Plasma sCD146 is a potential biomarker for acute exacerbation of chronic obstructive pulmonary disease.

This study examined the levels of soluble CD146 (sCD146) in plasma samples from patients with chronic obstructive pulmonary disease (COPD) and assessed the relationship between sCD146 and the severity of COPD. A total of 97 COPD patients were recruited from 20 medical centers in Jiangsu, China, including 13 stable subjects and 84 exacerbated subjects. The plasma sCD146 level in exacerbated subjects (28.77 ± 10.80 ng/mL) was significantly lower than that in stable subjects (38.84 ± 15.00 ng/mL). In the high sCD146 group, the proportion of subjects with modified Medical Research Council (mMRC) scores of 0-1 was higher, the proportion of subjects with the Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 was lower, and the proportion of subjects with ≥1 hospitalizations in the past year was lower. The plasma sCD146 level was negatively correlated with the COPD Assessment Test (CAT) score (r = -0.2664, p = 0.0087). Logistic regression analysis showed that sCD146 was an independent risk factor for acute exacerbation of COPD (AECOPD). Receiver operating characteristic (ROC) analysis suggested that sCD146 combined with sex, age, pulmonary function, and acute exacerbations in the past year had clinical value for the accurate identification of AECOPD, with an area under the ROC curve (AUC) of 0.908 (95% CI: 0.810-1.000, p < 0.001). In addition, there was a significant negative correlation between plasma sCD146 and S100A9 (r = -0.3939, p < 0.001).

Observation of Higher-Order Nodal-Line Semimetal in Phononic Crystals.

Higher-order topological insulators and semimetals, which generalize the conventional bulk-boundary correspondence, have attracted extensive research interest. Among them, higher-order Weyl semimetals feature twofold linear crossing points in three-dimensional momentum space, 2D Fermi-arc surface states, and 1D hinge states. Higher-order nodal-point semimetals possessing Weyl points or Dirac points have been implemented. However, higher-order nodal-line or nodal-surface semimetals remain to be further explored in experiments in spite of many previous theoretical efforts. In this work, we realize a second-order nodal-line semimetal in 3D phononic crystals. The bulk nodal lines, 2D drumhead surface states guaranteed by Zak phases, and 1D flat hinge states attributed to k_{z}-dependent quadrupole moments are observed in simulations and experiments. Our findings of nondispersive surface and hinge states may promote applications in acoustic sensing and energy harvesting.

LincR-PPP2R5C Promotes Th2 Cell Differentiation Through PPP2R5C/PP2A by Forming an RNA-DNA Triplex in Allergic Asthma.

PURPOSE: The roles and mechanisms of long noncoding RNAs (lncRNAs) in T helper 2 (Th2) differentiation from allergic asthma are poorly understood. We aimed to explore a novel lncRNA, LincR-protein phosphatase 2 regulatory subunit B' gamma (PPP2R5C), in Th2 differentiation in a mouse model of asthma. METHODS: LincR-PPP2R5C from RNA-seq data of CD4+ T cells of asthma-like mice were validated and confirmed by quantitative reverse transcription polymerase chain reaction, northern blotting, nuclear and cytoplasmic separation, and fluorescence in situ hybridization (FISH). Lentiviruses encoding LincR-PPP2R5C or shRNA were used to overexpress or silence LincR-PPP2R5C in CD4+ T cells. The interactions between LincR-PPP2R5C and PPP2R5C were explored with western blotting, chromatin isolation by RNA purification assay, and fluorescence resonance energy transfer. An ovalbumin-induced acute asthma model in knockout (KO) mice (LincR-PPP2R5C KO, CD4 conditional LincR-PPP2R5C KO) was established to explore the roles of LincR-PPP2R5C in Th2 differentiation. RESULTS: LncR-PPP2R5C was significantly higher in CD4+ T cells from asthmatic mice ex vivo and Th2 cells in vitro. The lentivirus encoding LincR-PPP2R5C suppressed Th1 differentiation; in contrast, the short hairpin RNA (shRNA) lentivirus decreased LincR-PPP2R5C and Th2 differentiation. Mechanistically, LincR-PPP2R5C deficiency suppressed the phosphatase activity of the protein phosphatase 2A (PP2A) holocomplex, resulting in a decline in Th2 differentiation. The formation of an RNA-DNA triplex between LincR-PPP2R5C and the PPP2R5C promoter enhanced PPP2R5C expression and activated PP2A. LincR-PPP2R5C KO and CD4 conditional KO decreased Th2 differentiation, airway hyperresponsiveness and inflammatory responses. CONCLUSIONS: LincR-PPP2R5C regulated PPP2R5C expression and PP2A activity by forming an RNA-DNA triplex with the PPP2R5C promoter, leading to Th2 polarization in a mouse model of acute asthma. Our data presented the first definitive evidence of lncRNAs in the regulation of Th2 cells in asthma.

