Klebsiella pneumoniae (KP) is an important opportunistic pathogen that can persist in the gastrointestinal tract and serve as a reservoir for subsequent infection. The increasing prevalence of multidrug-resistant KP highlights the need for non-antibiotic strategies to limit intestinal KP burden and associated host injury. Lactiplantibacillus plantarum GUANKE (L. plantarum GUANKE) is a candidate probiotic strain with reported effects on mucosal barrier protection and inflammatory regulation, but its role in intestinal KP challenge remains unclear. In this study, the effects of L. plantarum GUANKE and its metabolite phenyllactic acid (PLA) on KP growth, intestinal KP burden, and associated inflammatory injury were investigated using antibacterial assays in vitro, metabolomic analyses, an antibiotic-pretreated mouse model of intestinal KP challenge, and an influenza A virus (IAV)/KP intestinal co-exposure model. L. plantarum GUANKE and its culture-derived products inhibited KP growth in vitro. Metabolomic analysis identified PLA as a metabolite enriched in L. plantarum GUANKE fermentation supernatants, and exogenous PLA directly inhibited KP growth in a dose-dependent manner. In an antibiotic-pretreated mouse model of intestinal KP challenge, oral administration of L. plantarum GUANKE reduced intestinal KP burden and was associated with changes in gut microbiota composition, increased cecal PLA abundance, improved intestinal barrier-related parameters, and reduced inflammatory responses, while exogenous PLA partially reproduced these effects. IAV infection increased susceptibility to intestinal KP expansion, and oral L. plantarum GUANKE reduced KP burden in the IAV/KP intestinal co-exposure model. In mice challenged with multidrug-resistant KP strain NK04152, L. plantarum GUANKE and PLA reduce intestinal KP burden and associated tissue injury in mice, supporting their potential as candidate microbiota and metabolite strategies against intestinal KP challenge.

Background/Objectives: To investigate the antagonistic effect of probiotic Lactiplantibacillus plantarum GUANKE against respiratory syncytial virus (RSV) and its underlying molecular mechanisms. Methods: in vitro cell models (A549 and HEp2 cells) and an in vivo mouse model (BALB/c mice) were employed. RT-qPCR, TCID50 assay, immunofluorescence, ELISA, Western blot, and histopathological analysis were used to investigate the effects of GUANKE on RSV replication, inflammatory responses, and the type I interferon pathway. Results: Oral administration of GUANKE effectively cleared RSV and alleviated RSV-induced pulmonary inflammatory responses. GUANKE inhibited viral replication. The GUANKE intervention group exhibited significantly reduced pathological damage to lung tissue and decreased the expression of inflammatory cytokines (IL-1β, IL-6, MCP-1, TNF-α). GUANKE augmented the early type I interferon response and activated the STING-TBK1-IRF3-IFN signaling pathway. Conclusions: GUANKE exerts anti-RSV effects by enhancing the early type I interferon response and activating the STING-TBK1-IRF3-IFN signaling pathway, thereby inhibiting RSV replication and alleviating pulmonary inflammatory responses. This suggests its potential value as an anti-RSV agent.

Background: Kai-Bi-Bu-Fei Decoction (KBD) is derived from the canonical Traditional Chinese Medicine formulas Xuan-Bai-Cheng-Qi and Ma-Xing-Shi-Gan. It has been employed for decades in the treatment of severe pneumonia with significant clinical efficacy. This study aimed to evaluate the protective effects of KBD against influenza virus-induced severe pneumonia in a murine model and to elucidate the underlying molecular mechanisms. Methods: The chemical profile of KBD was characterized using UPLC-Q-TOF-MS. A severe pneumonia model was established in C57BL/6J mice via intranasal infection with influenza A/Puerto Rico/8/34 (H1N1, PR8). Multiple parameters, including 14-day survival rate, body weight, lung index, histopathological changes, viral load, and pulmonary cytokine/chemokine levels, were assessed. Furthermore, multi-omics analyses were integrated to characterize the gut microbiota and metabolic profiles. Fecal microbiota transplantation (FMT) was subsequently performed to validate the functional role of the gut microbiota and its metabolites. Results: KBD treatment significantly improved the survival rate by 40%, reduced the lung index by 27.85%, and alleviated lung injury. It also markedly lowered the viral load by 80.88%, suppressed pro-inflammatory cytokine levels, and restored intestinal barrier integrity. Mechanistically, KBD restored gut microbiota diversity by increasing the abundance of Firmicutes and Bacteroidetes, enriching beneficial genera such as Bifidobacterium and Faecalibaculum, and reducing Verrucomicrobiota. Integrated transcriptomic and metabolomic analyses revealed that KBD enhanced short-chain fatty acid (SCFA) metabolism and up-regulated pyruvate metabolism. Finally, FMT confirmed that the therapeutic benefits of KBD were transferable via the microbiota to microbiota-depleted mice. Conclusions: KBD exerts robust protection against severe influenza pneumonia, a process primarily mediated by the gut microbiota-SCFA axis. The enhancement of mitochondrial energy metabolism also appears to play a critical role in its therapeutic mechanism.

