## 1 Introduction  
Commensal bacteria that inhabit the surfaces exposed to the external environment, collectively known as microbiota, engage in a symbiotic relationship with the host, and their role in health and disease is increasingly being recognized [1]. This relationship takes on particular significance in the context of defense against pathogen invasion. Indeed, the microbiota can directly interfere with pathogen colonization by competing for space and nutrients, and the local immune system can promptly respond to pathogenic threats. In parallel, the microbiota and the immune system cross-regulate each other's activity to optimize their response against potential pathogen encounters [2, 3]. For instance, the microbiota may produce immunomodulatory metabolites, such as indole-containing metabolites from the utilization of tryptophan [4], or short-chain fatty acids (SCFAs) from the fermentation of indigestible fibers [5]. SCFAs have five or less carbons and include formic acid, acetic acid, propionic acid, butyric acid, isobutyric acid, valeric acid, and isovaleric acid.  
SCFAs participate in a variety of physiological functions. For instance, butyrate not only represents the primary energy source for colonocytes in the gut, but also modulates the immune system, for instance by regulating the differentiation of regulatory T cells [6; 7] or the activity of macrophages [8; 9]. Mechanistically, butyrate is a ligand for three G protein-coupled receptors, GPR41, GPR43 and GPR109A, and works as a potent inhibitor of specific classes of histone deacetylases [10]. In turn, the microbiota can be modulated by the immune system, for instance via the release of antimicrobial peptides [11] or IgA [12]. While these mechanisms are being unraveled in the gastrointestinal tract, how the microbiota and the host immune system crosstalk in the respiratory tract to protect from infection remains less studied.  
_Aspergillus_ species are environmental fungi and are a potential cause of diseases in susceptible individuals, ranging from asthmatic forms to the more severe invasive aspergillosis [13]. The immune response to _Aspergillus_ has been the object of intense research, and the mechanisms employed by the innate and the adaptive arms of the immune system are increasingly being elucidated [14]. It has been noted that the microbiome may also be involved in protection against _Aspergillus_[15; 16]. In this regard, we have recently shown that the composition of the oropharyngeal microbiome could predict the risk of fungal pneumonia in hematological patients [17]. In particular, an increased risk of fungal pneumonia was associated with the loss of protective anaerobes such as Clostridiales and Bacteriodota and the expansion of pathogenic Proteobacteria, as confirmed in a murine model of aspergillosis [17]. However, the mechanisms at the basis of the protection as well as how the microbiota integrates with the immune system during the response to infection have not been investigated.  
Based on these premises, in this study we have resorted to a murine model of _Aspergillus fumigatus_ infection in immune-deficient mice, and found alterations in the composition of the lung microbiota and in the pulmonary abundance of SCFAs along characteristic patterns, supporting a role for the microbiota-immune system crosstalk in the regulation of antifungal immunity in the lung.