CD146 deficiency aggravates chronic obstructive pulmonary disease via the increased production of S100A9 and MMP-9 in macrophages.

Chronic obstructive pulmonary disease (COPD) is a leading cause of global death. As a molecule beyond adhesion, CD146 is involved in COPD pathogenesis. However, the mechanisms of CD146 in COPD remain largely elusive. We hypothesized that CD146 regulates the production of matrix metalloproteinase-9 (MMP-9) in macrophages and thereby contributes to COPD. Here, we constructed a murine model of COPD using lipopolysaccharide (LPS) and porcine pancreatic elastase (PPE). In COPD-like mice, LPS and PPE decreased the pulmonary expression of CD146. MMP-9 expression and bioactivity were increased in CD146 knockout COPD-like mice. In vitro, LPS decreased CD146 expression in macrophages. With or without LPS challenge, CD146-defective macrophages produced more MMP-9. Transcriptome analysis based on next-generation sequencing (NGS) revealed that S100A9 regulated MMP-9 production in CD146-defective macrophages. Targeting S100A9 with paquinimod decreased lung inflammation and alleviated alveolar destruction in COPD-like mice. Collectively, our study suggests that CD146 negatively regulates MMP-9 production in macrophages via the S100A9 pathway in COPD.

Up-to-date advance in the relationship between OSA and stroke: a narrative review.

PURPOSE: Obstructive sleep apnea (OSA) and stroke affect each other. In this review, we summarized the effect of OSA on the onset and recurrence of stroke, the prognosis, and the treatment of poststroke patients with OSA. METHODS: Pubmed/MEDLINE were searched through May 2023 to explore the relationship between OSA and stroke. The relevant papers included OSA and stroke, OSA and recurrent stroke, and the prognosis and treatment of poststroke patients with OSA. RESULTS: The results showed that OSA can promote the onset and recurrence of stroke and that OSA may adversely affect the prognosis of poststroke patients. The application of continuous positive airway pressure (CPAP) and other treatments may benefit poststroke patients with OSA, though the long term effects of treatment are not well documented. CONCLUSION: Both the onset and recurrence of stroke closely correlated with OSA, but the specific mechanisms remain unclear. Further studies should be carried out to explore effective treatments in patients with stroke and OSA.

Acoustic Higher-Order Weyl Semimetal with Bound Hinge States in the Continuum.

Higher-order topological phases have raised widespread interest in recent years with the occurrence of the topological boundary states of dimension two or more less than that of the system bulk. The higher-order topological states have been verified in gapped phases, in a wide variety of systems, such as photonic and acoustic systems, and recently also observed in gapless semimetal phase, such as Weyl and Dirac phases, in systems alike. The higher-order topology is signaled by the hinge states emerging in the common band gaps of the bulk states and the surface states. In this Letter, we report our first prediction and observation of a new type of hinge states, the bound hinge states in the continuum (BHICs) bulk band, in a higher-order Weyl semimetal implemented in phononic crystal. In contrast to the hinge state in gap, which is characterized by the bulk polarization, the BHIC is identified by the nontrivial surface polarization. The finding of the topological BHICs broadens our insight to the topological states, and may stimulate similar researches in other systems such as electronic, photonic, and cold atoms systems. Our Letter may pave the way toward high-Q acoustic devices in application.

Fine particulate matter (PM2.5) induces inhibitory memory alveolar macrophages through the AhR/IL-33 pathway.

