The Molecular Mechanisms of Neuroinflammation in Alzheimer's Disease, the Consequence of Neural Cell Death.

Alzheimer's disease (AD) is accompanied by neural cell loss and memory deficit. Neural cell death, occurring via apoptosis and autophagy, is widely observed in the AD brain in addition to neuroinflammation mediated by necroptosis and the NLRP3 inflammasome. Neurotoxicity induced by amyloid-beta (Aß) and tau aggregates leads to excessive neural cell death and neuroinflammation in the AD brain. During AD progression, uncontrolled neural cell death results in the dysregulation of cellular activity and synaptic function. Apoptosis mediated by pro-apoptotic caspases, autophagy regulated by autophagy-related proteins, and necroptosis controlled by the RIPK/MLKL axis are representative of neural cell death occurred during AD. Necroptosis causes the release of cellular components, contributing to the pro-inflammatory environment in the AD brain. Inordinately high levels of neural cell death and pro-inflammatory events lead to the production of pro-inflammatory cytokines and feed-forward hyper neuroinflammation. Thus, neural cell death and neuroinflammation cause synaptic dysfunction and memory deficits in the AD brain. In this review, we briefly introduce the mechanisms of neural cell death and neuroinflammation observed in the AD brain. Combined with a typical strategy for targeting Aß and tau, regulation of neural cell death and neuroinflammation may be effective for the amelioration of AD pathologies.

Naturally-Occurring Tyrosinase Inhibitors Classified by Enzyme Kinetics and Copper Chelation.

Currently, there are three major assaying methods used to validate in vitro whitening activity from natural products: methods using mushroom tyrosinase, human tyrosinase, and dopachrome tautomerase (or tyrosinase-related protein-2, TRP-2). Whitening agent development consists of two ways, melanin synthesis inhibition in melanocytes and downregulation of melanocyte stimulation. For melanin levels, the melanocyte cell line has been used to examine melanin synthesis with the expression levels of TRP-1 and TRP-2. The proliferation of epidermal surfaced cells and melanocytes is stimulated by cellular signaling receptors, factors, or mediators including endothelin-1, α-melanocyte-stimulating hormone, nitric oxide, histamine, paired box 3, microphthalmia-associated transcription factor, pyrimidine dimer, ceramide, stem cell factors, melanocortin-1 receptor, and cAMP. In addition, the promoter region of melanin synthetic genes including tyrosinase is upregulated by melanocyte-specific transcription factors. Thus, the inhibition of growth and melanin synthesis in gene expression levels represents a whitening research method that serves as an alternative to tyrosinase inhibition. Many researchers have recently presented the bioactivity-guided fractionation, discovery, purification, and identification of whitening agents. Melanogenesis inhibition can be obtained using three different methods: tyrosinase inhibition, copper chelation, and melanin-related protein downregulation. There are currently four different types of inhibitors characterized based on their enzyme inhibition mechanisms: competitive, uncompetitive, competitive/uncompetitive mixed-type, and noncompetitive inhibitors. Reversible inhibitor types act as suicide substrates, where traditional inhibitors are classified as inactivators and reversible inhibitors based on the molecule-recognizing properties of the enzyme. In a minor role, transcription factors can also be downregulated by inhibitors. Currently, the active site copper iron-binding inhibitors such as kojic acid and chalcone exhibit tyrosinase inhibitory activity. Because the tyrosinase catalysis site structure is important for the mechanism determination of tyrosinase inhibitors, understanding the enzyme recognition and inhibitory mechanism of inhibitors is essential for the new development of tyrosinase inhibitors. The present review intends to classify current natural products identified by means of enzyme kinetics and copper chelation to exhibit tyrosinase enzyme inhibition.

The Impact of Light Wavelength and Darkness on Metabolite Profiling of Korean Ginseng: Evaluating Its Anti-Cancer Potential against MCF-7 and BV-2 Cell Lines.

