Research published between 21 July and 3 August 2026
Recent aspergillosis research has highlighted the relationship between corticosteroid treatment and pulmonary aspergillosis, a possible future method for restoring the activity of azole antifungals, and the importance of the immune response during recovery from invasive aspergillosis.
The most immediately relevant study found a strong, dose-related association between corticosteroid exposure and pulmonary aspergillosis. The other studies are earlier-stage research but may contribute to more personalised monitoring and new treatments in the future.
1. Corticosteroid use linked to an increased risk of pulmonary aspergillosis
A large Danish population-based study has examined whether inhaled and oral corticosteroids are associated with chronic pulmonary aspergillosis (CPA) and invasive pulmonary aspergillosis (IPA).
The researchers identified 1,351 people diagnosed with pulmonary aspergillosis other than allergic bronchopulmonary aspergillosis (ABPA). Each person was matched with five controls of the same age and sex.
Both inhaled and oral corticosteroid use were associated with an increased risk of pulmonary aspergillosis:
- Lower-dose inhaled corticosteroids were associated with approximately 1.7 times the risk.
- Higher-dose inhaled corticosteroids were associated with approximately 2.8 times the risk.
- Lower-dose oral corticosteroids were associated with approximately three times the risk.
- Higher-dose oral corticosteroids were associated with approximately four times the risk.
Higher-dose inhaled corticosteroids were associated with invasive pulmonary aspergillosis, while oral corticosteroid exposure was associated with both CPA and IPA. The association became weaker as more time passed since corticosteroid exposure.
The presence of a dose-response relationship strengthens the evidence: people exposed to higher corticosteroid doses generally had a greater risk. However, this was an observational study and cannot prove that corticosteroids directly caused every case. People requiring higher doses may also have more severe COPD or other lung damage that independently increases their risk.
An accompanying editorial by Professor David Denning argues that the findings should increase awareness of potentially fatal aspergillosis among people with COPD receiving corticosteroids.
What does this mean for patients?
Corticosteroids are important medicines that control inflammation and can prevent serious asthma or COPD exacerbations. This study does not mean that people should stop inhaled or oral corticosteroids.
Instead, it supports careful prescribing, using the lowest effective dose and regularly reviewing whether continued corticosteroid treatment is necessary. Clinicians should also consider aspergillosis when someone with COPD or another chronic lung condition develops unexplained or persistent deterioration, particularly during repeated or high-dose corticosteroid treatment.
Patients should not reduce or stop corticosteroids without discussing this with their clinical team. Suddenly stopping oral corticosteroids can be dangerous, particularly after prolonged treatment.
Read the corticosteroid study in Thorax
Read the accompanying editorial
2. Could resistant Aspergillus be made sensitive to azoles again?
Azole antifungals—including itraconazole, voriconazole, posaconazole and isavuconazole—are central to the treatment of many forms of aspergillosis. Unfortunately, some strains of Aspergillus fumigatus are resistant to one or more azoles, leaving patients with fewer treatment options.
Laboratory researchers have now investigated a different part of the fungal pathway used to produce ergosterol, an essential component of the fungal cell membrane.
They identified an enzyme called Erg7A, or lanosterol synthase, as a potential treatment target. Genetically disrupting this enzyme made resistant Aspergillus more sensitive to azoles. This effect was seen in clinical isolates with different resistance mechanisms, including mutations affecting cyp51A and hmg1.
The researchers also tested an experimental lanosterol-synthase inhibitor called Ro 48-8071. When combined with itraconazole or posaconazole, it produced a strong synergistic effect and restored azole susceptibility in resistant isolates.
What does this mean for patients?
This is promising laboratory research, but it is not yet a treatment that can be offered to patients. Ro 48-8071 also affects the human version of lanosterol synthase, so researchers would need to develop safer compounds that selectively target the fungal enzyme.
Further testing in animal models would be required before any human clinical trial could begin. Nevertheless, the study provides an interesting strategy: instead of abandoning azoles when resistance develops, a future combination treatment might make the fungus responsive to them again.
3. Aspergillus-specific immune cells may help predict recovery
Successful treatment of invasive aspergillosis depends on antifungal medication and on the patient’s immune system recovering sufficiently to control the infection.
The OPTIFIL study examined 39 people with haematological malignancies who had localised invasive pulmonary aspergillosis. Researchers measured immune cells that recognised Aspergillus and produced interferon-gamma, an important immune signalling molecule.
These Aspergillus-specific T cells were detected in 41% of patients. Their presence was associated with better outcomes after six weeks, while their absence was associated with uncontrolled infection.
One important limitation was lymphopenia—a very low number of lymphocytes in the blood—which made the test difficult to interpret in some patients.
What does this mean for patients?
The study supports the idea that monitoring the recovery of antifungal immunity might provide useful information alongside scans, cultures, biomarkers and clinical symptoms.
In the future, this type of test might help identify people whose immune systems are recovering and those who remain at particularly high risk. It could also contribute to research into immune-based treatments.
However, this was a small study involving a highly selected group of patients with blood cancers. The test is not ready for routine clinical use and requires validation in larger and more varied patient populations.
Read the study in The Journal of Infectious Diseases
4. How immune-cell metabolism can weaken antifungal defence
A separate laboratory study investigated itaconate, a naturally produced metabolite that helps regulate inflammation during infection.
Although limiting excessive inflammation can protect lung tissue, the researchers found that itaconate can also suppress parts of the innate immune response during fungal pneumonia. This may reduce the immune system’s ability to control fungal growth.
The study adds to growing evidence that immune responses to fungal infection require a careful balance. Too little immune activity can allow infection to progress, while excessive inflammation can damage the lungs.
What does this mean for patients?
This is early mechanistic research and does not currently change treatment. Itaconate should not simply be considered “good” or “bad”: its effects depend on the infection, immune response and stage of disease.
Understanding these metabolic pathways may eventually help researchers develop treatments that improve antifungal immunity without causing damaging inflammation.
Overall message
The clearest clinical finding from this fortnight is the dose-related association between corticosteroid exposure and pulmonary aspergillosis. It reinforces the importance of reviewing corticosteroid treatment and recognising aspergillosis as a possible explanation for unexplained deterioration in people with chronic lung disease.
The remaining studies point towards two longer-term possibilities: overcoming azole resistance by making resistant fungi sensitive again, and using measurements of antifungal immunity to understand prognosis and personalise care.
Neither approach is ready for routine treatment, but both address major unmet needs in aspergillosis care.
This update summarises recently published research for patients, carers and non-specialist healthcare professionals. Observational associations do not necessarily establish cause and effect, while laboratory findings may not translate into safe or effective treatments in humans. Some appraisal is based on abstracts and available publisher information; full-text review may refine individual details.
This information is educational and does not replace advice from your clinical team. Do not start, stop or alter corticosteroid or antifungal treatment without medical guidance.
