Category: Diseases, Syndromes and Conditions

Categories : Diseases, Syndromes and Conditions Injury & TraumaTags :

A New Treatment for Chronic Tendon Disease

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Photo by Nino Liverani on Unsplash

The Achilles tendon can endure a load nearly 8 times body weight during exercise, rendering it vulnerable to injury despite its strength, which can be worsened by a failure to properly heal, forming bone instead of new tendon. A new study found that by inhibiting blood vessel formation, the anomalous bone growth can be prevented.

Due to the unique nature of tendons, failing to consult a doctor soon after an injury can lead to chronic tendon disease, which is characterised by pain, swelling, and movement problems. Tendon heterotopic ossification (HO) is a rare type of chronic tendon disease where new bone grows the tendon, causing even more damage. Famous athletes have had to retire early from sports due to a lack of a radical solution for Achilles tendon injuries.

Using single-cell sequencing technology, a team led by Professor Ouyang Hongwei found that changes in the tissue microenvironment of tendon HO alterations in gene expression and in tendon stem progenitor cells. These findings were published in Bone Research, providing a novel treatment for tendon heterotopic ossification.

The researchers firstly found that the tendon specific transcription factor MKX decreased significantly in heterotopic ossified human tendon, and deletion of MKX led to spontaneous ossification of mouse tendon, suggesting that MKX plays a critical role in tendon HO.

Further studies revealed that MKX knockout mouse tendon cells expressed high levels of genes related to blood vessel formation, resulting in vascular invasion and remodelling of the tendon extracellular matrix. This also resulted in abnormal activation of genes related to bone and cartilage in tendon stem cells. These data indicated that inhibition of blood vessel formation may improve the tendon tissue microenvironment and prevent HO progression.

Armed with this knowledge, Prof Ouyang and his colleagues searched for drugs that can inhibit the angiogenesis process. They found that local injection of a small molecule inhibitor known as BIBF1120 significantly inhibited the neovascularisation of tendon after injury, thus alleviating the progression of tendon HO.

Source: MedicalXpress

Categories : Diseases, Syndromes and ConditionsTags :

Study Shows New Possibilities of Treating Rare Ossifying Disease

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Source: National Cancer Institute on Unsplash

Fibrodysplasia ossificans progressiva (FOP) is a rare disease characterised by anomalous bone growth at the site of even minor injuries. It results in what some term a “second skeleton,” which locks up joint movement and even making breathing difficult. However, new research shows that forming extra-skeletal bone might not be the only driver of the disease. Impaired muscle tissue regeneration allows unwanted bone to form instead of muscle regeneration after injury.

This study was published in NPJ Regenerative Medicine.

“While we have made great strides toward better understanding this disease, this work shows how basic biology can provide great insights into appropriate regenerative medicine therapies,” said the study’s lead author, Foteini Mourkioti, PhD. “From the lab, we’re now able to show that there is potential for a whole new realm of therapies for patients with this devastating condition.”

About 15 years ago, researchers discovered that a mutation in the ACVR1 gene was responsible for FOP. In that study, the team found that the mutation changed cells within muscles and connective tissues, causing them to behave like bone cells and create new, extraneus bone.

“However, while investigations of how the FOP mutation alters the regulation of cell fate decisions have been extensively pursued in recent years, little attention has been paid to the effects of the genetic mutation on muscle and its impact on the cells that repair muscle injuries,” Shore said. “We were convinced that pursuing research in this area could provide clues not only for preventing extra bone formation but also for improving muscle function and regeneration, bringing new clarity to FOP as a whole.”

The researchers studied muscle from mice with the same mutation in the ACVR1 gene that people with FOP have. They focused on two specific types of muscle tissue stem cells: fibro-adipogenetic progenitors (FAPs) and muscle stem cells (MuSCs). Typically, muscle injury repair requires a careful balance of these two cell types. Injured tissue responds by an expansion of FAP cells, which are assigned to recruit muscle stem cells that will regenerate the damaged muscle tissue. After about three days, FAPs die off, their job done. At the same time, MuSCs transition toward a more mature, differentiated state, called muscle fibre, essential to organised movement of our muscles.