Influenza is an acute, highly contagious respiratory infection and remains a major global health threat. Previous studies have shown that the probiotic Lactiplantibacillus plantarum strain GUANKE (GUANKE) alleviates intestinal barrier disruption and lung pathology in influenza A virus (IAV)–infected mice, but its efficacy as a standalone intervention is modest. This study evaluated whether combining GUANKE with picolinic acid (PA) enhances protection through complementary mechanisms. The results showed that oral co-administration of GUANKE and PA provided greater protection than either agent alone in IAV-infected mice. Time-course analyses that PA primarily suppresses viral replication during early infection, whereas GUANKE attenuates inflammation at later stages. Metabolomic profiling and follow-up experiments identified phenyllactic acid is a major mediator of GUANKE’s anti-inflammatory activity. In summary, PA limits early viral burden while GUANKE restrains subsequent inflammatory injury, together improving overall protection against IAV in mice. These findings support a probiotic–small-molecule combination strategy that leverages mechanistic complementarity to mitigate influenza.

Background: Gut microbiota dysbiosis is critically implicated in the pathogenesis of allergic airway inflammation (AAI) via the gut-lung axis. While Latilactobacillus curvatus is a promising probiotic candidate, its specific immunomodulatory mechanisms in respiratory diseases remain poorly understood. Objective: In this study, we investigated the protective effects and underlying mechanisms of L. curvatus IM01 in an ovalbumin (OVA)-induced murine AAI model using an integrated multi-omics approach. Results: Our results demonstrated that oral administration of L. curvatus IM01 significantly attenuated airway inflammation, suppressed Th2-type immune responses, and reduced serum IgE levels. Crucially, our multi-omics integration revealed a coherent gut-lung axis narrative driven by microbial and metabolic crosstalk. Specifically, 16S rRNA sequencing indicated that L. curvatus IM01 was closely linked to structural shifts in the gut microbial community, notably characterized by an enrichment trend for beneficial genera such as Odoribacter and Lactobacillus. This microbial restructuring was closely associated with a modulated cecal metabolic profile, as untargeted metabolomics exhibited a clear trend toward the restoration of key systemically active immunoregulatory metabolites, including indolelactic acid (ILA) and choline, which have been previously linked to the alleviation of AAI symptoms. Further linking this metabolic shift to respiratory immune tolerance, lung transcriptomic analysis showed that the treatment is strongly associated with the promotion of the differentiation of CD4(+) T cells into Foxp3(+) regulatory T cells (Tregs). Conclusions: Collectively, these findings suggest a novel potential pathway by which L. curvatus IM01 modulates the gut-lung axis through coordinated microbial and metabolic interventions, highlighting its potential as a therapeutic functional food ingredient for AAI.

The gut-lung axis is a critical regulator of systemic immune homeostasis, however, the precise mechanisms linking gut-derived metabolites to distal airway inflammation remain incompletely understood. Here, we show that oral administration of viable Leuconostoc mesenteroides MY2024 engages a metabolite-host enzyme circuit that protects against allergic airway inflammation (AAI). Viable, but not heat-inactivated, MY2024 significantly attenuated ovalbumin (OVA)-induced Th2-driven eosinophilic asthma by suppressing pathogenic M2-like macrophage responses in the lung. Mechanistically, MY2024 increased gut-derived cinnamic acid (CA), which activated a colonic STAT1-SAT1 signaling axis to accelerate systemic spermidine catabolism. Reduced systemic spermidine availability was associated with reduced pulmonary eIF5A hypusination, a metabolic checkpoint known to support alternative macrophage activation. Notably, these protective effects and the associated metabolic reprogramming were preserved in microbiota-depleted mice, highlighting a direct bacterium-to-host metabolic axis. Together, our findings delineate a probiotic-metabolite-host enzyme circuit and identify colonic epithelial SAT1-dependent spermidine catabolism as a potential metabolic checkpoint for regulating type 2 AAI.

