Rosa Rubicondior: Malevolent Design - How 'Intelligent Design' Exposes Divine Malevolence

Tuesday, 12 August 2025

Malevolent Design - How 'Intelligent Design' Exposes Divine Malevolence

Schistosoma mansoni

Parasitic Worms Evolved to Suppress Neurons in Skin - AAI News

It gets tedious repeating this point so often, but so long as creationists keep using what they claim is irreducible complexity and/or complex specified genetic information as evidence for intelligent design, they need to be reminded that the same argument can also be used as evidence of their putative designer’s malevolence.

Creationists, of course, ignore the fact that parasites are no less “designed” than humans and have structures and processes that are “irreducibly complex” and depend on “complex specified information” in order to succeed in their environments. Yet their existence, and how they interact with and even manipulate their hosts, inevitably increases suffering in the world – a theological problem that creationist disinformation organisations such as the Discovery Institute avoid like the plague.

Parasite–host relationships also inevitably involve evolutionary arms races – the antithesis of intelligence if both “sides” are supposedly designed by the same designer.

So, to keep reminding them: if their justification for designating their god as the designer of living systems holds true, then it is also justification for designating the same god as the cause of suffering. Here is another example of a parasite that falls within their definition of an organism “designed” to do what it does and to participate in an arms race with its host in order to do so. This concerns the discovery that the parasitic worm Schistosoma mansoni, which causes schistosomiasis, is able to suppress neurons in the skin to evade detection as it burrows into its victim’s body (usually the leg).

Background^ Schistosoma mansoni. Origins and Evolution

Schistosoma mansoni is a parasitic flatworm (trematode) in the blood fluke group. Genetic evidence suggests schistosomes evolved from free-living flatworms that became parasites of molluscs, later adapting to vertebrate hosts. The genus Schistosoma likely originated in Asia, with S. mansoni diverging in Africa several million years ago after its ancestors switched from infecting rodents and other mammals to infecting primates, including humans. Today it is widespread in sub-Saharan Africa, with pockets in the Middle East, South America, and the Caribbean, largely spread through the slave trade during the 16th–19th centuries.

Life Cycle

Egg Stage – Adult worms live in the blood vessels of the intestines. Female worms lay hundreds of eggs daily, many of which pass into the host’s intestines and are excreted in faeces.
Hatching – In freshwater, eggs hatch into free-swimming larvae called miracidia.
Snail Host – The miracidia must quickly find and infect a freshwater snail of the genus Biomphalaria. Inside the snail, they undergo several developmental stages, multiplying asexually.
Cercariae Release – After several weeks, the snails release free-swimming larvae called cercariae.
Human Infection – Cercariae actively seek a mammalian host, penetrate the skin, and shed their tails, becoming schistosomula. These enter the bloodstream, migrate through the lungs and liver, and mature into adults in the mesenteric veins.
Adult Stage – Adult worms live in pairs, with the slender female residing in a groove along the thicker male’s body. They can survive for years, continually producing eggs and perpetuating the cycle.

Key Point

The pathology of schistosomiasis is mainly caused by the host’s immune reaction to eggs trapped in tissues, leading to inflammation, scarring, and sometimes organ damage. The parasite’s life cycle is the result of a finely tuned arms race between evasion of host defences and the host’s attempts to eliminate it.

This discovery, by researchers from the Tulane School of Medicine, is published, open access, in The Journal of Immunology and explained in a news release from the American Association of Immunologists.

Parasitic Worms Evolved to Suppress Neurons in Skin
New research, published in The Journal of Immunology, discovered that a parasitic worm suppresses neurons in the skin to evade detection. The researchers suggest that the worm likely evolved this mechanism to enhance its own survival, and that the discovery of the molecules responsible for the suppression could aid in the development of new painkillers.
Schistosomiasis is a parasitic infection caused by helminths, a type of worm. Infection occurs during contact with infested water through activities like swimming, washing clothes, and fishing, when larvae penetrate the skin. Surprisingly, the worm often evades detection by the immune system, unlike other bacteria or parasites that typically cause pain, itching, or rashes.

