lung from within.

The term "idiopathic" means the cause remains unknown. Risk factors are identified — smoking, occupational exposures, gastroesophageal reflux, abnormal pulmonary microbiome, certain viral infections (EBV, CMV, herpesviruses) — but none is necessary or sufficient. Repeated epithelial microtrauma on a genetically predisposed background is the most widely accepted etiopathogenic theory.

Severe viral respiratory infections deserve particular mention. A significant proportion of survivors of severe COVID-19 develop persistent pulmonary fibrotic sequelae. Experimental data also show that severe H1N1 influenza infection induces persistent lung injury with collagen deposition. In both cases, the triggering mechanism is not the virus itself but the hyperinflammation it provokes. This is precisely the mechanism that helminths modulate, as shown by data on protection against post-viral immunopathology in the Nb/SCV2 and Nb/H1N1 murine models discussed in Part 3.

An epidemiological gradient worth noting

IPF primarily affects people over 60, with a clear male predominance. Its incidence is increasing in industrialised countries: current estimates place global prevalence between 3 and 9 cases per 100,000 inhabitants, depending on diagnostic criteria. This prevalence is markedly higher in Western Europe, North America and Japan than in sub-Saharan Africa, South-East Asia or Latin America — regions where helminth infections remain common in the general population.

This North-South gradient is not causal proof, but it fits within the conceptual framework of the "old friends" hypothesis formulated by Graham Rook: the millennia-long co-evolution between the human species and its commensals — helminths, soil saprophytic bacteria — shaped the immune system to maintain a baseline inflammatory regulation that the sanitisation of industrialised societies has progressively destabilised.

Three drugs that slow without curing

The prognosis of IPF is severe: median survival of 3 to 5 years without lung transplantation. Three agents are approved: pirfenidone (2014), nintedanib (2014) and nerandomilast (FDA, October 2025). In the phase 3 FIBRONEER-IPF trial (n = 1,177, 52 weeks), nerandomilast at 18 mg twice daily reduced FVC decline by 68.8 ml compared to placebo (p < 0.001) — but FVC continued to decline by 114.7 ml in the treated group (Richeldi et al., 2025).

Three agents available. The therapeutic ceiling is identical for all three: slowing a destruction that nothing, to date, can reverse.

A considerable therapeutic blind spot

IPF is driven by two cellular processes that feed each other. Alveolar epithelial dysfunction: type II pneumocytes (AT2 cells) enter aberrant states and secrete a pro-fibrotic microenvironment enriched in TGF-β, actively stimulating surrounding fibroblasts (Hoffman et al., 2025). Pathological fibroblast activation: these myofibroblasts result from a state transition from resident alveolar fibroblasts, under the control of the transcription factor RUNX2 — its conditional deletion attenuates experimental fibrosis (Fang et al., 2025).

All currently approved strategies intervene downstream of "fibrotic lock-in" — they slow collagen accumulation without acting on the mechanisms that establish and maintain the fibrotic state. It is precisely in this space — the upstream immunological mechanisms — that helminthic therapy finds a potentially original point of entry.

Part 1 — The legitimate concern, then its reassessment

1.1 Why helminthic therapy does not seem indicated a priori

The initial concern rests on concrete biological data. Helminths induce type 2 responses — IL-4, IL-5, IL-13, IL-33 — several of which are documented as pro-fibrotic in the chronic pulmonary context.

The IL-33/ST2 axis is one of the main alarmin axes in IPF. In human IPF tissue, the predominant form is the full-length nuclear form (flIL-33), which acts in an ST2-independent manner (Luzina et al., 2013). The mature extracellular form activates M2 macrophages and ILC2s via ST2, inducing IL-13 and TGF-β1 (Li et al., 2014; McHedlidze et al., 2013).

The IL-13/arginase axis constitutes a second pro-fibrotic axis independent of TGF-β: IL-13 induces arginase in M2 macrophages, producing proline and hydroxyproline — direct collagen precursors (Kaviratne et al., 2004).

The IL-25/ILC2 axis adds a third TGF-β-independent pathway, documented as active in human IPF (Hams et al., 2014).

The IL-33/amphiregulin axis: ST2hi memory Th2 cells produce amphiregulin that activates eosinophil EGFR receptors, inducing osteopontin secretion and contributing to bronchial fibrotic remodelling (Morimoto et al., 2018).

