Sera from 20 ICU sufferers without microbiological or clinical proof IA, including 8 sufferers with chronic obstructive pulmonary disease, 6 sufferers with chronic renal disease, 3 sufferers with renal transplantation, and 3 sufferers with acute pancreatitis (a long time, 33-75 years), were used seeing that negative handles. the lack of an obvious predisposing immunodeficiency. The medical diagnosis of IA is certainly tough because scientific symptoms aren’t particular and delicate, and serum galactomannan provides low awareness within this band of sufferers relatively. Therefore, even more accurate and prompt disease markers for early diagnosis are needed. To determine disease markers needs a thorough understanding of fungal antigens which might be discovered in the serum or various other body liquids of sufferers. Herein we survey book immunodominant antigens discovered from extracellular protein of em Aspergillus fumigatus /em . Outcomes Extracellular protein of em A. fumigatus /em were separated by two-dimensional electrophoresis (2-DE) and probed with the sera from critically ill patients with proven IA. The immunoreactive protein spots were identified by MALDI-TOF mass spectrometry (MALDI-TOF -MS). Forty spots from 2DE gels were detected and 17 different proteins were identified as immunogenic in humans. Function annotation revealed that most of these proteins were metabolic enzymes involved in carbohydrate, fatty acid, amino acid, and energy metabolism. One of the proteins, thioredoxin reductase GliT (TR), which showed the best immunoactivity, was analyzed further for secretory signals, protein localization, and homology. The results indicated that TR is a secretory protein with a signal sequence exhibiting a high probability for secretion. Furthermore, TR did not match any human proteins, and had low homology with most other fungi. The recombinant TR was recognized by the sera of all proven IA patients with different underlying diseases in this study. Conclusions The immunoreactive proteins identified in this study may be helpful for the diagnosis of IA in critically ill patients. Our results indicate that TR and other immunodominant antigens have potential as biomarkers for the serologic diagnosis of invasive aspergillosis. Background In recent decades, invasive aspergillosis (IA) has emerged as an important cause of morbidity and mortality in patients with prolonged neutropenia. However, several reports have recently described a rising incidence of IA in critically ill patients, even in the absence of an apparent predisposing immunodeficiency [1-6]. The incidence of IA in critically ill patients ranges from 0.3% to 5.8% [2,3,6], and carries an overall mortality rate 80%, with an attributable mortality of approximately 20% [4,5]. Critically ill patients are prone to develop immunologic derangement, which renders them more vulnerable for em Aspergillus /em infections. The risk factors for IA include chronic obstructive pulmonary disease (COPD) and other chronic lung diseases [1-4,7,8], prolonged P005091 use of steroids [2,9], advanced liver disease [2-4,10], chronic renal replacement therapy [11,12], near-drowning [4,13-15], and diabetes mellitus [2,3,9]. The diagnosis of such IA is difficult because signs and symptoms are non-specific. The conventional diagnostic methods, such as tissue examination and microbial cultivation, may lack sensitivity in the first stages of infection in critically ill patients. As a result, the diagnosis of IA is often established after a long delay or following autopsy. Currently, the best-characterized circulating marker used in the diagnosis of IA is galactomannan (GM), which is present in the Vegfb cell walls of most em Aspergillus /em species. The commercial Platelia em Aspergillus P005091 /em assay (BioRad?, Marnes-La-Coquette, France) has been included in the EORTC/MSG criteria for probable IA. However, a recent meta-analysis indicated that GM testing is more P005091 useful in patients with prolonged neutropenia (sensitivity, P005091 72%-82%) than in non-neutropenic, critically ill patients (sensitivity, 40%-55%) [16]. Further studies suggested that the host immune status may influence GM release. It appears that GM production is proportional to the fungal load in tissues [17]. Although neutropenic patients and non-neutropenic, critically ill patients are susceptible to IA, the pathology of the disease is quite different in these two groups of patients. In neutropenic patients and animal models, IA is characterized by thrombosis and hemorrhage from rapid and extensive hyphal growth [18]. However, in non-neutropenic, critically ill patients and animal models, IA.