Skin Neurons

In this new study, researchers from Tulane School of Medicine aimed to find out why the parasitic worm Schistosoma mansoni doesn’t cause pain or itching when it penetrates the skin. Their findings show that S. mansoni causes a reduction in the activity of TRPV1+, a protein that sends signals the brain interprets as heat, pain, or itching. As part of pain-sensing in sensory neurons, TRPV1+ regulates immune responses in many scenarios such as infection, allergy, cancer, autoimmunity, and even hair growth.

The researchers found that S. mansoni produces molecules that suppress TRPV1+ to block signals from being sent to the brain, allowing S. mansoni to infect the skin largely undetected. It is likely S. mansoni evolved the molecules that block TRPV1+ to enhance its survival.

Potential Therapeutics

If we identify and isolate the molecules used by helminths to block TRPV1+ activation, it may present a novel alternative to current opioid based treatments for reducing pain. The molecules that block TRPV1+ could also be developed into therapeutics that reduce disease severity for individuals suffering from painful inflammatory conditions.

Professor De’Broski R. Herbert, senior author Department of Microbiology and Immunology
School of Medicine
Tulane University, New Orleans, LA, USA.

The study also found that TRPV1+ is necessary for initiating host protection against S. mansoni. TRPV1+ activation leads to the rapid mobilization of immune cells, including gd T cells, monocytes, and neutrophils, that induce inflammation. This inflammation plays a crucial role in host resistance to the larval entry into the skin. These findings highlight the importance of neurons that sense pain and itching in successful immune responses.

Identifying the molecules in S. mansoni that block TRPV1+ could inform preventive treatments for schistosomiasis. We envision a topical agent which activates TRPV1+ to prevent infection from contaminated water for individuals at risk of acquiring S. mansoni.

Professor De’Broski R. Herbert.

In this study, mice were infected with S. mansoi and evaluated for their sensitivity to pain as well as the role of TRPV1+ in preventing infection. Researchers next plan to identify the nature of the secreted or surface-associated helminth molecules that are responsible for blocking TRPV1+ activity and specific gd T cell subsets that are responsible for immune responses. The researchers also seek to further understand the neurons that helminths have evolved to suppress.

Publication:
Juan M Inclan-Rico, Adriana Stephenson, Camila M Napuri, Heather L Rossi, Li-Yin Hung, Christopher F Pastore, Wenqin Luo, De’Broski R Herbert.
TRPV1+ neurons promote cutaneous immunity against Schistosoma mansoni
The Journal of Immunology, 2025;, vkaf141, https://doi.org/10.1093/jimmun/vkaf141

Abstract
Immunity against skin-invasive pathogens requires mechanisms that rapidly detect, repel, or immobilize the infectious agent. While bacteria often cause painful cutaneous reactions, host skin invasion by the human parasitic helminth Schistosoma mansoni often goes unnoticed. This study interrogated whether pain-sensing skin afferents marked by expression of the ion channel Transient Receptor Potential Vanilloid 1 (TRPV1) contributed to the detection and initiation of skin immunity against S. mansoni. Data show that percutaneous S. mansoni infection significantly reduced thermal pain sensitivity evoked by TRPV1+ neurons. Consistently, isolated skin sensory neurons from infected mice had significantly reduced calcium influx and neuropeptide release in response to the TRPV1 agonist capsaicin compared to neurons from naïve controls. Using gain- and loss-of-function approaches to test whether TRPV1+ neurons initiate host-protective responses revealed that TRPV1+ neurons limit S. mansoni skin entry and migration into the pulmonary tract. Moreover, TRPV1+ neurons were both necessary and sufficient to promote proliferation and cytokine production from dermal γδ T cells and CD4+ T helper cells, as well as to enhance neutrophil and monocyte recruitment to the skin. Taken together, this work suggests that S. mansoni may have evolved to manipulate TRPV1+ neuron activation as a countermeasure to limit IL-17-mediated inflammation, facilitating systemic dissemination and chronic parasitism.