BACKGROUND:Qing-Fei-Yin Decoction (QFY), derived from the classical formula Ma-Xing-Shi-Gan Decoction, emphasized "clearing heat and detoxifying, ventilating the lungs, and relieving cough," has been widely used for the treatment of influenza and has demonstrated significant efficacy. However, the studies on its mechanism were limited. OBJECTIVE:This study aimed to systematically evaluate its efficacy and explore its action mechanism using murine model of influenza. METHODS:The chemical profile of QFY was analyzed using UPLC-MS. A murine model challenged by PR8 (H1N1) influenza virus was established with C57BL/6J mice. Mice were randomly assigned to QFY-treat, oseltamivir-treat, PBS-treat, control groups. Multiple indicators (including survival rate, pathological alteration of lungs and colon, viral load, and inflammatory cytokine levels in lung and serum) were assessed. In addition, transcriptomic sequencing of lung tissues and 16S rRNA sequencing of gut microbiota were conducted. RESULTS:QFY improved the 14-day survival rate of infected mice from 0 % (PBS group) to 40 %, though still below the 60 % observed in the oseltamivir group. It alleviated lung pathological injury, reduced viral load, and downregulated pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ, CCL2, CXCL10). Transcriptomic analysis of lung tissue revealed that QFY markedly suppressed the activation of NF-κB, TNF, IL-17, and NOD-like receptor signaling pathways, while enhancing the expression of genes related to epithelial barrier function. Furthermore, QFY restored gut microbiota homeostasis, increasing beneficial microbiota such as Barnesiella, which promotes short-chain fatty acid production, while inhibiting the overgrowth of pathogenic genera like Escherichia. CONCLUSION:QFY Decoction exhibited experimentally validated anti-influenza activity, mediated primarily through three mechanisms: inhibition of viral replication, suppression of excessive inflammation, and modulation of intestinal microbiota balance.

Background: Kugan granules (KGKL), a Chinese patent medicine, was used widely for the treatment of influenza in China and have demonstrated good efficacy. However, the underlying mechanism remains unclear. Objective: To investigate the anti-influenza efficacy of KGKL and to explore its mechanism of action. Materials and methods: Six-week-old C57BL/6J mice were divided into 3 groups: the blank group (control group), the infection group (model group), and the Kugan granules group (KGKL group). The latter 2 groups were administered either nonlethal or lethal doses of the influenza virus AH1N1 PR8. Tissue specimens, including those from the lungs and colon, were collected on days 1, 3, 7, and 14 postinfection (pi). The levels of IFN-β were measured on days 1 and 3 pi using ELISA, while the mRNA of interferon-related proteins was analyzed on day 1 pi using real-time polymerase chain reaction (PCR). The viral load in the lungs was quantified on days 3 and 7 pi using real-time PCR. On day 7 pi, the lung index and colon length were measured, and pathologic examinations of the lungs were conducted. In addition, multiple cytokines (IL-6, IL-1β, TNF-α, IFN-γ, CXCL-10, TGF-β, IL-4, and IL-10) in the lungs were assessed using ELISA. The expression levels of NLRP3 inflammasome-related proteins and tight junction proteins in the lungs were evaluated using Western blotting. Mouse survival was continuously monitored until day 14 pi. Results: The KGKL group exhibited significantly improved lung index ( P <0.01), colon length ( P <0.0001), and pathologic score ( P <0.05) when compared with the model group. The levels of multiple cytokines or chemokines (IL-6, IL-1β, TNF-α, IFN-γ, CXCL-10, and TGF-β) in lung of KGKL group were significantly reduced (IL-6, IL-1β, TNF-α, IFN-γ, CXCL-10: P <0.05; TGF-β: P <0.01), while the releases of IL-4 and IL-10 were significantly increased (IL-4: P <0.01; IL-10: P <0.05). The viral load in the lungs of the KGKL group was significantly reduced on day 3 ( P <0.05) and day 7 pi ( P <0.01). The levels of IFN-β in the lungs of the KGKL group were significantly elevated compared with the model group on day 1 pi ( P <0.05). The expression of interferon-related proteins was upregulated on day 1 pi. The expressions of NLRP3 inflammasome-related proteins (NLRP3, ASC, pro-caspase-1, and P20) were significantly reduced in lung ( P <0.05), while the expression levels of tight junction-related proteins (ZO-1, Occludin, and Claudin-5) were significantly increased on day 7 pi ( P <0.05). Conclusions: The primary mechanism of KGKL anti-influenza probably involved reducing viral load by directly inhibiting virus replication or inducing IFN-I in the early stage of the infection and suppressing excessive inflammatory response by down-regulating NLRP3-Caspase1-mediated pyroptosis in the late stage of the infection.

