Chitin synthase gene FgCHS8 affects virulence and fungal cell wall sensitivity to environmental stress in Fusarium graminearum

2016 ◽  
Vol 120 (5) ◽  
pp. 764-774 ◽  
Author(s):  
Ya-Zhou Zhang ◽  
Qing Chen ◽  
Cai-Hong Liu ◽  
Yu-Bin Liu ◽  
Pan Yi ◽  
...  
Keyword(s):  
Cell Wall ◽  
Environmental Stress ◽  
Fusarium Graminearum ◽  
Fungal Cell Wall ◽  
Chitin Synthase ◽  
Fungal Cell

scholarly journals Cryptococcus neoformans Chitin Synthase 3 (Chs3) Plays a Critical Role in Dampening Host Inflammatory Responses

2019 ◽  
Author(s):  
Camaron R. Hole ◽  
Woei C. Lam ◽  
Rajendra Upadhya ◽  
Jennifer K. Lodge
Keyword(s):  
Immune Response ◽  
Cell Wall ◽  
Cryptococcus Neoformans ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Pathogenic Fungi ◽  
Fungal Cell Wall ◽  
Chitin Synthase ◽  
Aids Patients ◽  
Fungal Cell

ABSTRACTCryptococcus neoformans infections are significant causes of morbidity and mortality among AIDS patients and the third most common invasive fungal infection in organ transplant recipients. One of the main interfaces between the fungus and the host is the fungal cell wall. The cryptococcal cell wall is unusual among human pathogenic fungi in that the chitin is predominantly deacetylated to chitosan. Chitosan deficient strains of C. neoformans were found to be avirulent and rapidly cleared from the murine lung. Moreover, infection with a chitosan deficient C. neoformans lacking three chitin deacetylases (cda1Δ2Δ3Δ) was found to confer protective immunity to a subsequent challenge with a virulent wild type counterpart. In addition to the chitin deacetylases, it was previously shown that chitin synthase 3 (Chs3) is also essential for chitin deacetylase mediated formation of chitosan. Mice inoculated with chs3Δ at a dose previously shown to induce protection with cda1Δ2Δ3Δ die within 36 hours after installation of the organism. Mortality was not dependent on viable fungi as mice inoculated with heat-killed preparation of chs3Δ died at the same rate as mice inoculated with live chs3Δ, suggesting the rapid onset of death was host mediated likely caused by an over exuberant immune response. Histology, cytokine profiling, and flow cytometry indicates a massive neutrophil influx in the mice inoculated with chs3Δ. Mice depleted of neutrophils survived chs3Δ inoculation indicating that death was neutrophil mediated. Altogether, these studies lead us to conclude that Chs3, along with chitosan, plays critical roles in dampening cryptococcal induced host inflammatory responses.IMPORTANCECryptococcus neoformans is the most common disseminated fungal pathogen in AIDS patients, resulting in ∼200,000 deaths each year. There is a pressing need for new treatments for this infection, as current antifungal therapy is hampered by toxicity and/or the inability of the host’s immune system to aid in resolution of the disease. An ideal target for new therapies is the fungal cell wall. The cryptococcal cell wall is different than many other pathogenic fungi in that it contains chitosan. Strains that have decreased chitosan are less pathogenic and strains that are deficient in chitosan are avirulent and can induce protective responses. In this study we investigated the host responses to chs3Δ, a chitosan-deficient strain, and found mice inoculated with chs3Δ all died within 36 hours and death was associated with an aberrant hyperinflammatory immune response driven by neutrophils, indicating that chitosan is critical in modulating the immune response to Cryptococcus.

ChemInform Abstract: Novel Nikkomycin Analogues: Inhibitors of the Fungal Cell Wall Biosynthesis Enzyme Chitin Synthase.

ChemInform ◽  
2000 ◽  
Vol 31 (41) ◽  
pp. no-no
Author(s):  
Kikoh Obi ◽  
Jun-ichiro Uda ◽  
Kazuhiko Iwase ◽  
Osamu Sugimoto ◽  
Hiroyuki Ebisu ◽  
...  
Keyword(s):  
Cell Wall ◽  
Fungal Cell Wall ◽  
Chitin Synthase ◽  
Cell Wall Biosynthesis ◽  
Fungal Cell

Novel nikkomycin analogues: inhibitors of the fungal cell wall biosynthesis enzyme chitin synthase

2000 ◽  
Vol 10 (13) ◽  
pp. 1451-1454 ◽  
Author(s):  
Kikoh Obi ◽  
Jun-ichiro Uda ◽  
Kazuhiko Iwase ◽  
Osamu Sugimoto ◽  
Hiroyuki Ebisu ◽  
...  
Keyword(s):  
Cell Wall ◽  
Fungal Cell Wall ◽  
Chitin Synthase ◽  
Cell Wall Biosynthesis ◽  
Fungal Cell

scholarly journals Cryptococcus neoformans Chitin Synthase 3 Plays a Critical Role in Dampening Host Inflammatory Responses

mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Camaron R. Hole ◽  
Woei C. Lam ◽  
Rajendra Upadhya ◽  
Jennifer K. Lodge
Keyword(s):  
Immune Response ◽  
Cell Wall ◽  
Cryptococcus Neoformans ◽  
Inflammatory Responses ◽  
Pathogenic Fungi ◽  
Fungal Cell Wall ◽  
Chitin Synthase ◽  
Aids Patients ◽  
Fungal Cell ◽  
Content Type