Fine particulate matter (PM2.5) concentrations have decreased in the past decade. The adverse effects of acute PM2.5 exposure on respiratory diseases have been well recognized. To explore the long-term effects of PM2.5 exposure on chronic obstructive pulmonary disease (COPD), mice were exposed to PM2.5 for 7 days and rest for 21 days, followed by challenges with lipopolysaccharide (LPS) and porcine pancreatic elastase (PPE). Unexpectedly, PM2.5 exposure and rest alleviated the disease severity and airway inflammatory responses in COPD-like mice. Although acute PM2.5 exposure increased airway inflammation, rest for 21 days reversed the airway inflammatory responses, which was associated with the induction of inhibitory memory alveolar macrophages (AMs). Similarly, polycyclic aromatic hydrocarbons (PAHs) in PM2.5 exposure and rest decreased pulmonary inflammation, accompanied by inhibitory memory AMs. Once AMs were depleted, pulmonary inflammation was aggravated. PAHs in PM2.5 promoted the secretion of IL-33 from airway epithelial cells via the aryl hydrocarbon receptor (AhR)/ARNT pathway. High-throughput mRNA sequencing revealed that PM2.5 exposure and rest drastically changed the mRNA profiles in AMs, which was largely rescued in IL-33-/- mice. Collectively, our results indicate that PM2.5 may mitigate pulmonary inflammation, which is mediated by inhibitory trained AMs via IL-33 production from epithelial cells through the AhR/ARNT pathway. We provide the rationale that PM2.5 plays complicated roles in respiratory disease.

A comparative study of IL-33 and its receptor ST2 in a C57BL/6 J mouse model of pulmonary Cryptococcus neoformans infection.

It has been reported that IL-33 receptor ST2 deficiency mitigates Cryptococcus neoformans (C. neoformans) pulmonary infection in BALB/c mice. IL-33 may modulate immune responses in ST2-dependent and ST2-independent manners. The host genetic background (i.e., BALB/c, C57BL/6 J) influences immune responses against C. neoformans. In the present study, we aimed to explore the roles of IL-33 and ST2 in pulmonary C. neoformans-infected mice on a C57BL/6 J genetic background. C. neoformans infection increased IL-33 expression in lung tissues. IL-33 deficiency but not ST2 deficiency significantly extended the survival time of C. neoformans-infected mice. In contrast, either IL-33 or ST2 deficiency reduced fungal burdens in lung, spleen and brain tissues from the mice following C. neoformans intratracheal inoculation. Similarly, inflammatory responses in the lung tissues were more pronounced in both the IL-33-/- and ST2-/- infected mice. However, mucus production was decreased in IL-33-/- infected mice alone, and the level of IL-5 in bronchoalveolar lavage fluid (BALF) was substantially decreased in the IL-33-/- infected mice but not ST2-/- infected mice. Moreover, IL-33 deficiency but not ST2 deficiency increased iNOS-positive macrophages. At the early stage of infection, the reduced pulmonary fungal burden in the IL-33-/- and ST2-/- mice was accompanied by increased neutrophil infiltration. Collectively, IL-33 regulated pulmonary C. neoformans infection in an ST2-dependent and ST2-independent manner in C57BL/6 J mice.

Exosomes in malignant pleural effusion from lung cancer patients impaired the cytotoxicity of double-negative T cells.

CD3+CD4-CD8- double-negative T (DNT) cells are new weapons in cancer immunotherapy. Here, we explored DNT cells in malignant pleural effusions (MPEs) from lung cancer patients. DNT cells, especially TCRαß+CD56- DNT cells, were increased in MPE from lung cancer patients. DNT cells highly expressed PD-1, TRAIL, NKG2D and DNAM-1. In contrast, FasL was barely detected in DNT cells. Compared with non-MPE cells, MPE-derived DNT cells expressed much higher levels of PD-1 and TRAIL. DNT cells from healthy peripheral blood donors potentially killed lung cancers, which was decreased by MPE supernatant. Exosomes from MPE supernatant expressed PD-1 and CEACAM1 and impaired the cytotoxicity of DNT cells. Blocking PD-1 and TIM3 rescued the cytotoxicity of DNT cells treated with MPE-derived exosomes. Overall, we demonstrated that the frequency of DNT cells in MPE from lung cancer patients was increased and that MPE-derived exosomes impaired the cytotoxicity of DNT cells via the PD-1/PD-L1 and CEACAM1/TIM3 pathways.

Observation of boundary induced chiral anomaly bulk states and their transport properties.

The most useful property of topological materials is perhaps the robust transport of topological edge modes, whose existence depends on bulk topological invariants. This means that we need to make volumetric changes to many atoms in the bulk to control the transport properties of the edges in a sample. We suggest here that we can do the reverse in some cases: the properties of the edge can be used to induce chiral transport phenomena in some bulk modes. Specifically, we show that a topologically trivial 2D hexagonal phononic crystal slab (waveguide) bounded by hard-wall boundaries guarantees the existence of bulk modes with chiral anomaly inside a pseudogap due to finite size effect. We experimentally observed robust valley-selected transport, complete valley state conversion, and valley focusing of the chiral anomaly bulk states (CABSs) in such phononic crystal waveguides. The same concept also applies to electromagnetics.