In the mice with the ACVR1 mutation being studied, apoptosis – the process through which FAP cells die as a part of proper muscle regeneration – had slowed significantly, leading to a high presence of FAPs past their usual lifespan, altering their balance with the MuSCs. The injured tissue also showed a diminished capacity for muscle stem cell maturation and, as a result, muscle fibres were considerably smaller in mice carrying the ACVR1 mutation compared to muscle fibres in mice lacking the mutation.

“The prolonged persistence of diseased FAPs within the regenerating muscle contributes to the altered muscle environment in FOP, which reduces muscle regeneration and allows the over-abundant FAPs to contribute to the formation of extra-skeletal bone,” Mourkioti said. “This provides a completely new perspective on how excess extra-skeletal bone is formed – and how it could be prevented.”

The current targets for treating FOP focus on slowing extra-skeletal bone growth. This research may provide a pivotal new direction. “We propose that therapeutic interventions should consider promoting the regenerating potential of muscles together with the reduction of ectopic bone formation,” the authors wrote. “By addressing both stem cell populations and their roles in the origin of FOP, there is the possibility of greatly enhanced therapies.”

Source: University of Pennsylvania School of Medicine

Categories : Antibiotics Diseases, Syndromes and ConditionsTags :

Signs of Antibiotic ‘Pre-resistance’ Identified for the First Time

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Drug-resistant, Mycobacterium tuberculosis bacteria, the pathogen responsible for causing the disease tuberculosis (TB). A 3D computer-generated image. Credit: CDC

In a first of its kind study, researchers have spotted signs of antibiotic ‘pre-resistance’ in bacteria for the first time, indicating that they have the potential to develop drug resistance in the future.

The findings, published in Nature Communications, will allow doctors in the future to select the best treatments for bacterial infections.

Mycobacterium tuberculosis (TB) was the second leading infectious cause of death after COVID in 2020, killing 1.5m people. It can be cured if treated with the right antibiotics, but treatment is lengthy and many people most at risk lack access to adequate healthcare. Drug-resistant TB can develop when people do not finish their full course of treatment, or when drugs are not available or are of poor quality.

Multi-drug resistant TB represents a huge, unsustainable burden and totally drug resistant strains have been detected in a handful of countries. As health systems struggle to cope with the pandemic, progress on TB treatment globally has slowed.

To better understand TB for developing new drugs, this study has identified for the first time how to pre-empt drug resistance mutations before they have occurred. Dubbed ‘pre-resistance’ when a pathogen has a greater inherent risk of developing resistance to drugs in the future.

By analysing thousands of bacterial genomes, the study has potential application to other infectious diseases and paves the way towards personalised pathogen ‘genomic therapy’ – which chooses drugs according to the pathogen, preventing drug resistance.

The culmination of 17 years’ work, the study built up a TB bacterial ‘family tree’  from 3135 different tuberculosis samples. Computational analysis identified the ancestral genetic code of bacteria that then went on to develop drug resistance. The team identified the key changes associated with the development of resistance by looking through the ‘branches’ of the family tree to see which had the most potential for developing drug resistance.

Variations in the TB genome predicted that a particular branch would likely become drug resistant, and then validated their findings in an independent global TB data set.

Dr Grandjean, senior author of the study, said: “We’re running out of options in antibiotics and the options we have are often toxic – we have to get smarter at using what we have to prevent drug resistance.

“This is the first example of showing that we can get ahead of drug resistance. That will allow us in the future to use the pathogen genome to select the best treatments.”

Source: EurekAlert!

Categories : Diseases, Syndromes and ConditionsTags :

Apaxiban is an Option in Severe Renal Dysfunction

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Photo by Robina Weermeijer on Unsplash

The anticoagulation options for patients with concomitant renal impairment are limited and until recently, warfarin was the only recommended option due to insufficient data supporting alternative drugs in such patients. A new study published in Blood Advances suggests that apixaban is a viable option in patients with severe renal dysfunction.

Apixaban in patients with impaired renal function is supported by limited data. Landmark clinical trials evaluating apixaban in patients with atrial fibrillation and/or acute venous thromboembolism excluded patients with creatinine clearance (CrCl) <25 mL/min. 

A multicentre, retrospective chart review was conducted to evaluate the safety and effectiveness of apixaban compared with warfarin in patients with CrCl <25 mL/min. Included patients were newly initiated on apixaban or warfarin for at least 45 days with a CrCl <25 mL/min.