Background/Objectives: Gut microbiota is essential for maintaining host immune homeostasis and has been confirmed to be closely related to some intestinal and extraintestinal diseases. Bacteroides, as the dominant bacterial genus in the human gut, has attracted great attention due to its excellent metabolic activity, but there are few studies on Bacteroides dorei species. In our previous study, a gut commensal strain, Bacteroides dorei RX2020 (B. dorei), was isolated from healthy human feces and exhibited superior flavonoid metabolic activity, prompting further analysis of its uncharacterized genomic features, probiotic potential, safety, and immunomodulatory activity. Results: The results showed that B. dorei exhibited intrinsic probiotic functionalities with preserved genomic and phenotypic stability, demonstrated safety profiles in murine models through in vivo assessments, and conferred antagonistic activity against enteric foodborne pathogens via competitive exclusion. The strain also demonstrated abundant metabolic activity and was involved in the metabolism of tryptophan and bile acids (BAs). Moreover, B. dorei can promote the production of IFNβ by dendritic cells (DCs) to inhibit the replication of influenza virus in epithelial cells, which may be achieved by regulating host metabolism. Conclusions: This study reveals the potential of B. dorei as next-generation probiotics (NGPs), contributing to a broader understanding and application of these novel probiotics in health and disease management.

BACKGROUND:The role of the gut microbiome in respiratory infections is increasingly recognized. We have found that a gut commensal strain, Bacteroides dorei RX2020 (B. dorei) previously isolated from healthy human fecal microbiota, alleviates influenza virus infection, but the underlying mechanisms remain elusive. METHODS:To explore the mechanism by which B. dorei alleviates influenza, we administered it via gavage to influenza virus-infected mice. Gene knockout mice were then used to verify the underlying signaling pathways involved in the antiviral action of B. dorei. Metabolomics analysis was conducted to identify effective metabolites of B. dorei against influenza, followed by complementary verification to confirm these metabolites. RESULTS:Metabolomics reveals that influenza virus infection significantly reduced the concentrations of secondary bile acid (BA) in feces at 7 post-infection (dpi). Oral administration of B. dorei increased bile salt hydrolase (BSH) activity and restored the BA metabolism, thereby protecting wild-type but not TGR5-deficient mice from influenza virus infection. B.dorei-mediated TGR5 activation inhibited influenza virus-induced lung inflammation via cAMP-PKA pathway. Supplementing exogenous Ursodeoxycholic acid (UDCA) and Hyodeoxycholic acid (HDCA), two metabolites changed dramatically after B. dorei treatment, reproduced the protective effect of B. dorei. CONCLUSIONS:Overall, our work elucidates the protective efficacy of commensal microbes against influenza virus infection by modulating lung immunity and restoring BA metabolism, suggesting a potential strategy to intervene in distal infections by regulating gut microbial metabolism.