Korean ginseng is a source of functional foods and medicines; however, its productivity is hindered by abiotic stress factors, such as light. This study investigated the impacts of darkness and different light wavelengths on the metabolomics and anti-cancer activity of ginseng extracts. Hydroponically-grown Korean ginseng was shifted to a light-emitting diodes (LEDs) chamber for blue-LED and darkness treatments, while white fluorescent (FL) light treatment was the control. MCF-7 breast cancer and lipopolysaccharide (LPS)-induced BV-2 microglial cells were used to determine chemo-preventive and neuroprotective potential. Overall, 53 significant primary metabolites were detected in the treated samples. The levels of ginsenosides Rb1, Rb2, Rc, Rd, and Re, as well as organic and amino acids, were significantly higher in the dark treatment, followed by blue-LED treatment and the FL control. The dark-treated ginseng extract significantly induced apoptotic signaling in MCF-7 cells and dose-dependently inhibited the NF-κB and MAP kinase pathways in LPS-induced BV-2 cells. Short-term dark treatment increased the content of Rd, Rc, Rb1, Rb2, and Re ginsenosides in ginseng extracts, which promoted apoptosis of MCF-7 cells and inhibition of the MAP kinase pathway in BV-2 microglial cells. These results indicate that the dark treatment might be effective in improving the pharmacological potential of ginseng.

Amyloid Against Amyloid: Dimeric Amyloid Fragment Ameliorates Cognitive Impairments by Direct Clearance of Oligomers and Plaques.

Amyloid-ß (Aß) in the form of neurotoxic aggregates is regarded as the main pathological initiator and key therapeutic target of Alzheimer's disease. However, anti-Aß drug development has been impeded by the lack of a target needed for structure-based drug design and low permeability of the blood-brain barrier (BBB). An attractive therapeutic strategy is the development of amyloid-based anti-Aß peptidomimetics that exploit the self-assembling nature of Aß and penetrate the BBB. Herein, we designed a dimeric peptide drug candidate based on the N-terminal fragment of Aß, DAB, found to cross the BBB and solubilize Aß oligomers and fibrils. Administration of DAB reduced amyloid burden in 5XFAD mice, and downregulated neuroinflammation and prevented memory impairment in the Y-maze test. Peptide mapping assays and molecular docking studies were utilized to elucidate DAB-Aß interaction. To further understand the active regions of DAB, we assessed the dissociative activity of DAB with sequence modifications.

Caspase-8 blocks kinase RIPK3-mediated activation of the NLRP3 inflammasome.

Caspase-8 deficiency in certain cells prompts chronic inflammation. One mechanism suggested to account for this inflammation is enhanced signaling for necrotic cell death, mediated by the protein kinases RIPK1 and RIPK3 that caspase-8 can cleave. We describe an activity of caspase-8 in dendritic cells that controls the initiation of inflammation in another way. Caspase-8 deficiency in these cells facilitated lipopolysaccharide-induced assembly and function of the NLRP3 inflammasome. This effect depended on the functions of RIPK1 and RIPK3, as well as of MLKL and PGAM5, two signaling proteins recently shown to contribute to RIPK3-mediated induction of necrosis. However, although enhancement of inflammasome assembly in the caspase-8-deficient cells shares proximal signaling events with the induction of necrosis, it occurred independently of cell death. These findings provide new insight into potentially pathological inflammatory processes to which RIPK1- and RIPK3-mediated signaling contributes.

Natural Products Targeting Amyloid Beta in Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by severe brain damage and dementia. There are currently few therapeutics to treat this disease, and they can only temporarily alleviate some of the symptoms. The pathogenesis of AD is mainly preceded by accumulation of abnormal amyloid beta (Aß) aggregates, which are toxic to neurons. Therefore, modulation of the formation of these abnormal aggregates is strongly suggested as the most effective approach to treat AD. In particular, numerous studies on natural products associated with AD, aiming to downregulate Aß peptides and suppress the formation of abnormal Aß aggregates, thus reducing neural cell death, are being conducted. Generation of Aß peptides can be prevented by targeting the secretases involved in Aß-peptide formation (secretase-dependent). Additionally, blocking the intra- and intermolecular interactions of Aß peptides can induce conformational changes in abnormal Aß aggregates, whereby the toxicity can be ameliorated (structure-dependent). In this review, AD-associated natural products which can reduce the accumulation of Aß peptides via secretase- or structure-dependent pathways, and the current clinical trial states of these products are discussed.

The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics.