ABSTRACT Cryptococcus neoformans infections are significant causes of morbidity and mortality among AIDS patients and the third most common invasive fungal infection in organ transplant recipients. One of the main interfaces between the fungus and the host is the fungal cell wall. The cryptococcal cell wall is unusual among human-pathogenic fungi in that the chitin is predominantly deacetylated to chitosan. Chitosan-deficient strains of C. neoformans were found to be avirulent and rapidly cleared from the murine lung. Moreover, infection with a chitosan-deficient C. neoformans strain lacking three chitin deacetylases (cda1Δcda2Δcda3Δ) was found to confer protective immunity to a subsequent challenge with a virulent wild-type counterpart. In addition to the chitin deacetylases, it was previously shown that chitin synthase 3 (Chs3) is also essential for chitin deacetylase-mediated formation of chitosan. Mice inoculated with the chs3Δ strain at a dose previously shown to induce protection with the cda1Δcda2Δcda3Δ strain die within 36 h after installation of the organism. Mortality was not dependent on viable fungi, as mice inoculated with a heat-killed preparation of the chs3Δ strain died at the same rate as mice inoculated with a live chs3Δ strain, suggesting that the rapid onset of death was host mediated, likely caused by an overexuberant immune response. Histology, cytokine profiling, and flow cytometry indicate a massive neutrophil influx in the mice inoculated with the chs3Δ strain. Mice depleted of neutrophils survived chs3Δ inoculation, indicating that death was neutrophil mediated. Altogether, these studies lead us to conclude that Chs3, along with chitosan, plays critical roles in dampening cryptococcus-induced host inflammatory responses. IMPORTANCE Cryptococcus neoformans is the most common disseminated fungal pathogen in AIDS patients, resulting in ∼200,000 deaths each year. There is a pressing need for new treatments for this infection, as current antifungal therapy is hampered by toxicity and/or the inability of the host’s immune system to aid in resolution of the disease. An ideal target for new therapies is the fungal cell wall. The cryptococcal cell wall is different from the cell walls of many other pathogenic fungi in that it contains chitosan. Strains that have decreased chitosan are less pathogenic and strains that are deficient in chitosan are avirulent and can induce protective responses. In this study, we investigated the host responses to a chs3Δ strain, a chitosan-deficient strain, and found that mice inoculated with the chs3Δ strain all died within 36 h and that death was associated with an aberrant hyperinflammatory immune response driven by neutrophils, indicating that chitosan is critical in modulating the immune response to Cryptococcus.

Recent Status and Advancements in the Development of Antifungal Agents: Highlights on Plant and Marine Based Antifungals

2019 ◽  
Vol 19 (10) ◽  
pp. 812-830 ◽  
Author(s):  
P. Marie Arockianathan ◽  
Monika Mishra ◽  
Rituraj Niranjan
Keyword(s):  
Cell Wall ◽  
Antifungal Agents ◽  
Fungal Diseases ◽  
Fungal Cell Wall ◽  
Fungal Resistance ◽  
Ergosterol Biosynthesis ◽  
Fungal Cell ◽  
Ergosterol Synthesis ◽  
Glucan Synthesis ◽  
Anti Fungal

The developing resistance in fungi has become a key challenge, which is being faced nowadays with the available antifungal agents in the market. Further search for novel compounds from different sources has been explored to meet this problem. The current review describes and highlights recent advancement in the antifungal drug aspects from plant and marine based sources. The current available antifungal agents act on specific targets on the fungal cell wall, like ergosterol synthesis, chitin biosynthesis, sphingolipid synthesis, glucan synthesis etc. We discuss some of the important anti-fungal agents like azole, polyene and allylamine classes that inhibit the ergosterol biosynthesis. Echinocandins inhibit β-1, 3 glucan synthesis in the fungal cell wall. The antifungals poloxins and nikkomycins inhibit fungal cell wall component chitin. Apart from these classes of drugs, several combinatorial therapies have been carried out to treat diseases due to fungal resistance. Recently, many antifungal agents derived from plant and marine sources showed potent activity. The renewed interest in plant and marine derived compounds for the fungal diseases created a new way to treat these resistant strains which are evident from the numerous literature publications in the recent years. Moreover, the compounds derived from both plant and marine sources showed promising results against fungal diseases. Altogether, this review article discusses the current antifungal agents and highlights the plant and marine based compounds as a potential promising antifungal agents.

Fungal Cell Wall‐Graphene Oxide Microcomposite Membrane for Organic Solvent Nanofiltration

2021 ◽  
pp. 2100110
Author(s):  
Liyuan Zhang ◽  
Mengchen Zhang ◽  
Gongping Liu ◽  
Wanqin Jin ◽  
Xiaoyan Li
Keyword(s):  
Cell Wall ◽  
Graphene Oxide ◽  
Organic Solvent ◽  
Fungal Cell Wall ◽  
Fungal Cell ◽  
Organic Solvent Nanofiltration
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