Probiotics show anti-influenza activity, offering a potential variant-resistant alternative for infection prevention and control. In this study, we evaluated whether a specially formulated yogurt enriched with synbiotics (named yogurt 1) with 7 probiotics and 6 prebiotics, has anti-influenza effects and its underlying mechanisms using a mouse model challenged with influenza virus H1N1 PR8 strain. The mice were treated with phosphate-buffered saline (negative control), yogurt matrix, yogurt 1, and oseltamivir (positive control), respectively. Yogurt 1 treatment improved the survival of infected mice (from 0% to 30%), alleviated pathological injuries in the lungs and colon, and reduced the viral load of influenza virus on day 3 and day 7 post-infection. Yogurt 1 also downregulated some inflammation-related signaling pathways and reduced the levels of proinflammatory cytokines or chemokines in the lungs or serum, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α) and keratinocyte chemoattractant (KC). The levels of short-chain fatty acids in the cecal content were increased, the diversity of the intestinal flora was partially restored, and influenza-specific IgG and interferon-secreting lymphocytes were enhanced following yogurt 1 administration. Thus, yogurt 1, as a commercial and easily accessible dairy product, demonstrated a notable anti-influenza effect in mice by inhibiting viral proliferation, suppressing excessive inflammatory responses, and promoting influenza virus-specific adaptive humoral and cellular immune responses, demonstrating its potential for influenza epidemic prevention and control.

Symbiotic flora exhibits a strong association with the pathogenesis of allergic disorders. Certain Bacteroides species have demonstrated potential in ameliorating allergic conditions. However, the specific role of Bacteroides uniformis in allergic asthma and its underlying mechanisms remain incompletely understood. This study demonstrates that oral administration of B.uniformis IM01 significantly enhanced the production of indole-3-acetic acid (IAA), suppressed airway inflammatory cell airway infiltration and aberrant T helper 2 (Th2) immune responses, and improved the epithelial barrier function in a murine model of asthma. Mechanistically, B.uniformis IM01 upregulated tryptophan metabolism, elevating IAA levels in both colon and serum, which activated the aryl hydrocarbon receptor (AhR) and induced interleukin-22 (IL-22) production. Activated AhR may inhibit NF-κB/NLRP3 signaling pathway and facilitate the splenic differentiation of Foxp3+ regulatory T cells (Tregs), thus attenuating lung barrier dysfunction and improving allergic asthma symptoms. In summary, our results revealed that B.uniformis IM01 upregulated production of IAA to activate AhR leading to inhibited NF-κB/NLRP3-mediated immune responses, and ameliorated allergic asthma through the gut-lung axis. B.uniformis IM01 upregulated production of IAA to active AhR leading to inhibited NF-κB/NLRP3-mediated immune responses, and ameliorated allergic asthma symptoms through the gut-lung axis.

Influenza, a highly transmissible acute respiratory illness caused by influenza viruses, is responsible for annual seasonal epidemics and poses a substantial global disease burden. While primarily recognized for its respiratory manifestations, influenza infection exhibits significant extrapulmonary effects, particularly through disrupting gut microbiota composition and compromising intestinal barrier integrity. This study investigates the protective efficacy of Lactiplantibacillus plantarum strain GUANKE against influenza-associated intestinal pathology in a murine model. Building on GUANKE's established safety profile and immunomodulatory capabilities, we employed a multi-faceted approach examining three key defense mechanisms: (1) maintenance of intestinal epithelial integrity, (2) preservation of chemical mucosal secretions, and (3) modulation of microbial homeostasis. Our findings establish crucial scientific evidence for probiotic-mediated protection of gastrointestinal function during influenza infection, potentially informing novel therapeutic strategies for virus-induced gut dysbiosis.

Hyperuricemia (HUA) is a widespread metabolic disorder. Probiotics have drawn increasing attention as an adjunctive treatment with fewer side effects. However, thus far the effective strains are limited and the mechanisms for their serum uric acid (SUA)-lowering effect are not well understood. Along this line, we conducted the current study using a hyperuricemia mouse model induced by potassium oxonate and adenine. A novel strain of Lactococcus cremoris named D2022 was identified to have significant SUA-lowering capability. Lactococcus cremoris D2022 significantly reduced SUA levels by inhibiting uric acid synthesis and regulating uric acid transportation. It was also found that Lactococcus cremoris D2022 alleviated HUA-induced renal inflammatory injury involving multiple signaling pathways. By focusing on the expression of NLRP3-related inflammatory genes, we found correlations between the expression levels of these genes and free fatty acid receptors (FFARs). In addition, oral administration of Lactococcus cremoris D2022 increased short-chain fatty acids (SCFAs) in cecal samples, which may be one of the mechanisms by which oral probiotics alleviate renal inflammation. Serum untargeted metabolomics showed changes in a variety of serum metabolites associated with purine metabolism and inflammation after oral administration of Lactococcus cremoris D2022, further confirming its systemic bioactivity. Finally, it was proved that Lactococcus cremoris D2022 improved intestinal barrier function. In conclusion, Lactococcus cremoris D2022 can alleviate HUA and HUA-induced nephropathy by increasing the production of SCFAs in the gut and systemic metabolism.