Tumor necrosis factor alpha (TNF-α) was initially recognized as a factor that causes the necrosis of tumors, but it has been recently identified to have additional important functions as a pathological component of autoimmune diseases. TNF-α binds to two different receptors, which initiate signal transduction pathways. These pathways lead to various cellular responses, including cell survival, differentiation, and proliferation. However, the inappropriate or excessive activation of TNF-α signaling is associated with chronic inflammation and can eventually lead to the development of pathological complications such as autoimmune diseases. Understanding of the TNF-α signaling mechanism has been expanded and applied for the treatment of immune diseases, which has resulted in the development of effective therapeutic tools, including TNF-α inhibitors. Currently, clinically approved TNF-α inhibitors have shown noticeable potency in a variety of autoimmune diseases, and novel TNF-α signaling inhibitors are being clinically evaluated. In this review, we briefly introduce the impact of TNF-α signaling on autoimmune diseases and its inhibitors, which are used as therapeutic agents against autoimmune diseases.

Postharvest Drying Techniques Regulate Secondary Metabolites and Anti-Neuroinflammatory Activities of Ganoderma lucidum.

Ganoderma lucidum extract is a potent traditional remedy for curing various ailments. Drying is the most important postharvest step during the processing of Ganoderma lucidum. The drying process mainly involves heat (36 h at 60 °C) and freeze-drying (36 h at -80 °C). We investigated the effects of different postharvest drying protocols on the metabolites profiling of Ganoderma lucidum using GC-MS, followed by an investigation of the anti-neuroinflammatory potential in LPS-treated BV2 microglial cells. A total of 109 primary metabolites were detected from heat and freeze-dried samples. Primary metabolite profiling showed higher levels of amino acids (17.4%) and monosaccharides (8.8%) in the heat-dried extracts, whereas high levels of organic acids (64.1%) were present in the freeze-dried samples. The enzymatic activity, such as ATP-citrate synthase, pyruvate kinase, glyceraldehyde-3-phosphatase dehydrogenase, glutamine synthase, fructose-bisphosphate aldolase, and D-3-phosphoglycerate dehydrogenase, related to the reverse tricarboxylic acid cycle were significantly high in the heat-dried samples. We also observed a decreased phosphorylation level of the MAP kinase (Erk1/2, p38, and JNK) and NF-κB subunit p65 in the heat-dried samples of the BV2 microglia cells. The current study suggests that heat drying improves the production of ganoderic acids by the upregulation of TCA-related pathways, which, in turn, gives a significant reduction in the inflammatory response of LPS-induced BV2 cells. This may be attributed to the inhibition of NF-κB and MAP kinase signaling pathways in cells treated with heat-dried extracts.

RIG-I RNA helicase activation of IRF3 transcription factor is negatively regulated by caspase-8-mediated cleavage of the RIP1 protein.

Excessive responses to pattern-recognition receptors are prevented by regulatory mechanisms that affect the amounts and activities of the downstream signaling proteins. We report that activation of the transcription factor IRF3 by the ribonucleic acid sensor RIG-I was restricted by caspase-8-mediated cleavage of the RIP1 protein, which resulted in conversion of RIP1 from a signaling enhancer to a signaling inhibitor. The proteins RIP1 and caspase-8 were recruited to the RIG-I complex after viral infection and served antagonistic regulatory roles. Conjugation of ubiquitin chains to RIP1 facilitated assembly of the RIG-I complex, resulting in enhanced phosphorylation of IRF3. However, the ubiquitination of RIP1 also rendered it susceptible to caspase-8-mediated cleavage that yielded an inhibitory RIP1 fragment. The dependence of RIP1 cleavage on the same molecular change as that facilitating RIG-I signaling allows for RIG-I signaling to be restricted in its duration without compromising its initial activation.

Rhizolutin, a Novel 7/10/6-Tricyclic Dilactone, Dissociates Misfolded Protein Aggregates and Reduces Apoptosis/Inflammation Associated with Alzheimer's Disease.

Rhizolutin (1) was discovered as a natural product of ginseng-rhizospheric Streptomyces sp. WON17. Its structure features an unprecedented 7/10/6-tricyclic dilactone carbon skeleton composed of dimethylcyclodecatriene flanked by a 7-membered and a 6-membered lactone ring based on spectroscopic analysis. During an unbiased screening of natural product libraries, this novel compound was found to dissociate amyloid-ß (Aß) plaques and tau tangles, which are key pathological hallmarks of Alzheimer's disease (AD). Rhizolutin treatment of APP/PS1 double transgenic mice with AD significantly dissociated hippocampal plaques. In vitro, rhizolutin substantially decreased Aß-induced apoptosis and inflammation in neuronal and glial cells. Our findings introduce a unique chemical entity that targets Aß and tau concurrently by mimicking misfolded protein clearance mechanisms of immunotherapy, which is prominently investigated in clinical trials.