Graphical Abstract

Introduction
The skin is populated by hematopoietic and non-hematopoietic cells that coordinately assemble the first line of defense against pathogen invasion. Certain bacterial and fungal skin infections evoke painful and itchy reactions, which are transmitted by diverse subsets of sensory neurons (afferents) whose cell bodies emanate from dorsal root ganglia (DRG) or trigeminal ganglia (TG).^1–3 Notably, the predominant subset of pain-sensing neurons (nociceptors) that express the non-selective cation channel transient receptor potential vanilloid member 1 (TRPV1) have been recognized as central regulators of barrier tissue immune responses during infection, autoimmunity, allergy, cancer, wound healing, hair growth, and tolerance.^1–14 TRPV1+ afferents not only respond to canonical stimuli like heat or capsaicin but also directly respond to bacterial and/or fungal products.^1–4 Activation of TRPV1+ neurons leads to secretion of neuropeptides such as calcitonin gene-related peptide (CGRP) and Substance P (SP) that in turn, direct effector functions of skin-resident hematopoietic cells.^1,3,8 While several bacterial species induce TRPV1 neuron-derived CGRP to suppress neutrophil responses that favor bacterial colonization, fungal antigen-induced CGRP from TRPV1+ neurons was shown to stimulate myeloid antigen-presenting cells (APC) to induce host-protective IL-17 responses.^1–4 TRPV1+ neurons can also promote detrimental skin inflammation in the context of psoriasis or allergic disease.^5,7–9 These studies highlight the importance and context-dependent contributions of sensory neurons that transmit pain and itch as regulators of skin inflammatory responses.

The skin-penetrating helminth Schistosoma mansoni causes chronic parasitism in ∼250 million people worldwide.^15,16 Upon exposure to human skin, S. mansoni infectious stage larvae (cercariae) rapidly penetrate within minutes through muscular actions and secretion of proteolytic enzymes that degrade extracellular matrix proteins and facilitate dissemination from cutaneous tissue into the pulmonary tract.^17,18 Surprisingly, the cutaneous stage of S. mansoni pathogenesis is usually asymptomatic, infrequently causing mild dermatitis and/or itch.^15,16,19 Conversely, zoonotic exposure to other avian schistosome species is marked by severe dermatitis and pruritus, known as “Swimmer’s itch,” with worsening manifestations upon repeated exposures proposed to prevent systemic parasite dissemination.^20–22 Our recent work demonstrated that itch-transmitting neurons bearing the receptor Mas-related G-coupled protein receptor A3 (MrgprA3) are inactivated upon exposure to S. mansoni antigens.²³ Prior activation of MrgprA3+ neurons repelled S. mansoni skin infection through induction of pro-inflammatory cytokine secretion by myeloid APC that induced IL-17-mediated inflammation.²³ TRPV1 is broadly expressed in DRG and TG nociceptors, including MrgprA3+ neurons,^24,25 suggesting that the broad population of TRPV1+ neurons may elicit immunity against S. mansoni. However, whether nociceptive TRPV1+ neurons are activated and contribute to host-protective immune responses against S. mansoni has not been addressed.

This study interrogated the hypothesis that S. mansoni evolved to suppress pain-transmitting TRPV1+ neurons that would otherwise elicit host-protective skin inflammation and block parasitism. Data show that S. mansoni percutaneous infection reduces thermal pain sensitivity as well as calcium influx and neuropeptide release evoked by TRPV1+ neurons. Local optogenetic TRPV1+ neuron activation prior to S. mansoni exposure conferred resistance to skin invasion and attenuated parasite dissemination into the lungs. TRPV1+ neuron activation significantly induced IL-17, IL-13, and Ki67 expression in skin γδ T cells, and moderately in CD4+ T cells, increased swelling and promoted the accumulation of inducible nitric oxide synthetase (iNOS+) neutrophils and monocytes within 1 day of S. mansoni infection. Conversely, chemical denervation of TRPV1+ neurons increased larval burden in the lungs and diminished γδ T cell, neutrophil, and monocyte responses. Taken together, these data support a model wherein S. mansoni suppresses nociceptor effector function(s) that would otherwise initiate host-protective inflammation to limit dissemination and chronic parasitism.