Patients were evaluated for thrombosis and bleeding outcomes six  months following initiation of anticoagulation. The primary outcome was the time to first bleeding or thrombosis event. A total of 128 patients met inclusion criteria in the apixaban group and 733 patients in the warfarin group. 

Time to first bleeding or thrombosis event was significantly different between the apixaban and warfarin groups. After controlling for atrial fibrillation and coronary artery bypass grafting, risk of thrombotic and bleeding events was lower in the apixaban group (hazard ratio 0.47). There was no statistical difference between time to thrombosis (83 days vs 54 days, P = .648), rate of thrombosis (5.5% vs 10.3%, P = .08), time to bleeding (46 days vs 54 days, P = .886), or rate of bleeding (5.5% vs 10.9%, P = .06). The severity of bleeding and thrombotic events was not different between groups. 

The results suggest apixaban may be a reasonable option for patients with severe renal dysfunction despite the known increase in apixaban exposure, the researchers concluded. They add that, “These results add to the growing body of evidence of real-world data that apixaban is a reasonable option for patients with severe renal dysfunction.”

The researchers recommend investigating the use of apixaban in patients with a severe renal dysfunction, especially those on haemodialysis, in order to definitively determine the role of apixaban in this patient population.

Source: Blood Advances

Categories : Diseases, Syndromes and ConditionsTags :

A Surprising Use for Ivermectin in Fighting West Nile Virus

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Mosquito
Photo by Егор Камелев on Unsplash

Putting ivermectin in bird-feeders in places where Culex mosquitoes congregate showed promise in reducing the number of infectious mosquitoes that could transmit West Nile virus to humans, according to a researcher presenting at the American Society of Tropical Medicine & Hygiene (ASTMH) virtual meeting.

A pilot trial found that when ivermectin-treated bird-feeders were placed in contiguous lots, there was up to a 16% additional reduction in infectious mosquito days compared to when the bird-feeders were randomly placed, where there was only a 5% additional decline, reported Karen Holcomb, PhD, of the University of California Davis.

Furthermore, with just 33% coverage of ivermectin-treated bird-feeders in a neighbourhood, infectious mosquito days fell by 15% to 45%, she stated.
Since no human vaccine exists for West Nile Virus, the primary strategy has been vector control, she added. However, insecticide has a low specificity in targeting mosquitoes involved in West Nile transmission, and Holcomb also discussed some “non-targeted effects” of spraying in the human population.

Her group hypothesised that because ivermectin could kill mosquitoes while being minimally toxic in mammals and birds, it might be possible to treat bird-feeders with ivermectin, where the mosquitoes would bite the birds, ingest the ivermectin, and die before they could pass the virus on to humans.

Two earlier studies laid the groundwork: one that treated chickens with ivermectin and found a decrease in seroconversion and fewer older mosquitoes near the treated flocks, and an increase in mortality of mosquitoes following a blood meal on treated chickens.

Nevertheless, “the link between ivermectin and West Nile virus transmission was not fully elucidated,” Dr Holcomb said, adding there was no significant difference in mosquito abundance or infection prevalence, as well as variable serum concentrations in chickens.

Next steps of the study included determining what type of set-up worked best for ivermectin-treated bird-feeders in neighborhoods: either contiguous (with all treated bird-feeders in a row) or random. Dr Holcomb’s group found similar reductions in infections in mosquitoes and birds, but the greatest reductions in treated lots were from contiguous, not random placement, she said.

Uncertainty about ivermectin-induced mortality in wild mosquitoes remains, as well as the proper dose of ivermectin to induce mortality.

As a result of ivermectin’s controversial demand during the COVID pandemic, Dr Holcomb said she encountered logistical hurdles.

“During the past year, our collaborators noted it’s become harder to obtain ivermectin, and the ivermectin they were getting was lower quality than prior to COVID,” she told MedPage Today.

In any case, this strategy won’t be used in field control trials for at least a couple more years, Dr Holcomb noted, and “during that time, there should be a reduction in demand for ivermectin.”.

Source: MedPage Today

Categories : Diseases, Syndromes and ConditionsTags :

How Shigella Bacteria Hijacks Cells

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Shigella bacteria Credit: S Bhimji, MD

Shigella, a bacterial pathogen that causes dysentery and is the leading cause of childhood diarrhoeal diseases, inserts a pore called a translocon into an infected person’s intestinal cells and then injects bacterial proteins into the cells. Once inside, the proteins hijack the cellular machinery to help Shigella multiply. In a study published in mBio, researchers report important details about Shigella’s translocon, which may help researchers develop an effective strategy to block this critical component of infection.

