The Experts below are selected from a list of 4137 Experts worldwide ranked by ideXlab platform
Michael Lierz - One of the best experts on this subject based on the ideXlab platform.
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Fungal Pneumonia as a major cause of mortality in white stork ciconia ciconia chicks
Avian Diseases, 2010Co-Authors: Philipp Olias, Boehmer Winfried, Hafez M Hafez, Achim D Gruber, Michael LierzAbstract:Abstract White stork (Ciconia ciconia) chicks have previously been suggested to be particularly susceptible to environmental conditions such as climatic changes during their first 3 wk of life. However, limited data are available on causes of mortality in free-ranging birds prior to fledging in general. One hundred and one white stork chicks found dead in 2007 and 2008 were examined and the causes of death identified. Of these, 44.6% had Fungal granulomatous Pneumonia resulting in obstruction and compression of airways. Of note, 94.1% of pulmonary infections occurred in white stork chicks below 23 days of age. PCR amplification and sequencing of the Fungal internal transcribed spacer region 1 identified Aspergillus fumigatus and various zygomycetes as primary causative agents. Thermomyces lanuginosus, previously unknown to cause pulmonary infections, was identified in one chick. The findings suggest that Fungal Pneumonia plays a major role in the loss of white stork chicks of up to 3 wk of age and represe...
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Fungal Pneumonia as a major cause of mortality in white stork ciconia ciconia chicks
Avian Diseases, 2010Co-Authors: Philipp Olias, Boehmer Winfried, Hafez M Hafez, Achim D Gruber, Michael LierzAbstract:White stork (Ciconia ciconia) chicks have previously been suggested to be particularly susceptible to environmental conditions such as climatic changes during their first 3 wk of life. However, limited data are available on causes of mortality in free-ranging birds prior to fledging in general. One hundred and one white stork chicks found dead in 2007 and 2008 were examined and the causes of death identified. Of these, 44.6% had Fungal granulomatous Pneumonia resulting in obstruction and compression of airways. Of note, 94.1% of pulmonary infections occurred in white stork chicks below 23 days of age. PCR amplification and sequencing of the Fungal internal transcribed spacer region 1 identified Aspergillus fumigatus and various zygomycetes as primary causative agents. Thermomyces lanuginosus, previously unknown to cause pulmonary infections, was identified in one chick. The findings suggest that Fungal Pneumonia plays a major role in the loss of white stork chicks of up to 3 wk of age and represents a major threat, similar to the threat posed to young poultry.
Bruce S Klein - One of the best experts on this subject based on the ideXlab platform.
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cblb constrains inactivated vaccine induced cd8 t cell responses and immunity against lethal Fungal Pneumonia
Journal of Immunology, 2018Co-Authors: Som G Nanjappa, M Suresh, Srinivasu Mudalagiriyappa, Scott J Fites, Bruce S KleinAbstract:Fungal infections in CD4+ T cell immunocompromised patients have risen sharply in recent years. Although vaccines offer a rational avenue to prevent infections, there are no licensed Fungal vaccines available. Inactivated vaccines are safer but less efficacious and require adjuvants that may undesirably bias toward poor protective immune responses. We hypothesized that reducing the TCR signaling threshold could potentiate antiFungal CD8+ T cell responses and immunity to inactivated vaccine in the absence of CD4+ T cells. In this study, we show that CBLB, a negative regulator of TCR signaling, suppresses CD8+ T cells in response to inactivated Fungal vaccination in a mouse model of CD4+ T cell lymphopenia. Conversely, Cblb deficiency enhanced both the type 1 (e.g., IFN-γ) and type 17 (IL-17A) CD8+ T cell responses to inactivated Fungal vaccines and augmented vaccine immunity to lethal Fungal Pneumonia. Furthermore, we show that immunization with live or inactivated vaccine yeast did not cause detectable pathologic condition in Cblb-/- mice. Augmented CD8+ T cell responses in the absence of CBLB also did not lead to terminal differentiation or adversely affect the expression of transcription factors T-bet, Eomes, and RORγt. Additionally, our adoptive transfer experiments showed that CBLB impedes the effector CD8+ T cell responses in a cell-intrinsic manner. Finally, we showed that ablation of Cblb overcomes the requirement of HIF-1α for expansion of CD8+ T cells upon vaccination. Thus, adjuvants that target CBLB may augment inactivated vaccines and immunity against systemic Fungal infections in vulnerable patients.
