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10.1371/journal.ppat.1005644 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1005644 C4880299!4880299 !27223610     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27223610 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       PLoS+Pathog 2016 ; 12 (5 ): e1005644 Nephropedia Template TP {{tp|p=27223610 |t=2016. Neutrophil Attack Triggers Extracellular Trap-Dependent Candida Cell Wall Remodeling and Altered Immune Recognition |pdf=|usr=}}{{27223610 }} gab.com Text Neutrophil Attack Triggers Extracellular Trap-Dependent Candida Cell Wall Remodeling and Altered Immune Recognition JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27223610 #FOAvip Pathogens hide immunogenic epitopes from the host to evade immunity, persist and cause infection. The opportunistic human fungal pathogen Candida albicans, which can cause fatal disease in immunocompromised patient populations, offers a good example as it masks the inflammatory epitope ?-glucan in its cell wall from host recognition. It has been demonstrated previously that ?-glucan becomes exposed during infection in vivo but the mechanism behind this exposure was unknown. Here, we show that this unmasking involves neutrophil extracellular trap (NET) mediated attack, which triggers changes in fungal cell wall architecture that enhance immune recognition by the Dectin-1 ?-glucan receptor in vitro. Furthermore, using a mouse model of disseminated candidiasis, we demonstrate the requirement for neutrophils in triggering these fungal cell wall changes in vivo. Importantly, we found that fungal epitope unmasking requires an active fungal response in addition to the stimulus provided by neutrophil attack. NET-mediated damage initiates fungal MAP kinase-driven responses, particularly by Hog1, that dynamically relocalize cell wall remodeling machinery including Chs3, Phr1 and Sur7. Neutrophil-initiated cell wall disruptions augment some macrophage cytokine responses to attacked fungi. This work provides insight into host-pathogen interactions during disseminated candidiasis, including valuable information about how the C. albicans cell wall responds to the biotic stress of immune attack. Our results highlight the important but underappreciated concept that pattern recognition during infection is dynamic and depends on the host-pathogen dialog. Twit Text FOAVip Neutrophil Attack Triggers Extracellular Trap-Dependent Candida Cell Wall Remodeling and Altered Immune Recognition ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27223610 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27223610 #FOAvip English Wikipedia <ref>{{Cite pmid|27223610 }}</ref> Neutrophil Attack Triggers Extracellular Trap-Dependent Candida Cell Wall Remodeling and Altered Immune Recognition #MMPMID27223610 Hopke A ; Nicke N ; Hidu EE ; Degani G ; Popolo L ; Wheeler RT PLoS Pathog 2016[May]; 12 (5 ): e1005644 PMID27223610 show ga Pathogens hide immunogenic epitopes from the host to evade immunity, persist and cause infection. The opportunistic human fungal pathogen Candida albicans, which can cause fatal disease in immunocompromised patient populations, offers a good example as it masks the inflammatory epitope ?-glucan in its cell wall from host recognition. It has been demonstrated previously that ?-glucan becomes exposed during infection in vivo but the mechanism behind this exposure was unknown. Here, we show that this unmasking involves neutrophil extracellular trap (NET) mediated attack, which triggers changes in fungal cell wall architecture that enhance immune recognition by the Dectin-1 ?-glucan receptor in vitro. Furthermore, using a mouse model of disseminated candidiasis, we demonstrate the requirement for neutrophils in triggering these fungal cell wall changes in vivo. Importantly, we found that fungal epitope unmasking requires an active fungal response in addition to the stimulus provided by neutrophil attack. NET-mediated damage initiates fungal MAP kinase-driven responses, particularly by Hog1, that dynamically relocalize cell wall remodeling machinery including Chs3, Phr1 and Sur7. Neutrophil-initiated cell wall disruptions augment some macrophage cytokine responses to attacked fungi. This work provides insight into host-pathogen interactions during disseminated candidiasis, including valuable information about how the C. albicans cell wall responds to the biotic stress of immune attack. Our results highlight the important but underappreciated concept that pattern recognition during infection is dynamic and depends on the host-pathogen dialog. |Animals [MESH] |Antigens, Fungal/immunology [MESH] |Candida albicans/immunology [MESH] |Candidiasis/*immunology [MESH] |Cell Wall/immunology [MESH] |Disease Models, Animal [MESH] |Extracellular Traps/*immunology [MESH] |Female [MESH] |HEK293 Cells [MESH] |Host-Pathogen Interactions/*immunology [MESH] |Humans [MESH] |Image Processing, Computer-Assisted [MESH] |Immune Evasion/*immunology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Microscopy, Fluorescence [MESH] |Neutrophils/immunology [MESH]Neutrophil Attack Triggers Extracellular Trap-Dependent Candida Cell W(epmc).pdf DeepDyve Pubget Overpricing