Discovery of Chemicals to Either Clear or Indicate Amyloid Aggregates by Targeting Memory-Impairing Anti-Parallel Aß Dimers.

Amyloid-ß (Aß) oligomers are implicated in Alzheimer disease (AD). However, their unstable nature and heterogeneous state disrupts elucidation of their explicit role in AD progression, impeding the development of tools targeting soluble Aß oligomers. Herein parallel and anti-parallel variants of Aß(1-40) dimers were designed and synthesized, and their pathogenic properties in AD models characterized. Anti-parallel dimers induced cognitive impairments with increased amyloidogenesis and cytotoxicity, and this dimer was then used in a screening platform. Through screening, two FDA-approved drugs, Oxytetracycline and Sunitinib, were identified to dissociate Aß oligomers and plaques to monomers in 5XFAD transgenic mice. In addition, fluorescent Astrophloxine was shown to detect aggregated Aß in brain tissue and cerebrospinal fluid samples of AD mice. This screening platform provides a stable and homogeneous environment for observing Aß interactions with dimer-specific molecules.

Electrochemical Characteristics of All-Solid Lithium Ion Battery with Lithium Titanate/Lithium Lanthanum Zirconium Oxide Composite Electrode.

Composite anodes for all solid-state lithium secondary batteries based on lithium titanate (Li4Ti5O12) were fabricated by a wet process. The effect of the content of polyethylene oxide in the lithium titanate composite anode on the interfacial control for enhancing the ionic conductivity and binding between the constituent materials in the electrode was examined. The content of Super-P and garnet-type lithium lanthanum zirconium oxide in the composite lithium titanate electrode was fixed and the electrochemical characteristics of a half-cell were evaluated as a function of the lithium titanate and polyethylene oxide content in the electrode, where the polyethylene oxide content was varied from 35-70 wt%. A maximum discharge capacity of about 160 mAh g-1 was obtained with the electrode comprising lithium titanate, lithium lanthanum zirconium oxide, Super-P, and polyethylene oxide in a weight ratio of 40:10:10:40. This value is about 94% of the theoretical capacity (170 mAh g-1) of the lithium titanate electrode, and was almost equal to the half-cell capacity of the liquid-type congener. Furthermore, when this composite lithium titanate electrode was fabricated and evaluated in the full cell of an all-solid lithium secondary battery, a discharge capacity of about 140 mAh g-1 was obtained.

Anti-Obesity Effect of Standardized Extract of Microalga Phaeodactylum tricornutum Containing Fucoxanthin.

Fucoxanthin (FX), a marine carotenoid found in macroalgae and microalgae, exhibits several beneficial effects to health. The anti-obesity activity of FX is well documented, but FX has not been mass-produced or applied extensively or commercially because of limited availability of raw materials and complex extraction techniques. In this study, we investigated the anti-obesity effect of standardized FX powder (Phaeodactylum extract (PE)) developed from microalga Phaeodactylum tricornutum as a commercial functional food. The effects of PE on adipogenesis inhibition in 3T3-L1 adipocytes and anti-obesity in high-fat diet (HFD)-fed C57BL/6J mice were evaluated. PE and FX dose-dependently decreased intracellular lipid contents in adipocytes without cytotoxicity. In HFD-fed obese mice, PE supplementation for six weeks decreased body weight, organ weight, and adipocyte size. In the serum parameter analysis, the PE-treated groups showed attenuation of lipid metabolism dysfunction and liver damage induced by HFD. In the liver, uncoupling protein-1 (UCP1) upregulation and peroxisome proliferator activated receptor γ (PPARγ) downregulation were detected in the PE-treated groups. Additionally, micro computed tomography revealed lower fat accumulation in PE-treated groups compared to that in the HFD group. These results indicate that PE exerts anti-obesity effects by inhibiting adipocytic lipogenesis, inducing fat mass reduction and decreasing intracellular lipid content, adipocyte size, and adipose weight.

Multifunctionalized Reduced Graphene Oxide Biosensors for Simultaneous Monitoring of Structural Changes in Amyloid-ß 40.

