Dectin-1 Fc Targeting of
            <i>Aspergillus fumigatus</i>
            Beta-Glucans Augments Innate Defense against Invasive Pulmonary Aspergillosis

Mattila, Polly E.; Metz, Allison E.; Rapaka, Rekha R.; Bauer, Lynne; Steele, Chad

doi:10.1128/aac.01274-07

Cited by 30 publications

(44 citation statements)

References 13 publications

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“…For lung fungal burden analysis, the left lungs were collected and homogenized in 1 ml of PBS. Total RNA was extracted from 0.1 ml of unclarified lung homogenate using the MasterPure yeast RNA purification kit (Epicentre Biotechnologies, Madison, WI), which includes a DNAse treatment step to eliminate genomic DNA as previously reported (36). Total RNA was also extracted from serial 1:10 dilutions of live A. fumigatus conidia (10 1 to 10 9 ) and DNAse treated to form a standard curve.…”

Section: Methodsmentioning

confidence: 99%

“…Lung A. fumigatus burden was analyzed with real-time PCR measurement of the A. fumigatus 18S rRNA [GenBank accession no. AB008401 (11)] and quantified using a standard curve of A. fumigatus conidia as previously described (36). As a validation of the real-time PCR method, heat-killed A. fumigatus did not yield a signal by real-time PCR and were unable to grow on potato dextrose agar plates (36).…”

Section: Methodsmentioning

confidence: 99%

“…AB008401 (11)] and quantified using a standard curve of A. fumigatus conidia as previously described (36). As a validation of the real-time PCR method, heat-killed A. fumigatus did not yield a signal by real-time PCR and were unable to grow on potato dextrose agar plates (36). In addition, no amplification controls (i.e., no reverse transcriptase included in the cDNA reaction) yielded a signal of Ͻ0.001% by real-time PCR, indicating that the DNAse treatment step was efficient at eliminating contaminating A. fumigatus DNA [since DNA is not predicative of organism viability (27)].…”

Section: Methodsmentioning

confidence: 99%

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Chlorine gas exposure increases susceptibility to invasive lung fungal infection

Gessner¹,

Doran

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chlorine (Cl2) is a highly irritating and reactive gas with potential occupational and environmental hazards. Acute exposure to Cl2 induces severe epithelial damage, airway hyperreactivity, impaired alveolar fluid clearance, and pulmonary edema in the presence of heightened inflammation and significant neutrophil accumulation in the lungs. Herein, we investigated whether Cl2 exposure affected the lung antimicrobial immune response leading to increased susceptibility to opportunistic infections. Mice exposed to Cl2 and challenged intratracheally 24 h thereafter with the opportunistic mold Aspergillus fumigatus demonstrated an >500-fold increase in A. fumigatus lung burden 72 h postchallenge compared with A. fumigatus mice exposed to room air. Cl2-exposed A. fumigatus challenged mice also demonstrated significantly higher lung resistance following methacholine challenge and increased levels of plasma proteins (albumin and IgG) in the bronchoalveolar lavage fluid. Despite enhanced recruitment of inflammatory cells to the lungs of Cl2-exposed A. fumigatus challenged mice, these cells (>60% of which were neutrophils) demonstrated a profound impairment in generating superoxide. Significantly higher A. fumigatus burden in the lungs of Cl2 exposed mice correlated with enhanced production of IL-6, TNF-α, CXCL1, CCL2, and CCL3. Surprisingly, however, Cl2-exposed A. fumigatus challenged mice had a specific impairment in the production of IL-17A and IL-22 in the lungs compared with mice exposed to room air and challenged with A. fumigatus. In summary, our results indicate that Cl2 exposure markedly impairs the antimicrobial activity and inflammatory reactivity of myeloid cells in the lung leading to increased susceptibility to opportunistic pathogens.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Chlorine gas exposure increases susceptibility to invasive lung fungal infection

Gessner¹,

Doran

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…However, it was observed that the non-endocytosed Aspergillus fumigatus (located between the cell membrane and cell) was also able to incorporate dectin-1, which indicated that dectin-1 was secreted outside the cells. The effect of this phenomenon on the body is unknown yet, although previous findings demonstrated that dectin-1-Fc IgG was able to regulate the endocytosis process (13,14).…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 2 and dectin-1 function as promising biomarker for Aspergillus fumigatus infection

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. In recent years, along with the wide application of organ transplantation and immunosuppressive agents, as well as the abuse of broad spectrum antibiotics, the incidence of invasive fungal infections has been increasing gradually. The present study aimed to identify novel biomarkers in cells infected with Aspergillus fumigatus. Human umbilical vein endothelial cells (HUVECs) were infected with Asper gillus fumigatus and then harvested at different time-points (0, 1, 2, 4 and 6 h). The expression Toll-like receptor 2 (TLR2) and dectin-1 expression were examined using flow cytometry and western blotting, and fluorescence-based microscopy was used to evaluate their distribution. The results indicated that TLR2 and dectin-1 protein levels were localized on the surface of HUVECs, and that dectin-1 was distributed on HUVEC membranes as observed under confocal microscope.

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“…Transient transfection experiments in neutropenic mice have demonstrated protective effects of augmenting expression of native dectin-1 or of a fusion protein consisting of the extracellular domain of dectin-1 linked to the Fc portion of murine immunoglobulin G1. 100,101 Human studies of dectin-1-based therapeutics have not been reported.…”

Section: Innate Immune Defenses Against Invasive Aspergillosis In Hscmentioning

confidence: 99%

Aspergillosis and stem cell transplantation: An overview of experimental pathogenesis studies

Al-Bader

Sheppard

2016

Virulence

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Invasive aspergillosis is a life-threatening infection caused by the opportunistic filamentous fungus Aspergillus fumigatus. Patients undergoing haematopoietic stem cell transplant (HSCT) for the treatment of hematological malignancy are at particularly high risk of developing this fatal infection. The susceptibility of HSCT patients to infection with A. fumigatus is a consequence of a complex interplay of both fungal and host factors. Here we review our understanding of the hostpathogen interactions underlying the susceptibility of the immunocompromised host to infection with A. fumigatus with a focus on the experimental validation of fungal and host factors relevant to HSCT patients. These include fungal factors such as secondary metabolites, cell wall constituents, and metabolic adaptations that facilitate immune evasion and survival within the host microenvironment, as well as the innate and adaptive immune responses involved in host defense against A. fumigatus.

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Dectin-1 Fc Targeting of Aspergillus fumigatus Beta-Glucans Augments Innate Defense against Invasive Pulmonary Aspergillosis

Cited by 30 publications

References 13 publications

Chlorine gas exposure increases susceptibility to invasive lung fungal infection

Chlorine gas exposure increases susceptibility to invasive lung fungal infection

Toll-like receptor 2 and dectin-1 function as promising biomarker for Aspergillus fumigatus infection

Aspergillosis and stem cell transplantation: An overview of experimental pathogenesis studies

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