However, such constitutive expression is costly for the host in terms of nutrient conservation, self-toxicity and resistance development. Multicellular organisms with high levels of cellular specialization, such as mammals, have evolved adaptations to circumvent these fitness costs, including nutrient depots, sacrificial cells and redundancy in their immune responses. Even so, the Loganin production and secretion of antimicrobial agents during mammalian immune responses generally occurs on a facultative basis. This is well exemplified by the prevalence of situation-dependent production of antimicrobial peptides in the human gut. We reason that fungi, which exhibit a lower degree of multicellular complexity than mammals, should be more sensitive to the fitness costs associated with superfluous antimicrobial production, and thus even more inclined toward facultative production. An unfortunate implication of this line of reasoning is that when fungi and other organisms pass through typical antibiotic screening programs, much of their arsenal is likely to remain uninduced and undetected. The results presented herein indicate the existence of one or several PAMP-recognition systems in A. fumigatus, although these systems are not yet characterized. Furthermore, we show that these PAMPs have significant and specific effect on the release of an antimicrobial secondary metabolite. This highlights the need for a re-evaluation of traditional approaches to fungal antibiotic screening. Molds of the genus Aspergillus are ubiquitous in nature, growing in soils, on Gomisin-D plants and on organic debris. They are common in both outdoor and indoor air, including that of hospitals as well as in water, food items and dust. People are therefore widely exposed to airborne Aspergillus spp. conidia and at risk of colonization, primarily in the respiratory tract. Normally, fungi that manage to penetrate the respiratory mucosa are destroyed quickly by innate immune cells. Aspergillus spp. infections are therefore exceedingly rare in immunocompetent individuals. However, patients with conditions that cause immunodeficiency or who are undergoing immunosuppressive treatments are at a high risk of contracting invasive aspergillosis, especially if the polymorphonuclear neutrophils and T-cells are affected. The effector cells of the innate immune system play a crucial role in the transition from early colonization to invasive aspergillosis. Alveolar macrophages can rapidly phagocytose and destroy conidia, while PMNs prevent the germination of the conidia and their subsequent transition to the hyphal form, which is a key prerequisite for invasion. A number of antimicrobial molecules secreted by the respiratory epithelium also seem to be important in the elimination of conidia. While the condition of the host immune response is the most decisive factor in the development of aspergillosis, the results presented herein demonstrate that the presence of bacteria-associated molecules can increase the fungal toxin production and thereby increase its virulence. Gliotoxin has been shown to induce apoptosis and inhibit multiple processes associated with the activation, differentiation and function of macrophages, PMNs and T-cells. After inhalation of spores, germination leads to gliotoxin secretion.