Experimental Observation of Non-Abelian Earring Nodal Links in Phononic Crystals.

Nodal lines are symmetry-protected one-dimensional band degeneracies in momentum space, which can appear in numerous topological configurations such as nodal rings, chains, links, and knots. Very recently, non-Abelian topological physics have been proposed in space-time inversion (PT) symmetric systems. One of the most special configurations in such systems is the earring nodal link, composing of a nodal chain linking with an isolated nodal line. Such earring nodal links have not been observed in real systems. We designed phononic crystals with earring nodal links, and experimentally observed two different kinds of earring nodal links by measuring the band structures. We found that the order of the nodal chain and line can be switched after band inversion but their link cannot be severed. Our Letter provides experimental evidence for phenomena unique to non-Abelian band topology and our acoustic system provides a convenient platform for studying the new materials carrying non-Abelian charges.

KIF2A decreases IL-33 production and attenuates allergic asthmatic inflammation.

BACKGROUND: The microtubule-dependent molecular motor protein Kinesin Family Member 2A (KIF2A) is down-regulated in asthmatic human airway epithelium. However, little is known about the roles of KIF2A as well as the possible underlying mechanisms in asthma. METHODS: House dust mite (HDM) extract was administered to establish a murine model of asthma. The expression of KIF2A, IL-33 and the autophagy pathways were detected. The plasmid pCMV-KIF2A was used to overexpress KIF2A in the airway epithelial cells in vitro and in vivo. IL-4, IL-5, IL-33 and other cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues homogenates were measured. RESULTS: In response to the challenge of house dust mite (HDM) in vitro and in vivo, airway epithelial cells displayed decreased production of KIF2A. Meanwhile, autophagy and IL-33 were increased in HMD-treated epithelial cells. Mechanistically, KIF2A decreased autophagy via suppressing mTORC1 pathway in HDM-treated epithelial cells, which contributed to the reduced production of IL-33. Moreover, in vivo KIF2A transfection reduced IL-33 and autophagy in the lung, leading to the attenuation of allergic asthma. CONCLUSION: KIF2A suppressed mTORC1-mediated autophagy and decreased the production of epithelial-derived cytokine IL-33 in allergic airway inflammation. These data indicate that KIF2A may be a novel target in allergic asthma.

Multifocal micronodular pneumocyte hyperplasia lacking typical clinical features of the tuberous sclerosis complex: a case report and literature review.

BACKGROUND: Multifocal micronodular pneumocyte hyperplasia (MMPH) is a rare pulmonary manifestation of the tuberous sclerosis complex (TSC) with distinctive histological characteristics. Most case reports of MMPH associated with TSC usually have a history and typical clinical features (seizures, mental retardation, and skin lesions) of TSC. We present a peculiar asymptomatic MMPH case that lacked the history and typical clinical features of TSC. CASE PRESENTATION: A 56-year-old man was referred to our hospital with bilateral ground-glass opacities (GGOs) on chest computed tomography (CT) lasting 8 months, with no complaint of any discomfort. Because of the lack of clinical manifestations, the diagnosis of MMPH and TSC was confirmed by lung biopsy histopathology and gene sequencing of nonsense mutations in the TSC1 gene. Considering the relevant literature review and that the prognosis of most patients with MMPH is generally stable, no special treatment was given. We followed up with the patient for three years after discharge, and the clinical manifestations and imaging features of the patient were stable. CONCLUSION: To our best knowledge, this is the first case of MMPH lacking typical clinical manifestations of TSC confirmed by histopathology combined with gene sequencing. MMPH should be considered as one of the differential diagnoses of multiple GGOs in the lung even when the findings of TSC are not recognized.

IL-33/ST2 axis deficiency exacerbates neutrophil-dominant allergic airway inflammation.