A direct experimental finding reinforces this concern: co-infection with Ascaris suum in a bleomycin model worsens pulmonary inflammation and increases IL-33 and IL-13 levels (Oliveira et al., 2019). But a critical nuance is required: these data concern Ascaris at high burden — they cannot be generalised to a controlled therapeutic inoculation with another species at low dose (Caraballo et al., 2015).

1.2 The paradox resolved: two distinct axes

This is where the picture becomes instructively complex. Data on helminthic immunomodulation in the fibrotic context show that there are at least two distinct axes operating in parallel — and that the concern described in 1.1 primarily concerns the chronic Th2 axis, while a second axis, Th17/Treg, plays a demonstrated anti-fibrotic role.

The Th17/Treg axis in dermal fibrosis was studied in a murine bleomycin model with Heligmosomoides polygyrus (Hp). Mice exposed to Hp are protected against bleomycin-induced dermal fibrosis. The causal mechanism was established by anti-CD25 depletion: protection is abolished when CD4⁺ regulatory T cells (Tregs) are eliminated. The active axis is therefore Hp → CD4⁺ Tregs → Th17 suppression → ↓IL-17 → ↓collagen (Sekiguchi et al., 2025). This axis does not conflict with the concern described in 1.1: it does not involve amplification of IL-13 or IL-33, but a correction of the Th17/Treg imbalance that is also documented in human IPF.

A second complementary mechanism was characterised the following year: Hp reprogrammes Th17 cells themselves toward a Tr1/Treg-like phenotype, with increased IL-10 and Foxp3, and reduced IFN-γ (Metwali et al., 2026). These two findings — Treg depletion abolishing protection, and direct Th17 reprogramming — articulate as two complementary mechanisms of the same anti-fibrotic axis.

Converging clinical data reinforce the plausibility of this lead. Administration of rmIL-35 and rmIL-10 — two regulatory cytokines induced by helminths — significantly reduces the Ashcroft histological score, total hydroxyproline, collagen I mRNA and α-SMA in a bleomycin model of systemic sclerosis (Huang et al., 2025). Moreover, low-dose IL-2 administration (1 MIU/day, phase I/IIa, n = 9, systemic sclerosis) induces a selective Treg expansion of ×1.8 at day 8 (p = 0.0015), without expansion of effector cells — establishing the human clinical feasibility of manipulating the Treg axis in systemic fibroses (Barde et al., 2024).

The initial concern is therefore real but partial. It concerns a specific scenario: uncontrolled chronic Th2 stimulation, with sustained elevation of IL-13 and IL-33, in an already compromised lung. This scenario is biologically credible for certain high-burden species, but does not necessarily describe what a controlled therapeutic inoculation with a selected species would produce.

1.3 The systemic sclerosis clinical signal

A further clinical signal deserves mention here, though it remains to be rigorously documented. Self-treaters with systemic sclerosis report functional benefits after helminth inoculation, including measured respiratory parameters — DLCO and FVC. Systemic sclerosis is particularly relevant here: interstitial pulmonary fibrosis is its leading cause of mortality, with fibrotic mechanisms largely shared with IPF. Access to objective medical records for these individuals would be of great interest (Helminthic Therapy Wiki).

1.4 Clinical trials: heterogeneous results

Helminthic therapy has been the subject of a substantial number of clinical trials across various inflammatory conditions, with heterogeneous results requiring case-by-case analysis. A detailed register is available on the Helminthic Therapy Wiki. Among the documented sources of variability, the physicochemical conditions of inoculum preparation play an underestimated role (Venkatakrishnan et al., 2021).

Part 2 — Fibrotic axes and helminthic mechanisms

2.1 Why NLRP3 and TLR4 are central

Beyond the classical cytokine axes, two helminthic mechanisms deserve particular attention in the IPF context.

The NLRP3 inflammasome is activated in human IPF tissue. Its activation produces mature IL-1β — which directly stimulates fibroblasts and amplifies TGF-β — and IL-18, which promotes Th17 polarisation. NLRP3 also induces pyroptosis of alveolar epithelial cells. Nlrp3 knockout mice develop attenuated bleomycin fibrosis.