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intrinsic myd88 akt1 mtor signaling coordinates disparate tc17 and tc1 responses during vaccine immunity against Fungal Pneumonia
PLOS Pathogens, 2015Co-Authors: Som G Nanjappa, Nydiaris Hernandezsantos, Kevin Galles, Marcel Wuthrich, M Suresh, Bruce S KleinAbstract:Fungal infections have skyrocketed in immune-compromised patients lacking CD4+ T cells, underscoring the need for vaccine prevention. An understanding of the elements that promote vaccine immunity in this setting is essential. We previously demonstrated that vaccine-induced IL-17A+ CD8+ T cells (Tc17) are required for resistance against lethal Fungal Pneumonia in CD4+ T cell-deficient hosts, whereas the individual type I cytokines IFN-γ, TNF-α and GM-CSF, are dispensable. Here, we report that T cell-intrinsic MyD88 signals are crucial for these Tc17 cell responses and vaccine immunity against lethal Fungal Pneumonia in mice. In contrast, IFN-γ+ CD8+ cell (Tc1) responses are largely normal in the absence of intrinsic MyD88 signaling in CD8+ T cells. The poor accumulation of MyD88-deficient Tc17 cells was not linked to an early onset of contraction, nor to accelerated cell death or diminished expression of anti-apoptotic molecules Bcl-2 or Bcl-xL. Instead, intrinsic MyD88 was required to sustain the proliferation of Tc17 cells through the activation of mTOR via Akt1. Moreover, intrinsic IL-1R and TLR2, but not IL-18R, were required for MyD88 dependent Tc17 responses. Our data identify unappreciated targets for augmenting adaptive immunity against fungi. Our findings have implications for designing Fungal vaccines and immune-based therapies in immune-compromised patients.
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tc17 cells mediate vaccine immunity against lethal Fungal Pneumonia in immune deficient hosts lacking cd4 t cells
PLOS Pathogens, 2012Co-Authors: Som G Nanjappa, Marcel Wuthrich, Erika Heninger, David J Gasper, Bruce S KleinAbstract:Vaccines may help reduce the growing incidence of Fungal infections in immune-suppressed patients. We have found that, even in the absence of CD4(+) T-cell help, vaccine-induced CD8(+) T cells persist and confer resistance against Blastomyces dermatitidis and Histoplasma capsulatum. Type 1 cytokines contribute to that resistance, but they also are dispensable. Although the role of T helper 17 cells in immunity to fungi is debated, IL-17 producing CD8(+) T cells (Tc17 cells) have not been investigated. Here, we show that Tc17 cells are indispensable in antiFungal vaccine immunity in hosts lacking CD4(+) T cells. Tc17 cells are induced upon vaccination, recruited to the lung on pulmonary infection, and act non-redundantly in mediating protection in a manner that requires neutrophils. Tc17 cells did not influence type I immunity, nor did the lack of IL-12 signaling augment Tc17 cells, indicating a distinct lineage and function. IL-6 was required for Tc17 differentiation and immunity, but IL-1R1 and Dectin-1 signaling was unexpectedly dispensable. Tc17 cells expressed surface CXCR3 and CCR6, but only the latter was essential in recruitment to the lung. Although IL-17 producing T cells are believed to be short-lived, effector Tc17 cells expressed low levels of KLRG1 and high levels of the transcription factor TCF-1, predicting their long-term survival and stem-cell like behavior. Our work has implications for designing vaccines against Fungal infections in immune suppressed patients.
Barbara D Alexander - One of the best experts on this subject based on the ideXlab platform.
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Fungal diagnostics in Pneumonia
Seminars in Respiratory and Critical Care Medicine, 2011Co-Authors: Erika D Lease, Barbara D AlexanderAbstract:Fungal Pneumonia is increasingly common, particularly in highly immunosuppressed patients, such as solid organ or hematopoietic stem cell transplant recipients, and the diagnosis is evolving. Although standard techniques such as microscopy and culture remain the mainstays of diagnosis, relatively recent advances in serological and molecular testing are important additions to the field. This article reviews the laboratory tools used to diagnose Fungal respiratory disease.