OBJECTIVE: The IL-33/ST2 axis has been extensively investigated in type 2 eosinophilic inflammation. Here, we aimed to investigate the role of the IL-33/ST2 axis in neutrophil-dominant allergic airway inflammation. METHODS: House-dust mite (HDM) extract and lipopolysaccharide (LPS) were administered to establish a murine model of neutrophil-dominant allergic airway inflammation. The formation of neutrophilic extracellular traps (NETs) in the lung tissues was demonstrated by immunofluorescence imaging. Mature IL-33 in bronchoalveolar lavage fluid (BALF) was detected by Western blotting. The neutrophilic chemokine KC produced by bone marrow-derived macrophages (BMDMs) or primary alveolar epithelial cells was measured with a commercial ELISA kit. RESULTS: In the present study, we observed neutrophilic inflammation and tight junction damage in the lungs of mice sensitised with HDM and LPS. Furthermore, sensitisation with HDM and LPS resulted in the formation of NETs, accompanied by increased levels of mature IL-33 in the BALF. Moreover, LPS damaged the epithelial tight junction protein occludin directly or indirectly by inducing NET formation. Surprisingly, IL-33 deficiency augmented neutrophilia and epithelial barrier injury in the lungs of mice after sensitisation with HDM and LPS. Similarly, the absence of ST2 exacerbated the neutrophilic inflammatory response, decreased the expression of occludin and exacerbated the severity of neutrophil-dominant allergic airway inflammation in an HDM/LPS-induced mouse model. Mechanistically, BMDMs and alveolar epithelial cells from IL-33- or ST2-deficient mice tended to produce higher levels of the neutrophilic chemokine KC. CONCLUSIONS: These results demonstrated that the IL-33/ST2 axis may play a protective role in neutrophil-dominant allergic airway inflammation.

Neutrophil extracellular traps promote scar formation in post-epidural fibrosis.

Low back pain following spine surgery is a major complication due to excessive epidural fibrosis, which compresses the lumbar nerve. The mechanisms of epidural fibrosis remain largely elusive. In the drainage samples from patients after spine operation, neutrophil extracellular traps (NETs) and NETs inducer high-mobility group box 1 were significantly increased. In a mouse model of laminectomy, NETs developed in the wound area post epidural operation, accompanied with macrophage infiltration. In vitro, macrophages ingested NETs and thereby increased the elastase from NETs via the receptor for advanced glycation end product. Moreover, NETs boosted the expression of fibronectin in macrophages, which was dependent on elastase and could be partially blocked by DNase. NF-κB p65 and Smad pathways contributed to the increased expression fibronectin in NETs-treated macrophages. In the mouse spine operation model, post-epidural fibrosis was significantly mitigated with the administration of DNase I, which degraded DNA and cleaved NETs. Our study shed light on the roles and mechanisms of NETs in the scar formation post spine operation.

Epithelial-Mesenchymal Transition in Asthma Airway Remodeling Is Regulated by the IL-33/CD146 Axis.

Epithelial-mesenchymal transition (EMT) is essential in asthma airway remodeling. IL-33 from epithelial cells is involved in pulmonary fibrosis. CD146 has been extensively explored in cancer-associated EMT. Whether IL-33 regulates CD146 in the EMT process associated with asthma airway remodeling is still largely unknown. We hypothesized that EMT in airway remodeling was regulated by the IL-33/CD146 axis. House dust mite (HDM) extract increased the expression of IL-33 and CD146 in epithelial cells. Increased expression of CD146 in HDM-treated epithelial cells could be blocked with an ST2-neutralizing antibody. Moreover, HDM-induced EMT was dependent on the CD146 and TGF-ß/SMAD-3 signaling pathways. IL-33 deficiency decreased CD146 expression and alleviated asthma severity. Similarly, CD146 deficiency mitigated EMT and airway remodeling in a murine model of chronic allergic airway inflammation. Furthermore, CD146 expression was significantly elevated in asthma patients. We concluded that IL-33 from HDM extract-treated alveolar epithelial cells stimulated CD146 expression, promoting EMT in airway remodeling in chronic allergic inflammation.

Airway invasive aspergillosis with organizing pneumonia: a case report and review of literature.

Organizing pneumonia (OP) is a distinct clinical and pathologic entity. This condition can be cryptogenic (COP) or secondary to other known causes (secondary OP, SOP). Concomitant occurrence of invasive pulmonary aspergillosis (IPA) with SOP is unusual. Here, we report a case where SOP was a presenting feature in a patient with diagnosed IPA. A previously healthy 62-year-old man presented to the hospital with a month of intermittent fever accompanied by cough and expectoration. According to computed tomography (CT), sputum culture, and transbronchial lung biopsy, he was diagnosed as IPA. Despite undergoing voriconazole and dexamethasone therapy, the patient's condition did not improve after three weeks of therapy. CT-guided percutaneous lung biopsy performed in the left upper lung showed invasive airway aspergillosis with organizing pneumonia. Two months after the combination therapy of voriconazole and methylprednisolone, the CT scan indicated the pulmonary consolidations were almost entirely resolved. To the best of our knowledge, this is the first case of successful non-surgical treatment of IPA with SOP. In a review of the literature, we aimed to highlight the possibility of invasive airway aspergillosis concurrent with secondary organizing pneumonia. Physicians should be aware of the possibility of SOP in the case of IPA.

