Helminthic therapy and sepsis

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Is sepsis the result of a depleted biome and could its toll be reduced by helminth replacement?

Sepsis is hard to diagnose and treat, and is killing more people in developed countries. [1]

In the UK, sepsis claims more lives each year than breast, bowel and prostate cancer combined and, in 2004, it was the ninth leading cause of disease-related deaths in US hospitals. It is also currently the most expensive condition treated, so a huge drain on healthcare resources. [2]

Although researchers identified a biomarker for sepsis in the blood in 2013, which could possibly be utilised to create a test to diagnose the condition within two hours by screening at a patient's bedside [3] the available treatments were rapidly diminishing by 2014, and some were no longer working. [4]

Sepsis is of particular concern because it is an increasing cause of complications and death among women in the West, where rates of severe and fatal sepsis during labor and delivery are rising sharply, such that sepsis became the leading cause of direct maternal death in the UK in 2013. [5]

While certain conditions are known to increase the risk of severe and fatal sepsis, many cases occur in women with no recognised risk factors, so what is causing sepsis in these cases? Could it be the helminth deficiency that is now almost universal in developed countries?

We know that the exacerbated pro-inflammatory immune responses that occur during sepsis might be effectively countered, and prevented, if patients were hosting helminths. [6] And the human protein, resistin, which is turned on in humans by a helminth infection, may help in the treatment of sepsis. [7] (Media comment on this study here.)

Chronic filarial infection can provide protection against bacterial sepsis by functionally reprogramming macrophages [8] and a worm protein has been shown to reduce inflammation and mortality from sepsis in mice. [9]

In March 2017, the first effective treatment for sepsis was announced. The protocol, developed by Dr. Paul Marik, uses intravenous vitamin C with hydrocortisone and the B vitamin, thiamine. Of 150 patients treated with the protocol for severe sepsis and septic shock, only one went on to die from the sepsis itself, thus reducing the usual sepsis mortality rate from 30-50 percent utilising standard treatment protocols to less than 1 percent. [10] [11] [12] (video)

It will inevitably take time for the Marik protocol to be adopted into medical practice, but anyone wishing to avoid sepsis can protect themselves immediately by adding a modest number of mutualistic helminths to their biome, as well as ensuring that they are getting adequate amounts of vitamin D [13] and zinc. [14]

The scientific evidence[edit | edit source]

2025 Jul 8 Ascaris Lumbricoides Cystatin Impairs IL-1β Maturation and CD14 Expression in Human Monocytes -- Full text
2025 Jun 23 Quantitative Proteomics Reveals Fh15 as an Antagonist of TLR4 Downregulating the Activation of NF-κB, Inducible Nitric Oxide, Phagosome Signaling Pathways, and Oxidative Stress of LPS-Stimulated Macrophages (preprint)
2025 Mar 3 Nematode serine protease inhibitor SPI-I8 negatively regulates host NF-κB signalling by hijacking MKRN1-mediated polyubiquitination of RACK1 -- Full text | PDF. "treatment with recombinant Nb-SPI-I8 significantly increased the probability of survival of mice from lethal sepsis."
2022 Aug Trichinella spiralis cystatin alleviates polymicrobial sepsis through activating regulatory macrophages -- Full text
2021 Mar 24 Therapeutic Efficacy of Excretory-Secretory Products of Trichinella spiralis Adult Worms on Sepsis-Induced Acute Lung Injury in a Mouse Model -- Full text | PDF
2020 Mar 18 Effects of the dietary fibre inulin and Trichuris suis products on inflammatory responses in lipopolysaccharide-stimulated macrophages
2019 Feb 19 Fasciola hepatica GST downregulates NF-κB pathway effectors and inflammatory cytokines while promoting survival in a mouse septic shock model -- Full text | PDF
2018 Dec 19 Fh15 Blocks the Lipopolysaccharide-Induced Cytokine Storm While Modulating Peritoneal Macrophage Migration and CD38 Expression within Spleen Macrophages in a Mouse Model of Septic Shock — Full text | PDF. A helminth-derived molecule significantly suppressed the inflammation-driven cytokine storm in a mouse model of septic shock.
2017 Nov 13 Human resistin protects against endotoxic shock by blocking LPS-TLR4 interaction (For media comment on this study linking helminths with potential sepsis treatment, see here.)
2017 Oct 6 The immunomodulatory capacity of helminths on inflammation: Impact of eosinophils on E. coli-induced sepsis and genome-wide transcriptome profiling of human monocytes stimulated with helminth extract and LPS implicate immune functions and diseases (thesis)
2017 May 8 Therapeutic effect of Schistosoma japonicum cystatin on bacterial sepsis in mice -- Full text | PDF
2017 Mar Human Resistin Regulates Immunity to Helminths and Sepsis (thesis)
2015 Jan 22 Chronic filarial infection provides protection against bacterial sepsis by functionally reprogramming macrophages -- Full text | PDF
2014 Oct The helminth Trichuris suis suppresses TLR4-induced inflammatory responses in human macrophages -- Full txt
2013 Nov Helminths and their implication in sepsis - a new branch of their immunomodulatory behaviour? -- Full text | PDF
2013 Jul 11 Cathelicidin-like helminth defence molecules (HDMs): absence of cytotoxic, anti-microbial and anti-protozoan activities imply a specific adaptation to immune modulation -- Full text | PDF "This peptide adopts an amphipathic helix structure and, like LL-37, can bind to Escherichia coli lipopolysaccharide (LPS) to prevent its interaction with the toll-like receptor (TLR) 4/MD2/CD14 complex on macrophages"