Determination of the conformation (monomer, oligomer, or fibril) of amyloid peptide aggregates in the human brain is essential for the diagnosis and treatment of Alzheimer's disease (AD). Accordingly, systematic investigation of amyloid conformation using analytical tools is essential for precisely quantifying the relative amounts of the three conformations of amyloid peptide. Here, we developed a reduced graphene oxide (rGO) based multiplexing biosensor that could be used to monitor the relative amounts of the three conformations of various amyloid-ß 40 (Aß40) fluids. The electrical rGO biosensor was composed of a multichannel sensor array capable of individual detection of monomers, oligomers, and fibrils in a single amyloid fluid sample. From the performance test of each sensor, we showed that this method had good analytical sensitivity (1 pg/mL) and a fairly wide dynamic range (1 pg/mL to 10 ng/mL) for each conformation of Aß40. To verify whether the rGO biosensor could be used to evaluate the relative amounts of the three conformations, various amyloid solutions (monomeric Aß40, aggregated Aß40, and disaggregated Aß40 solutions) were employed. Notably, different trends in the relative amounts of the three conformations were observed in each amyloid solution, indicating that this information could serve as an important parameter in the clinical setting. Accordingly, our analytical tool could precisely detect the relative amounts of the three conformations of Aß40 and may have potential applications as a diagnostic system for AD.

Mucilaginibacter craterilacus sp. nov., isolated from sediment soil of a crater lake.

A novel bacterial strain, designated N60AT, was isolated from sediment soil of crater lake, Baekrokdam, Hallasan, Jeju, Republic of Korea. Cells of N60AT were Gram-reaction-negative, oxidase- and catalase-positive, non-motile rods and formed transparent white colonies on ten-fold diluted R2A agar. N60AT contained summed feature 3 (C16 : 1ω7c/C16 : 1ω6c), iso-C15 : 0 and iso-C17 : 0 3-OH as the major fatty acids and MK-7 as the predominant isoprenoid quinone. It contained phosphatidylethanolamine as the predominant polar lipid. The DNA G+C content was 44.4 mol%. Phylogenetic analysis based on 16S rRNA gene sequencing revealed that N60AT formed a separate lineage in the genus Mucilaginibacter and that it was most closely related to Mucilaginibacter frigoritolerans FT22T (96.5 % sequence similarity). Phenotypic, chemotaxonomic and phylogenetic characteristics supported the conclusion that N60AT represents a novel species of the genus Mucilaginibacter, for which the name Mucilaginibacter craterilacus sp. nov. is proposed. The type strain is N60AT (=KCTC 52404T=NRRL B-65396T).

Sphingomonas gotjawalisoli sp. nov., isolated from soil of a lava forest.

A bacterial strain, designated SN6-9T, was isolated from soil of the Gotjawal, lava forest, located in Jeju, Republic of Korea. Strain SN6-9T was Gram-stain-negative, motile, oxidase- and catalase-negative, yellow-pigmented and rod-shaped. It contained summed feature 3 (C16 : 1ω7c and/or C16 : 1ω6c) and summed feature 8 (C18 : 1ω7c and/or C18 : 1ω6c) as the major fatty acids, Q-10 as the predominant isoprenoid quinone, sym-homospermidine as the major polyamine and diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, phosphatidylcholine, sphingoglycolipid and two unidentified phospholipids as the polar lipids. The DNA G+C content was 64.1 mol%. Phylogenetic analysis based on 16S rRNA gene sequences revealed that the strain formed a separate lineage in the genus Sphingomonas. Based on the results from this polyphasic taxonomic study, it is concluded that strain SN6-9T represents a novel species in the genus Sphingomonas. The name Sphingomonas gotjawalisoli sp. nov. is proposed; the type strain is SN6-9T (=KCTC 52405T=NRRL B-65395T).

Taurine-Carbohydrate Derivative Stimulates Fibrillogenesis of Amyloid-ß and Reduce Alzheimer-Like Behaviors.

Amyloid-ß (Aß) aggregates are a hallmark of Alzheimer's disease (AD). Through the misfolding process of Aß in the brain, oligomeric forms of Aß accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. We hypothesized that decrease in Aß oligomers during the aggregation process might be able to reduce Aß-dependent brain damage. As taurine-like chemicals are often reported to have direct binding abilities to Aß, we prepared a chemical library that consisted of taurine-carbohydrate derivatives to search for molecules that target Aß and accelerate its fibrillogenesis. Here, we report that 1-deoxy-1-(2-sulfoethylamino)-D-fructose stimulates the formation of relatively less toxic Aß fibrils leading to prevention of cognitive deficits in AD acute model mice.