“Shigella infects our gut by manipulating our intestinal cells and tricking them into letting the Shigella inside. In fact, there are many bacterial pathogens that use this same, or similar, mechanism to infect us,” said lead author Poyin Chen, PhD, a postdoctoral fellow at MGH. “This translocon pore is essentially the gateway through which bacterial proteins get pumped into our cells. We know that this structure is made of two proteins – IpaB and IpaC – but what we don’t know is how these proteins fit together to make this pore.”

Using protein mapping techniques to look closely at translocons when they were embedded in cell membranes, the researchers were able to see that ipaB makes up the inner ring of the pore. “If you think of the translocon pore as a donut, this would be the walls of the donut hole. This finding is important because this is the part of the translocon pore that directly interacts with bacterial proteins as they are injected into our cells,” Dr Chen explained. “With the findings from this study, we can begin to understand if this pore acts as a slippery tube that bacterial proteins travel through or if the translocon pore can control the flow of bacterial proteins into our cells.”

Such details may help investigators target the translocon and block the entry of Shigella proteins into cells. “For something that is so essential to establishing infection, we know terribly little of how it’s made and how it works,” said Dr Chen. “As we gain a better understanding of its parts, we will be able to approach the structure as a whole and maybe even find ways to neutralise the function of this structure to prevent infection before it can begin.”

Source: Massachusetts General Hospital

Categories : COVID Diseases, Syndromes and ConditionsTags :

Is Malaria Behind Low COVID Burden in Sub-Saharan Africa?

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Mosquito
Photo by Егор Камелев on Unsplash

In both rural and urban areas of Mali, there was a high seroprevalence of COVID, but a low burden of symptomatic disease, a researcher said in a presentation at the American Society of Tropical Medicine & Hygiene (ASTMH) virtual meeting. This could be tentatively attributable to the prevalence of malaria.

From spring to autumn (northern hemisphere) 2020, the seropositivity rate among those with self-reported symptoms jumped from 20.8% to 48.6%, while those reporting symptoms but were seronegative also increased from 9.8% to 49.3% in the cohort, reported John Woodford, MD, of the National Institute of Allergy and Infectious Diseases (NIAID).

However, he said that during March to July, the COVID-attributable fraction was 11%, and from August to December, the COVID-attributable fraction was 0%.

In addition, the percentage of seropositive people with symptomatic illness over the background illness reporting rate was 0%-11%, well below the age-adjusted 33% of cases expected, based on the US case rate.

Only three hospitalisations occurred throughout spring and autumn 2020, also far below the expected 11-30 hospitalisations, and no deaths.

Dr Woodford pointed to “a lot of anecdotal reports that there was a limited disease burden in Mali.”

“It was repeated over and over again for a variety of sub-Saharan African settings, but there’s very limited data to back this up,” he clarified.

His group performed a serosurvey of urban and rural areas of Mali, using two-antigen ELISA qualified for use in that country. Participants were also given a questionnaire asking about self-reported symptoms, medical, and social history.

Overall, they obtained serosurvey data from 3671 participants at four sites, who were a median age of 15. They noted the dates of the symptom questionnaires were March to July 2020 and August to December 2020.

No symptoms were independently associated with seropositivity, Dr Woodford said. There was no greater change of seropositive people being absent from work, seeking medical care, or being hospitalised compared to seronegative people in the cohort during spring. However they were more likely to seek medical care in the autumn than seronegative people (63.4% vs 45.9%, respectively).
The second follow-up visit was during the malaria season, when there was a high percentage of seropositivity, but the proportion of those with self-reported symptoms was comparable with background illness. MedPage Today asked Dr Woodford as to whether malaria infection might have a protective effect, to which he responded: “That is a question much larger than me, and much larger than COVID.” He added that the rural areas in their study had higher rates of malaria than the urban sites, while the reverse was true for COVID.

“What that means, I’m not sure, but there’s certainly a blunt association there,” Dr Woodford noted.

He referenced a recent study of hospitalised patients in Uganda, which found that patients with low previous malaria exposure had higher risk of severe or critical COVID clinical presentation compared to those with high previous exposure, even among patients with no comorbidities.