Enterovirus A71 capsid protein VP1 increases blood-brain barrier permeability and virus receptor vimentin on the brain endothelial cells.

Enterovirus A71 (EV-A71) is the major cause of severe hand-foot-and-mouth diseases (HFMD), especially encephalitis and other nervous system diseases. EV-A71 capsid protein VP1 mediates virus attachment and is the important virulence factor in the EV-A71pathogenesis. In this study, we explored the roles of VP1 in the permeability of blood-brain barrier (BBB). Sera albumin, Evans blue, and dextran leaked into brain parenchyma of the 1-week-old C57BL/6J mice intracranially injected with VP1 recombinant protein. VP1 also increased the permeability of the brain endothelial cells monolayer, an in vitro BBB model. Tight junction protein claudin-5 was reduced in the brain tissues or brain endothelial cells treated with VP1. In contrast, VP1 increased the expression of virus receptor vimentin, which could be blocked with VP1 neutralization antibody. Vimentin expression in the VP1-treated brain endothelial cells was regulated by TGF-ß/Smad-3 and NF-κB signal pathways. Moreover, vimentin over-expression was accompanied with compromised BBB. From these studies, we conclude that EV-A71 virus capsid protein VP1 disrupted BBB and increased virus receptor vimentin, which both may contribute to the virus entrance into brain and EV-A71 CNS infection.

Neutrophil extracellular traps induced by VP1 contribute to pulmonary edema during EV71 infection.

Pulmonary edema is a fatal complication of EV71-associated hand, foot, and mouth disease (HFMD). The pathogenesis of EV71-induced pulmonary edema remains largely unclear. In this study, we aimed to explore the roles of the capsid protein VP1 in the occurrence of EV71-induced pulmonary edema. The intranasal inoculation of recombinant VP1 protein caused lung inflammation with an elevation of inflammatory cytokines and neutrophils infiltration. Moreover, neutrophil extracellular traps (NETs) were observed in the lung parenchyma of the mice treated with VP1. VP1 directly induced the formation of NETs, which depended on PAD4. VP1 also damaged the lung barrier via the reduction of the tight junction protein occludin. Moreover, the EV71 attachment receptor vimentin was increased upon VP1 administration. In contrast, NETs decreased vimentin levels, suggesting a novel role for NETs in viral immune defense. These results evidenced a direct role of VP1 in EV71-induced pulmonary edema and demonstrated that NETs may be both harmful and beneficial in EV71 infection.

Spatiotemporal drought variability on the Mongolian Plateau from 1980-2014 based on the SPEI-PM, intensity analysis and Hurst exponent.

Knowledge about variations of drought can provide a scientific basis for water resource planning and drought mitigation. In this study, the variations and patterns of drought identified by the Standardized Precipitation Evapotranspiration Index (SPEI) were investigated on the Mongolian Plateau for the period 1980-2014, based on intensity analysis, linear regression, the Mann-Kendall test, wavelet analysis, and Hurst exponent. The results show that: 1) the annual SPEI decreased at a rate of -0.0133/yr over the past 35years, and a major abrupt change occurred in 1999; 2) drought on the Mongolian Plateau intensified from 1980 to 2014, and the drought in Mongolia has been more serious than in Inner Mongolia since the beginning of the 21st century; 3) the rate of drought/wet changes in 1980s-1990s and 1990s-2000s were faster than in 2000s-2010s. In 1980s-1990s, the different drought levels were transformed into various wet levels. In 1990s-2000s, the wet levels were transformed into drought, and in 2000s-2010s, the losses of drought levels were larger than the gains in wet levels; 4) the Hurst exponent is a reliable way to predict drought tendency, with a predictive accuracy as high as 91.7%; 5) the mean H value of the SPEI time series during 1980-2014 was 0.533, indicating that the future drought trend is generally consistent with the current state. In the future, the proportion of area with increasingly severe drought (72.2%) will be larger than that with increasingly wetter conditions (27.8%) on the Mongolian Plateau.