Paenibacillus baekrokdamisoli sp. nov., isolated from soil of crater lake.

A novel bacterial strain, Back-11T, was isolated from sediment soil of a crater lake, Baekrokdam, Hallasan, Jeju, Republic of Korea. Cells of strain Back-11T were Gram-stain-positive, motile, endospore-forming, rod-shaped and oxidase- and catalase-positive. It contained anteiso-C15 : 0 as the major fatty acid, menaquinone-7 (MK-7) as the predominant isoprenoid quinone, diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine and four unidentified aminophospholipids as the main polar lipids, and meso-diaminopimelic acid as the diagnostic diamino acid in the cell-wall peptidoglycan. The DNA G+C content was 45.3 mol%. Phylogenetic analysis, based on 16S rRNA gene sequencing, showed that strain Back-11T was most closely related to Paenibacillus taihuensis THMBG22T (95.5 % similarity) and fell into a clade in the genus Paenibacillus. On the basis of phylogenetic, chemotaxonomic and phenotypic data, strain Back-11T represents a novel species in the genus Paenibacillus, for which the name Paenibacillus baekrokdamisoli sp. nov. is proposed. The type strain is Back-11T ( = KCTC 33723T = CECT 8890T).

Nocardioides baekrokdamisoli sp. nov., isolated from soil of a crater lake.

A novel actinobacterial strain, B2-12T, was isolated from soil of a crater lake, Baekrokdam, Hallasan, Jeju, Republic of Korea. Cells of strain B2-12T were Gram-stain-positive, non-motile, non-spore-forming and coccoid to short-rod-shaped. Phylogenetic analysis, based on 16S rRNA gene sequencing, showed that strain B2-12T belonged to the genus Nocardioides and shared highest sequence similarity with 'Nocardioidespaucivorans' KIS31-44 (98.4 %). The predominant isoprenoid quinone was MK-8(H4). The major fatty acids of strain B2-12T were C16 : 1 (ω7c and/or ω6c), summed feature 9 (iso-C17 : 1ω9c and/or C16 : 0 10-methyl), C17 : 0 10-methyl, iso-C16 : 0, C16 : 0 and C17 : 1ω6c. The diagnostic diamino acid in the cell-wall peptidoglycan was ll-diaminopimelic acid. It contained diphosphatidylglycerol, phosphatidylglycerol and phosphatidylinositol as the polar lipids. The DNA G+C content was 67.0 mol%. Based on phylogenetic, chemotaxonomic and phenotypic data, 16S rRNA gene sequence comparisons and DNA-DNA hybridization data, strain B2-12T represents a novel species in the genus Nocardioides, for which the name Nocardioidesbaekrokdamisolisp. nov. is proposed. The type strain is B2-12T (=KCTC 39748T=NRRL B-65313T=DSM 100725T).

Sphingomonas vulcanisoli sp. nov., isolated from soil of a lava forest.

A Gram-stain-negative, non-motile, yellow-pigmented and rod-shaped bacterial strain, designated SN6-13T, was isolated from soil of the Gotjawal, lava forest, located in Jeju, Republic of Korea. Cells of strain SN6-13T were oxidase- and catalase-positive. The isolate contained Q-10 as the predominant isoprenoid quinone, summed feature 8 (C18 : 1ω7c and/or C18 : 1ω6c) and C16 : 0 as the major fatty acids, sym-homospermidine as the major polyamine and diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, phosphatidylcholine, sphingoglycolipid, ninhydrinphosphatidylglycerol and two unidentified aminophospholipids as the polar lipids. The DNA G+C content was 64.6 mol%. In phylogenetic analyses based on 16S rRNA gene sequencing, strain SN6-13T was most closely related to Sphingomonas laterariae LNB2T (95.4 % sequence similarity) and formed a separate lineage in the genus Sphingomonas. Based on phenotypic, chemotaxonomic and phylogenetic characteristics, it is concluded that strain SN6-13T represents a novel species of the genus Sphingomonas, for which the name Sphingomonas vulcanisoli sp. nov. is proposed. The type strain is SN6-13T ( = KCTC 42454T = CECT 8804T).