Juan M Inclan-Rico, Adriana Stephenson, Camila M Napuri, Heather L Rossi, Li-Yin Hung, Christopher F Pastore, Wenqin Luo, De’Broski R Herbert.
TRPV1+ neurons promote cutaneous immunity against Schistosoma mansoni
The Journal of Immunology, 2025;, vkaf141, https://doi.org/10.1093/jimmun/vkaf141

Copyright: © 2025 The American Association of Immunologists.
Published by Oxford University Press. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Glossary of Technical Terms & Acronyms.

Antigen-presenting cells (APCs) - Immune cells (e.g., dendritic cells, macrophages) that display antigens to T cells, triggering immune reactions.
Chromatin accessibility - The openness of chromatin structure in a cell’s DNA, affecting how easily genes can be transcribed; used to infer active gene regulation.
Cytokine expression - Production and secretion of small proteins (cytokines) by immune and other cells to regulate immune responses.
Epidermal hyperplasia - Thickening of the outer skin layer due to increased proliferation of epidermal cells.
γδ T cells - A subset of T lymphocytes characterised by their gamma-delta (γδ) T-cell receptor; involved in innate-like immune responses in barrier tissues like the skin.
IL-1β - Interleukin-1 beta, a potent pro-inflammatory cytokine involved in signalling during infection or tissue damage.
IL-17 - Interleukin-17, a pro-inflammatory cytokine produced by certain T cells; here, specifically IL-17–positive γδ T cells.
IL-17/IL-23-dependent changes - Immune responses mediated through cytokines interleukin-17 and interleukin-23, known to influence inflammation and epidermal response.
IL-33 - Interleukin-33, a cytokine involved in promoting type-2 immune responses and inflammatory signalling (here, derived from myeloid cells).
Itch-sensing afferents - Nerve fibres in the skin that detect itch stimuli.
Macrophages - Innate immune cells responsible for engulfing pathogens and coordinating inflammatory responses.
MrgprA3 - Mas-related G-protein-coupled receptor A3; a receptor found on sensory neurons involved in itch perception.
Myeloid antigen-presenting cell subsets - Subtypes of APCs originating from the myeloid lineage (like macrophages or dendritic cells) that present antigens and coordinate varying immune functions.
Neuropeptide calcitonin gene-related peptide (CGRP) - A neuropeptide released by neurons; here implicated in modulating cytokine signalling in immune cells.
Pruritus - Medical term for itching.
Schistosoma mansoni - A human parasitic helminth (blood fluke) that causes schistosomiasis.
Tumour necrosis factor (TNF) - A key pro-inflammatory cytokine involved in immune responses, inflammation, and apoptosis.
Type 2 conventional dendritic cells - A subtype of dendritic cells that promote type-2 immune responses, often associated with allergy and anti-parasitic immunity.

Parasite–host relationships like that between *Schistosoma mansoni* and humans remain one of the most awkward subjects for creationists. Their entire design argument rests on the idea that complex, highly adapted biological systems must have been purposefully created. Yet here we have a textbook example of a system that is undeniably complex and exquisitely adapted—only its “purpose” is to invade a human body, bypass our defences, and cause long-term suffering.

Creationist organisations such as the Discovery Institute rarely, if ever, address this directly. They cannot easily reconcile the notion of a benevolent, all-powerful designer with the existence of a parasite that can slip into the body undetected by chemically silencing the victim’s nerve cells. To acknowledge that this, too, is “irreducibly complex” would mean accepting that their putative designer actively created a mechanism for pain and disease.

The reality is that parasite–host dynamics, like all such relationships in nature, make perfect sense in the light of evolution. They are the product of countless generations of reciprocal adaptation—an evolutionary arms race in which neither side is designed to produce a harmonious outcome. This is exactly the opposite of what you would expect from a single, intelligent designer supposedly concerned with the welfare of its creations. It’s no wonder creationists prefer to avert their gaze from such examples: they fit the evolutionary model perfectly and demolish the illusion of benevolent, purposeful design.

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