However, Dr Woodford explained that without a much larger sample size and more accurate tests such as PCR, there was no way to tease out asymptomatic versus symptomatic infections.
“You’d need a very large population to look at symptomatic versus asymptomatic in seropositive patients,” he said. “Logistically, it’s a very challenging study to put together.”

Source: MedPage Today

Categories : Diseases, Syndromes and Conditions Immune SystemTags :

Effective Psoriasis Treatment Could be a ‘TWEAK’ Away

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Source: CC0

A key protein called TWEAK damages skin cells in psoriasis patients, according to a new study in mice and with human skin cells, and targeting TWEAK may help control the disease.

Although there are effective treatments for psoriasis, an autoimmune disease that shows up as patches of red, inflamed skin and painful, scaly rashes, not everyone responds to these therapies – and for many, the relief is temporary.

“These therapies don’t reduce disease by 100 percent, and they don’t cure the disease” says La Jolla Institute for Immunology (LJI) Professor Michael Croft, PhD. “And if you take patients off those drugs, the disease almost always comes back.”

“We think TWEAK might be considered a potential target for the treatment of psoriasis,” said first author Rinkesh Gupta, PhD, a postdoctoral fellow at LJI. “It’s good to have this chance to develop a new therapeutic option.”

The findings build on the lab’s earlier research showing that TWEAK can interact with keratinocytes, the most common type of skin cell. By investigating TWEAK-deficient mice, the researchers found that TWEAK is a driver of inflammation in a model of psoriasis.
The new study, published in Science Immunology, shows that TWEAK does not work alone; it teams up with two other proteins, tumour necrosis factor (TNF) and interleukin-17 (IL-17), to trigger inflammation. These three seem to control inflammatory molecule production and the expression of additional inflammation-associated proteins in patients with psoriasis.

“The fact that they work together suggests the disease is essentially driven by all three of those particular proteins at the same time,” explained Prof Croft. “The primary implication is that TWEAK will also be a good drug target. as has already been proven for TNF and IL-17.”

The researchers tested this idea with a mouse model of psoriasis to compare how well a TWEAK-inhibitor measured up to therapies inhibiting IL-17 or TNF.

“If you inhibit TWEAK from working on its receptor on keratinocytes, you get the same therapeutic effect as when you inhibit TNF or IL-17,” said Dr Gupta. A particularly encouraging aspect of this finding since TNF and IL-17 are both FDA-approved drug targets for psoriasis.

Prof Croft thinks TWEAK inhibitors have potential as therapies for many types of skin diseases. “We think TWEAK is involved in skin inflammation in general,” he said.

His lab is now investigating the role of TWEAK in atopic dermatitis, and while a distinct disease from psoriasis, they do have a few things in common – and there are not as many good treatments for atopic dermatitis.

“There’s certainly a lot of room for improvement in treatment of atopic dermatitis patients,” he said.

Source: La Jolla Institute for Immunology

Categories : Diseases, Syndromes and Conditions New Compounds and TreatmentsTags :

An End to The ‘Therapeutic Drought’ in Atopic Dermatitis

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Source: NCI

The end of a longstanding “therapeutic drought” in atopic dermatitis (AD) is in sight as improved understanding of the pathogenesis and pathophysiology has stoked development of multiple drug candidates, according to a leading expert in the field.

“We did have treatments like cyclosporine, that are not specific as we know, and they are not treatments we can give our patients for long-term disease control,” said Emma Guttman-Yassky, MD, of the Icahn School of Medicine at Mount Sinai, during the Inflammatory Skin Diseases Summit.

She said that overcoming this drought was not easy, mostly because “we didn’t have enough understanding of the disease and its pathogenesis, really preventing therapeutic development for patients with atopic dermatitis,” she said.

New AD therapies built on the trail made for psoriasis treatment, starting with basic studies that produced insights into pathogenesis, leading to hypotheses that eventually could be tested in clinical trials, she said. Progress was accompanied by many failures in early stages of therapeutic development in psoriasis.

“One failure that I remember very vividly from psoriasis was the failure of interferon-gamma targeting,” Dr Guttman-Yassky recounted. “In atopic dermatitis, we also had our share of this type of failure, but these failures really helped shape therapeutic directions for all the diseases we are now targeting, including atopic dermatitis.”