NLRP3 activation requires two sequential signals. Signal 1 (priming) is provided by TLR4/MyD88/NF-κB: DAMPs released during repeated epithelial injury — EDA fibronectin, hyaluronan, HSP70 — activate TLR4, inducing NLRP3 transcription. Signal 2 (activation) triggers inflammasome assembly. The loop is thus closed: epithelial injury → DAMPs → TLR4 → NLRP3 → IL-1β → fibroblast activation → new DAMPs.

2.2 The helminthic convergence toward TLR4/NLRP3

Helminths simultaneously block both signals at several distinct levels of regulation — which illustrates precisely why living organisms are irreplaceable.

Blocking Signal 1 — TLR4/NF-κB. Excretory/secretory proteins of Haemonchus contortus directly downregulate TLR4 and MyD88 in PBMCs, reducing NF-κB p65 phosphorylation and downstream NLRP3 transcription. Wen et al. 2022 also documents inhibition of MAPK pathways (p38, JNK, ERK) downstream of TLR4 (Wen et al., 2022). This mechanism is conserved between species: Trichinella spiralis and Echinococcus granulosus also downregulate TLR2/TLR4 (Wen et al., 2022).

Blocking Signal 2 — NLRP3 assembly.

Butyrate (produced by the helminth-enriched microbiome) → GPR109A activation → direct NLRP3 inhibition
Helminthic products → upregulation of NLRP12 and NLRC3 (endogenous negative regulators of NF-κB/NLRP3) (Wang et al., 2019)
Treg/IL-10 expansion → reduced macrophage activation → ↓NLRP3 priming
Preliminary data (oral communication, non-peer-reviewed): soluble H. contortus extracts suppress NLRP3 expression via downregulation of circRNA_1599 — the circular RNA corresponding to the NLRP3 transcript (log2FC = −7.99, p_adj = 2.3 × 10⁻¹²). Reduction of circRNA_1599 releases NLRP3-inhibitory miRNAs, reducing its basal expression (Wang et al., Hydra Helminth Conference, 2018)

The GPR109A (HCAR2) double phenomenon deserves emphasis: helminths simultaneously increase butyrate production by the microbiome (↑ GPR109A ligand) AND directly upregulate GPR109A on circulating immune cells — HCAR2 being one of the most significantly upregulated receptors by HcAg (ANOVA: F(3,8) = 268.8; p < 0.0001) (Wang et al., 2019). These two synergistic effects cannot be reproduced by any purified molecule.

2.3 An additional mechanism: ILC2 exhaustion under chronic infection

A recent finding adds an unexpected complementary angle. During chronic H. polygyrus infection, intestinal ILC2s progressively shift toward a hypoproliferative state under prolonged IL-25 stimulation: they continue to produce IL-13 but lose their proliferative capacity — a phenomenon the authors explicitly compare to an immune exhaustion state (Feng et al., 2025).

If this mechanism proved operative in pulmonary ILC2s — which remains entirely to be demonstrated, as Feng et al.'s data are exclusively intestinal — a well-established chronic helminthic infection could naturally cap the IL-25/ILC2/IL-13 axis not through active molecular antagonism, but through exhaustion of the proliferative capacity of the effector cell itself. This is a mechanism distinct from all others described here, and constitutes an additional reason why living organisms in the chronic phase — Arms 1 and 2 — cannot be replaced by punctual purified molecules.

Part 3 — Preclinical programme on living organisms

William Parker, a scientist specialising in helminthic therapy, argues that helminths exert their effects via a network of co-evolutionary signals that isolated molecules cannot reproduce — and that the living organism approach is therefore irreplaceable. A living helminth simultaneously secretes hundreds of immunomodulatory molecules — proteins, extracellular vesicles loaded with miRNAs, bioactive lipids, carbohydrates — modifies the intestinal microbiome and induces pulmonary larval migration, producing network effects that no purified molecule can capture. This part therefore focuses on living organisms. Purified molecules are the subject of a separate article.

Two methodological rules apply across the entire programme:

Biochemical hydroxyproline assay is co-primary with the Ashcroft histological score
Interventions on established fibrosis are initiated at day 7-10 post-bleomycin

Arm 1 — Prophylactic conditioning

Two distinct questions.

The first is macrophagic: does pulmonary larval migration of Nb modify the macrophage microenvironment in a way that reduces subsequent bleomycin fibrosis?

