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Allergic bronchopulmonary aspergillosis (ABPA) is a rare disease characterized by a complex allergic inflam-matory reaction of airways against Aspergillus affecting patients with chronic respiratory diseases (asthma, cystic fibrosis). Exacerbation is often the way to diagnose ABPA and marks its evolution by its recurrent char-acter leading to cortico-requirement or long-term antifungal treatment. Early diagnosis allows treatment of ABPA at an initial stage, preventing recurrence of exacerbations and long-term complications, mainly repre-sented by bronchiectasis. This review of the literature aims to present the current state of the art in terms of diagnosis and treatment of ABPA from a multidisciplinary perspective. As there is no clinical, biological nor radiological specific sign, diagnostic criteria are regularly revised. They are mainly based on the elevation of total and specific IgE against Aspergillus fumigatus and the presence of suggestive CT abnormalities such as mucoid impaction and consolidations. ABPA management includes eviction of mold and pharmacological therapy. Exacerbations are treated in first line with a moderate dose of oral corticosteroids. Azole antifungal agents represent an alternative for the treatment of exacerbations and are the preferential strategy to reduce the future risk of exacerbations and for corticosteroids sparing. Asthma biologics may be of interest; how-ever, their place remains to be determined. Avoiding complications of ABPA while limiting the side effects of systemic drugs remains a major challenge of ABPA management. Several drugs, including new antifungals and asthma biologics, are currently being tested and may be useful in the future.(c) 2023 SFMM. Published by Elsevier Masson SAS. All rights reserved.

Introduction NOD1 is an innate pattern-recognition sensor for Gram-negative peptidoglycan (PG) that is involved in the development of allergic asthma and signals through the kinase RIPK2. The aim of this study was to investigate the role of NOD1 in HDM-induced asthma. Methods Nod1-/-, Ripk2-/− and WT mice were subjected to a protocol of HDM-induced asthma. Faecal microbiota transplantation from Nod1-/− and WT was performed in germ free (GF) mice before HDM asthma protocol. HDM content was analysed by mass spectrometry. A NOD1 reporter cell model and the human bronchial epithelial cell line Beas2B were stimulated with HDM. Results Nod1-/− and Ripk2-/− mice exhibited reduced asthma features, including decreased airway hyperresponsiveness (AHR), less pulmonary inflammation and lower levels of Th2-related cytokines and chemokines. However, no differences in any asthma parameters were found between GF mice transplanted with either Nod1-/− or WT microbiota. HDM mass spectrometry analysis evidenced the presence of PG-derived NOD1 ligands, and a PG-dependent activation was found in the NOD1 reporter model. Furthermore, the HDM stimulation of human epithelial Beas2B cells led to NOD1 activation and RIPK2 signalling. Accordingly, when WT mice were subjected to the asthma protocol with PG-depleted HDM, but not to LPS-reduced HDM, asthma features were notably reduced. Conclusions HDM-derived microbiota promotes allergic airway disease through NOD1 sensing, suggesting that this pathway may provide attractive therapeutic targets.

Obesity and asthma prevalence has dramatically and concomitantly increased over the last 25 years, and many epidemiological studies have highlighted obesity as an important risk factor for asthma. Although many studies have been performed, the underlying mechanisms remain poorly understood. Innate mechanisms have been involved in both diseases, in particular through the recently described innate lymphoid cells (ILCs). ILCs are subdivided into three groups that are defined by their cytokine production and by their master transcription factor expression, in sharp correlation with their T helper counterparts. However, unlike T helper cells, ILCs do not express antigen-specific receptors, but respond to damage-induced signals. ILCs have been found in target tissues of both diseases, and data have implicated these cells in the pathogenesis of both diseases. In particular group 2 ILCs (ILC2) are activated in both the adipose and lung tissues under the effect of interleukin-33 and interleukin-25 expression. However, counter-intuitively to the well-known association between obesity and asthma, ILC2 are beneficial for obesity but deleterious for asthma. This review will examine the roles of ILCs in each disease and recent data highlighting ILCs as a putative link between obesity and asthma.

Introduction: While there is increasing evidence that it exists a link between asthma development, early life exposure to allergens like house dust mite (HDM) and the microbiome composition, the underlying mechanisms remain elusive. While Nucleotide-binding oligomerization domain 1 (NOD1) has been shown to regulate the gut microbiota composition, our previous findings showed that a Nod1 agonist used as a systemic adjuvant exacerbates ovalbumin-induced Th2-mediated allergic asthma and more recently that HDM-induced asthma is improved in Nod1-deficient mice. Aims and objectives: The aim of his study was to evaluate if the intestinal dysbiosis present in Nod1 deficient mice may modify HDM-induced pulmonary inflammation. Methods: The role of NOD1 was investigated in the HDM-induced asthma model, using Wild-Type, NOD1 deficient mice and Ripk2 deficient mice. Fecal transplantation of Nod1 deficient or WT mice into germfree (GF) mice was performed and HDM-induced asthma evaluated. We measured airway hyperreactivity, total and differential cell counts in bronchoalveolar lavage (BAL), Th2 cytokines and chemokines in lung protein extracts and total IgE levels in the serum. Results: Our results show that HDM-sensitized/challenged NOD1 and Ripk2 deficient mice exhibited less pulmonary inflammation when compared to the wild-type mice. However there was no difference between GF mice transplanted with either Nod1 deficient or WT microbiota. Conclusion: Our results suggest that NOD1-deficient dysbiosis is not responsible for decreasing allergic inflammation parameters and suggest that the allergen may directly activate NOD1 receptor.