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non aspergillus Fungal Pneumonia in transplant recipients
Clinics in Chest Medicine, 2005Co-Authors: Sylvia F Costa, Barbara D AlexanderAbstract:Although species of Aspergillus and Candida account for most deeply invasive and life-threatening Fungal infections, the past decades have seen a rise in the immunocompromised population. With this increase, additional fungi have emerged as important agents of morbidity and mortality. These opportunistic fungi are characterized by their ubiquitous presence in the environment, their ability to cause disease in immunosuppressed patients, and their diminished susceptibility to the currently available antiFungal agents. Pneumonia, one aspect of a myriad of clinical manifestations caused by these Fungal pathogens, is discussed in this article.
David L Goldman - One of the best experts on this subject based on the ideXlab platform.
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persistence of Fungal Pneumonia 1 in the control and β a dual role for tgf
2013Co-Authors: David L GoldmanAbstract:Casadevall and David L. GoldmanXiuping Shao, Johanna Rivera, Ramata Niang, Arturohttp://www.jimmunol.org/content/175/10/6757J Immunol€2005; 175:6757-6763; ;Referenceshttp://www.jimmunol.org/content/175/10/6757.full#ref-list-1This article cites 44 articles, 23 of which you can access for free at: Subscriptionshttp://jimmunol.org/subscriptionsInformation about subscribing to The Journal of Immunology is online at: Permissionshttp://www.aai.org/ji/copyright.htmlSubmit copyright permission requests at: Email Alertshttp://jimmunol.org/cgi/alerts/etocReceive free email-alerts when new articles cite this article. Sign up at:
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a dual role for tgf β1 in the control and persistence of Fungal Pneumonia
Journal of Immunology, 2005Co-Authors: Xiuping Shao, Arturo Casadevall, Johanna Rivera, Ramata Niang, David L GoldmanAbstract:TGF-β1 (TGF) has been implicated in the pathogenesis of several chronic infections and is thought to promote microbial persistence by interfering with macrophage function. In rats with experimental pulmonary cryptococcosis, increased lung levels of TGF were present at 12 mo of infection. Within the lung, expression of TGF localized to epithelioid cells and foamy macrophages in areas of inflammation. Increased TGF expression was also observed in the lungs of experimentally infected mice and a patient with pulmonary cryptococcosis. TGF reduced Ab and serum-mediated phagocytosis of Cryptococcus neoformans by rat alveolar macrophages (AM) and peripheral blood monocytes, and this was associated with decreased chemokine production and oxidative burst. Interestingly, TGF-treated rat AM limited both intracellular and extracellular growth of C. neoformans. Control of C. neoformans growth by TGF-treated rat AM was due to increased secretion of lysozyme, a protein with potent antiFungal activity. The effects of TGF on the course of infection were dependent on the timing of TGF administration relative to the time of infection. TGF treatment of chronically infected rats resulted in reduced lung Fungal burden, while treatment early in the course of infection resulted in increased Fungal burden. In summary, our studies suggest a dual role for TGF in persistent Fungal Pneumonia whereby it contributes to the local control of infection by enhancing macrophage antiFungal efficacy through increased lysozyme secretion, while limiting inflammation by inhibiting macrophage/monocyte phagocytosis and reducing associated chemokine production and oxidative burst.
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an innate immune system cell is a major determinant of species related susceptibility differences to Fungal Pneumonia
Journal of Immunology, 2005Co-Authors: Xiuping Shao, Arturo Casadevall, Aron Mednick, Mauricio Alvarez, Nico Van Rooijen, David L GoldmanAbstract:Rats and mice are considered resistant and susceptible hosts, respectively, for experimental cryptococcosis. For both species, alveolar macrophages (AM) are central components of the host response to pulmonary Cryptococcus neoformans infection. We explored the role of AM in three strains of mice and three strains of rats during cryptococcal infection by comparing the outcome of infection after macrophage depletion using liposomal clodronate. AM depletion was associated with enhancement and amelioration of disease in rats and mice, respectively, as measured by lung Fungal burden. The apparent protective role for AM in rats correlated with enhanced anticryptococcal activity as measured by phagocytic activity, oxidative burst, lysozyme secretion, and ability to limit intracellular growth of C. neoformans. Furthermore, rat AM were more resistant to lysis in association with intracellular infection. In summary, differences in AM function in rats and mice suggest an explanation for the species differences in susceptibility to C. neoformans based on the inherent efficacy of a central effector cell of the innate immune system.