The second is immunoregulatory: can prior helminthic exposure — inducing chronic Treg expansion, sustained IL-10 production and Th17 suppression — prevent IPF development by maintaining immune balance upstream of the fibrotic trigger?

Justification. Pulmonary larval migration of Nippostrongylus brasiliensis (Nb) induces Arg1⁺ OXPHOS-enriched alveolar macrophages — NAMs — whose signature persists until day 45 post-infection (Oyesola et al., 2023; Damani-Yokota et al., 2026). These NAMs reduce immunopathology in heterologous viral challenge models — not by reducing viral load, but by limiting tissue damage linked to hyperinflammation. The Nb/SCV2 and Nb/H1N1 models are therefore not merely models of viral infection: they model pulmonary fibrotic immunopathology analogous to severe post-COVID sequelae. The transcriptional signature of trained NAMs — enriched in Arg1, FABP5, MERTK and SPP1 — is moreover enriched in human IPF macrophages (Damani-Yokota et al., 2026).

In parallel, Hp in the chronic phase maintains Treg expansion and IL-10 production that correct the Th17/Treg imbalance documented in human IPF (Sekiguchi et al., 2025; Metwali et al., 2026).

Protocol — two subgroups.

Nb subgroup: 500 L3 subcutaneous at day −28, full rest for 28 days, bleomycin challenge at day 0. Nb being eliminated in 7 days in mice, animals are helminth-free at the time of bleomycin challenge. The effect tested is therefore prior macrophage conditioning, not active immunomodulation at the time of fibrosis. NAM persistence until day 45 post-Nb corresponds to day 17 post-bleomycin — sacrifice at day 28 post-bleomycin (= day 56 post-Nb) captures the optimal window.

Hp subgroup: 200 L3 oral at day −28, maintenance of chronic infection until sacrifice, bleomycin challenge at day 0. Two sacrifice timepoints: day 28 post-bleomycin (= day 56 post-Hp, established chronic phase according to Mules et al. 2024) and day 42 post-bleomycin (= day 70 post-Hp, to confirm persistence). A re-dosing at day −14 may be considered to ensure infection maintenance in the chronic phase at the time of challenge. Helminthic effects on the microbiome and SCFAs are only established in the chronic phase — day 28 alone would be too short (Mules et al., 2023; 2024).

Critical internal control. Heligmosomoides polygyrus (Hp, intestinal, non-pulmonary-migrating) administered under the same temporal conditions. Oyesola et al. demonstrated that Hp at day −28 confers no survival benefit against a lethal viral challenge — confirming that larval pulmonary migration, not systemic immunomodulation alone, is the determining factor. This control is essential to attribute any observed effect specifically to pulmonary migration.

Pharmacological variant. An additional arm administering rIL-4C + rIL-5 (without infection) before bleomycin would test whether type 2 macrophage conditioning — independently of the living helminth — is sufficient to reproduce the protective effect.

Primary criteria: total hydroxyproline + Ashcroft score. Secondary criteria: macrophage phenotyping (Arg1, PDL2, CD301b, iNOS), pulmonary and splenic Treg/Th17 profile, cytokines TGF-β1, IL-13, IL-17, IL-10 in BAL, plasma and faecal SCFAs, intestinal 16S sequencing at day 0/14/28, scRNA-seq on pulmonary macrophage populations at day 28.

Arm 2 — Living organisms on established fibrosis

Question asked. Can living helminths, administered after fibrosis has been established, modify its evolution? This is the clinically relevant situation: IPF patients are diagnosed with already significant fibrosis.

Three organisms, three translational rationales.

H. polygyrus in the mouse: chronic systemic immunomodulation (Treg, IL-10, Th17 suppression) without pulmonary migration. Inoculation at day 10 post-bleomycin, sacrifice at day 28 and 42.

Nippostrongylus brasiliensis in the rat: natural host with prolonged persistence. Translationally, Nb in the rat is the closest model to Necator americanus in humans — same family (hookworms), same life cycle including pulmonary migration, same controlled therapeutic inoculation rationale. This arm addresses the question that self-treaters using N. americanus implicitly ask: does larval pulmonary passage in an already fibrotic lung worsen or modulate disease trajectory?

Hymenolepis diminuta (HDC) in the mouse: non-colonising cestode, expelled in 10-12 days in a STAT6-dependent manner, without pulmonary migration. Translationally, it is the animal model closest to the human therapeutic use of HDC — cysts of H. diminuta are used by some self-treaters precisely for their non-colonising nature. Re-dosing from day 10 post-bleomycin.