This rocky development has led to recognition that AD is a complex disease involving multiple pathogenetic components, including barrier dysfunction, immune abnormalities, disruption of the dermal microbiome, and the peripheral and central nervous systems that play a central role in itch and other disease manifestations.

“Of all the major components involved in AD pathogenesis, immune targeting is the most tractable,” said Dr Guttman-Yassky. “Immune abnormalities are the most important because they perpetuate the disease phenotype of atopic dermatitis, from the nonlesional skin to acute disease and chronic lesions.”

In contrast to psoriasis, AD is a more heterogeneous disease with multiple clinical phenotypes that correlate with differences in immune polarisation and barrier dysfunction. All of the phenotypes exhibit activation of the type 2 inflammatory pathway as a common feature. Across the spectrum of clinical phenotypes, additional cytokine targeting may be required to achieve disease control.

Understanding that AD arises from systemic inflammation has also helped therapy development. Several studies have suggested that, compared to psoriasis, AD is associated with higher levels of immune activation. Blood samples of patients with AD have shown increased levels of activated T cells, circulatory cytokines, and cardiovascular markers.
The accumulation of new insights into AD pathogenesis added no fewer than a dozen viable therapeutic candidates to the pipeline. Dupilumab (Dupixent) led the way in providing the proof of principle that Th2-specific targeting reverses key pathogenetic factors that drive the disease process in AD.

Dr Guttman-Yassky pointed out how targeting Th2 inflammation with dupilumab led to reversal of barrier defects and lichenisation typical of AD as early as 4 weeks, and that by 16 weeks lesional and nonlesional skin looked similar. Furthermore, markers of epidermal hyperplasia and proliferation were “completely wiped out.”

Dr Guttman-Yassky highlighted several key classes of AD drug candidates with potential to build on the success of targeting inflammation: Interleukin-13 inhibition, OX40 inhibition and JAK/STAT inhibition, which showed promising results.

“With these types of response rates, our treatment goals for our patients are evolving,” said Dr Guttman-Yassky.

Source: MedPage Today

Categories : Cancer Diseases, Syndromes and ConditionsTags :

Treating Cancer with the Toxoplasma Gondii Parasite

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Source: National Cancer Institute on Unsplash

Scientists have discovered that Toxoplasma gondii, a parasite known to cause illness in pregnant women and immunocompromised patients, could potentially enhance the treatment of various types of tumours.

The parasite Toxoplasma gondii is a single-celled opportunistic protozoan capable of infecting a broad range of warm-blooded animals and has been reported in nearly one-third of the world’s human population. It has a number of health effects, including a strong link to schizophrenia and has even been associated with increased suicide attempts in mothers.

While many treatments have been able to treat tumours and prolong the lives of patients, there is a need to further enhance these. In the study, published in the Journal for ImmunoTherapy Cancer, scientists found that the commonly found parasite  is able to sensitise ‘cold’  tumours, that is, tumours unlikely to trigger a strong immune response, to immune checkpoint blockade therapy.

The researchers believe that this finding could have broader therapeutic implications for many types of cancers.

T. gondii has to live inside the cells of its host and secretes numerous proteins to counter the host’s immune defences and to facilitate their own invasion and colonisation of the host cells. The researchers first built a T. gondii mutant strain with limited growth and disease-causing ability, but which is also able to manipulate the host immune system.

By directly injecting this mutant parasite into solid tumours, it induces inflammatory responses in those tumours and even in tumours located in a distant location in the mouse body. The researchers further demonstrated that this treatment approach has made tumours more responsive to treatment with immune checkpoint inhibitors.

This dual treatment significantly extended the survival of mice and reduced tumour growth in mouse models of melanoma, Lewis lung carcinoma, and colon adenocarcinoma.

Dr Hany Elsheikha, Associate Professor in the School of Veterinary Medicine and Science at the University of Nottingham, and one of the lead authors of the study, said: “The use of a mutant version of Toxoplasma gondii in the treatment of certain tumours in mice models has been previously reported. What makes this study different is the confirmation that intratumoural injection with mutant Toxoplasma gondii strain boosts antitumour immunity and the effectiveness of checkpoint inhibition therapy.

“These are significant findings and are relevant to future tumour therapy. The marked reduction in tumour size and the significant improvement in the survival of mice that received this novel combinational therapy is promising but should be interpreted with caution as further research is needed.”

Source: University of Nottingham