Minireview: host defence in invasive aspergillosis

Abstract

Aspergillus is a saprophytic fungus, which mainly becomes pathogenic in immunosuppressed hosts. A failure of host defences results in a diverse set of illnesses, ranging from chronic colonisation, aspergilloma, invasive disease and hypersensitivity. A key concept in immune responses to Aspergillus species is that host susceptibility determines the morphological form, antigenic structure and physical location of the fungus. Traditionally, innate immunity has been considered as a first line of defence and activates adaptive immune mechanisms by the provision of specific signals; innate and adaptive immune responses are intimately linked. The T-helper cell (TH 1) response is associated with increased production of inflammatory cytokines IFN-γ, IL-2 and IL-12 and stimulation of antifungal effector cells. Alternatively, TH 2-type responses are associated with suppression of antifungal effector cell activity, decreased production of IFN-γ and increased concentrations of IL-4 and IL-10, which promote humoral responses to Aspergillus. The host's defensive capacity is defined by the sum of resistance and tolerance. Resistance displays the ability to limit fungal burden and elimination of the pathogen, and tolerance means the ability to limit host damage caused by immune response.

Haploidentical hematopoietic transplantation from KIR ligand–mismatched donors with activating KIRs reduces nonrelapse mortality

“…[61][62][63][64][65][66] Protective immunity against A fumigatus depends on inflammatory cytokines and Th1 responses. 67 The KIR2DS1-triggered IFN-g release in response to A fumigatuspulsed DCs may have clinical implications because invasive Aspergillosis is a major cause of mortality in immune-compromised hosts.…”

Immunohistochemical Analysis of Leucocyte Subsets in the Sinonasal Mucosa of Cats with Upper Respiratory Tract Aspergillosis

“…Although additional mechanisms are believed to be involved, neutropenia or impaired neutrophil function is believed to be the predominant predisposing factor (Lass-Florl et al, 2013). Interestingly, in the cases of feline URTA reported here, neutrophilic inflammation was not identified commonly.…”

“…The immune response in invasive aspergillosis (IA) has been most fully elucidated in murine models of the infection and in human patients with pulmonary and disseminated disease (Mirkov et al, 2012;Lass-Florl et al, 2013). The innate immune response to SNA has been described in dogs (Peeters et al, 2005a(Peeters et al, , 2006(Peeters et al, , 2007Mercier et al, 2012;Vanherberghen et al, 2012), but in contrast to cats, which often have invasive fungal rhinosinusitis, this mycosis is non-invasive in dogs (Peeters et al, 2005a).…”

Promising immunotherapy against fungal diseases

“…Severity and pattern of fungal diseases are usually directed by the interplay of the pathogen and host immunity. Hence, host susceptibility is determined by the activity of cell-and humoral-mediated immunity [2]; in immunocompetent patients disease manifestation is linked to an excessed, in immunocompromised individuals to lack of adequate host response [3]. For successful infection, fungi adapt to hosts stressors and evade hosts' immunity; any failure to restore host immunity leads to worse outcome.…”