Common measures: hydroxyproline and Ashcroft at day 28 and 42, BAL cytokines (TGF-β1, IL-13, IL-17, IL-10, IL-33), macrophage phenotyping and pulmonary and splenic Treg/Th17, respiratory function by plethysmography (if available), plasma and faecal SCFAs, intestinal 16S.

3.3 Programme limitations

Timing is critical. Day 28 is too short to capture helminthic effects in the chronic phase. Effects on the microbiome and SCFAs are only established after 6-8 weeks (Mules et al., 2023; 2024). Multiple sacrifice timepoints at day 28, 42 and 56 are necessary.

Species and dose. Helminthic fibrosis data come almost exclusively from murine models. Necator americanus, the species used in human helminthic therapy, has no murine model. Translatability requires non-human primate models or directly phase I studies in humans — with the corresponding ethical and regulatory constraints.

NAMs: allies or aggravators? Trained NAMs are protective acutely, but their programme (Arg1, FABP5, MERTK, SPP1) is enriched in IPF macrophages — potentially maladaptive chronically. Helminthic therapy could activate this programme beneficially in the short term but deleteriously if sustained. This tension will need to be followed in Arm 1 experiments through longitudinal analysis at multiple sacrifice timepoints.

The microbiome/SCFAs/GPR109A axis. Post-bleomycin systemic inflammatory stress can indirectly disturb the intestinal microbiome. Arms 1 and 2 must include plasma SCFAs (primary measure of systemic effect), faecal SCFAs (intestinal production) and 16S sequencing as exploratory secondary criteria.

Conclusions

Idiopathic pulmonary fibrosis remains a disease without curative therapeutic options. Three approved agents slow its progression — pirfenidone, nintedanib, nerandomilast — but none stops it, still less reverses it. Faced with this therapeutic ceiling, identifying upstream immunological mechanisms capable of modifying the fibrotic trajectory before its lock-in constitutes a legitimate research priority.

Helminthic therapy is not an obvious answer to this question. The initial concern is founded: helminths induce type 2 responses whose cytokines — IL-13, IL-33, IL-25 — are documented as pro-fibrotic in the pulmonary context. This concern must not be minimised. It must be clearly stated, as we have done in Part 1, before being nuanced.

The nuance rests on three convergent axes. First, the Th17/Treg axis — distinct from the Th2 axis — exerts causally demonstrated anti-fibrotic effects in fibrotic models: helminths induce Treg expansion and Th17 suppression, correcting an imbalance documented in human IPF. Second, the pulmonary larval migration of certain species reprogrammes alveolar macrophages toward a persistent resolutive phenotype — NAMs — which reduces post-viral fibrotic immunopathology in preclinical models directly relevant for post-COVID and post-influenza IPF. Third, living helminths modulate the intestinal microbiome in favour of SCFA producers, whose butyrate activates GPR109A, inhibits NLRP3 and HDACs, and reinforces the M2/Treg macrophage phenotype — an indirect but mechanistically coherent axis that purified molecules cannot reproduce.

The proposed preclinical programme articulates these axes into testable experimental questions. Arm 1 dissociates macrophage conditioning through larval migration (Nb) from chronic immunoregulatory protection via the Treg/IL-10/Th17 axis (Hp). Arm 2 tests these same species on established fibrosis — the clinically relevant situation — with N. brasiliensis in the rat as a translational model of N. americanus in humans, and HDC as a model of the human therapeutic use of H. diminuta.

Two cross-cutting methodological constraints structure the whole: biochemical hydroxyproline assay as co-primary criterion with histology, and multiple sacrifice timepoints through day 56 to capture helminthic effects in the chronic phase — where the Mules 2023/2024 data show that immunoregulatory benefits are actually established.

This programme aims to produce the preclinical data that would, if positive, justify a phase I study in humans under methodologically rigorous conditions. The stakes are high: IPF kills faster than most cancers, and the available therapeutic arsenal does not fundamentally alter this prognosis. In this context, a mechanistically grounded, biologically plausible and clinically accessible lead deserves to be explored with the rigour it demands — neither rejected out of caution, nor adopted out of enthusiasm.

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Posted Jun 23, 2026, 10:13 AM UTC