RESUMO
Invasive aspergillosis is a classic fungal infection of immunocompromised hosts which rarely manifests in immunocompetent patients. In this report, we present a case of invasive aspergillosis which resulted from induced immunosuppression through corticosteroid treatment of chronic rhinosinusitis. Further investigation is necessary into the epidemiology of mixed fungal rhinosinusitis and providers should be wary of invasive disease in those receiving chronic steroids.
RESUMO
Neuroimmune interactions are crucial for regulating immunity and inflammation. Recent studies have revealed that the central nervous system (CNS) senses peripheral inflammation and responds by releasing molecules that limit immune cell activation, thereby promoting tolerance and tissue integrity. However, the extent to which this is a bidirectional process, and whether peripheral immune cells also promote tolerance mechanisms in the CNS remains poorly defined. Here we report that helminth-induced type 2 inflammation promotes monocyte responses in the brain that are required to inhibit excessive microglial activation and host death. Mechanistically, infection-induced monocytes express YM1 that is sufficient to inhibit tumor necrosis factor production from activated microglia. Importantly, neuroprotective monocytes persist in the brain, and infected mice are protected from subsequent lipopolysaccharide-induced neuroinflammation months after infection-induced inflammation has resolved. These studies demonstrate that infiltrating monocytes promote CNS homeostasis in response to inflammation in the periphery and demonstrate that a peripheral infection can alter the immunologic landscape of the host brain.