Sebastian N Nagel - One of the best experts on this subject based on the ideXlab platform.
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enhancing the differentiation of pulmonary lymphoma and Fungal Pneumonia in hematological patients using texture analysis in 3 t mri
European Radiology, 2020Co-Authors: Damon Kim, Thomas Elgeti, Tobias Penzkofer, Ingo G Steffen, Laura J Jensen, Stefan Schwartz, Bernd Hamm, Sebastian N NagelAbstract:To evaluate texture analysis in nonenhanced 3-T MRI for differentiating pulmonary Fungal infiltrates and lymphoma manifestations in hematological patients and to compare the diagnostic performance with that of signal intensity quotients (“nonenhanced imaging characterization quotients,” NICQs). MR scans were performed using a speed-optimized imaging protocol without an intravenous contrast medium including axial T2-weighted (T2w) single-shot fast spin-echo and T1-weighted (T1w) gradient-echo sequences. ROIs were drawn within the lesions to extract first-order statistics from original images using HeterogeneityCAD and PyRadiomics. NICQs were calculated using signal intensities of the lesions, muscle, and fat. The standard of reference was histology or clinical diagnosis in follow-up. Statistical testing included ROC analysis, clustered ROC analysis, and DeLong test. Intra- and interrater reliability was tested using intraclass correlation coefficients (ICC). Thirty-three Fungal infiltrates in 16 patients and 38 pulmonary lymphoma manifestations in 19 patients were included. Considering the leading lesion in each patient, diagnostic performance was excellent for T1w entropy (AUC 80.2%; p 0.81) for these parameters except for moderate intrarater reliability of T1w energy (ICC = 0.64). T1w entropy, uniformity, and energy and T2w energy showed the best performances for differentiating pulmonary lymphoma and Fungal Pneumonia and outperformed NICQs. Results of the texture analysis should be checked for their intrinsic consistency to identify possible incongruities of single parameters. • Texture analysis in nonenhanced pulmonary MRI improves the differentiation of pulmonary lymphoma and Fungal Pneumonia compared with signal intensity quotients. • T1w entropy, uniformity, and energy along with T2w energy show the best performances for differentiating pulmonary lymphoma from Fungal Pneumonia. • The results of the texture analysis should be checked for their intrinsic consistency to identify possible incongruities of single parameters.
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Enhancing the differentiation of pulmonary lymphoma and Fungal Pneumonia in hematological patients using texture analysis in 3-T MRI
European Radiology, 2020Co-Authors: Thomas Elgeti, Tobias Penzkofer, Ingo G Steffen, Laura J Jensen, Stefan Schwartz, Bernd Hamm, Sebastian N NagelAbstract:Objectives To evaluate texture analysis in nonenhanced 3-T MRI for differentiating pulmonary Fungal infiltrates and lymphoma manifestations in hematological patients and to compare the diagnostic performance with that of signal intensity quotients (“nonenhanced imaging characterization quotients,” NICQs). Methods MR scans were performed using a speed-optimized imaging protocol without an intravenous contrast medium including axial T2-weighted (T2w) single-shot fast spin-echo and T1-weighted (T1w) gradient-echo sequences. ROIs were drawn within the lesions to extract first-order statistics from original images using HeterogeneityCAD and PyRadiomics. NICQs were calculated using signal intensities of the lesions, muscle, and fat. The standard of reference was histology or clinical diagnosis in follow-up. Statistical testing included ROC analysis, clustered ROC analysis, and DeLong test. Intra- and interrater reliability was tested using intraclass correlation coefficients (ICC). Results Thirty-three Fungal infiltrates in 16 patients and 38 pulmonary lymphoma manifestations in 19 patients were included. Considering the leading lesion in each patient, diagnostic performance was excellent for T1w entropy (AUC 80.2%; p < 0.005) and slightly inferior for T2w energy (79.9%; p