Bacteroides. dorei (B. dorei) is regarded as the “next-generation probiotics”, and it has been demonstrated to fight influenza infection and alter the composition of gut microbiota. The role of the gut microbiota in the immune response to antiviral vaccination has been fully established in animal experiments and clinical studies. However, whether oral B. dorei can affect the immune response to COVID-19 vaccines remains unknown. This study reported that B. dorei enhanced SARS-CoV-2 vaccine efficacy as indicated by elevation in immunoglobulin G antibody and neutralizing antibody titers, mucosal immune response and Th1 immune response, and memory immune responses. Moreover, B. dorei alone could induce maturation of dendritic cells to promote Th1 response, which was crucial for antiviral immunity. These results suggest that B. dorei may potentially be used as an immunoadjuvant or immunopotentiator to enhance immune function, especially in individuals with impaired immune function.

Influenza, a severe respiratory disease caused by the influenza virus, has long been a prominent threat to human health. An increasing number of studies have demonstrated that oral administration with probiotics may increase the immune response to lung infection via the gut-lung axis leading to the alleviation of the pulmonary disease. In this study, we evaluated the effects of oral administration of Pediococcus pentosaceus MIANGUAN2 (MIANGUAN2) on influenza infection in a mouse model. Our results showed that oral administration of MIANGUAN2 significantly improved weight loss, lung index, and lung pathology, and decreased lung viral load of influenza-infected mice. Additionally, MIANGUAN2-treated mice showed significantly lower levels of TNF-α, IL-1β, IFN-γ, and IL-12p70 and higher production of IL-4 in the lung. In accordance with this, the transcriptome analysis of the lung indicated that MIANGUAN2-treated mice had reduced expression of inflammation markers, such as TNF, apoptosis, and the NF-Kappa B pathway. Furthermore, the administration of MIANGUAN2 restored the SCFAs profiles through regulating the gut microbiota. SCFA-producing bacteria, such as p_Firmicutes, f_Lachnospiraceae, and f_Ruminococcaceae, were enriched in the MIANGUAN2-treated group compared with PBS-treated group. Consistently, the concentrations of SCFAs in the MIANGUAN2 group were significantly higher than those in the PBS-treated group. In addition, the concentrations of SCFAs were positively correlated with SCFA-producing bacteria, such as Ruminococcus, while being negatively correlated with the virial titers and proinflammatory cytokines. In conclusion, this animal study suggests that Pediococcus pentosaceus MIANGUAN2 may alleviate the influenza infection by altering the gut microbiota composition and increasing the levels of gut microbiota-derived SCFAs.

GUANKE is a Lactobacillus plantarum isolated from the feces of healthy volunteer. We have previously shown that GUANKE enhances the efficacy of the SARS-CoV-2 vaccine and prolongs the duration of vaccine protection by upregulating the IFN pathway and T and B lymphocyte functions of the host. The purpose of this study was to evaluate the protective effects and mechanism of oral administration of Lactobacillus plantarum GUANKE in the influenza (A virus A/Puerto Rico/8/34) infection mouse model. In our experiment, oral administration of GUANKE significantly decreased viral load and increased tight junction proteins expression in lung tissues of influenza-infected mice. After GUANKE was co-cultured with mBMDCs in vitro, mBMDCs’ maturity and antiviral ability were enhanced, and matured mBMDCs induced polarization of naïve CD4+ T cells into T helper (Th) 1 cells. Adoptive transfer of GUANKE-treated mBMDCs could protect mice from influenza infections. This study suggests that oral administration of Lactobacillus plantarum GUANKE could provide protection against influenza infection in mice, and this protective effect may be mediated, at least in part, by dendritic cells.

目的 分析2020-2023年北京市副流感病毒(HPIVs)的流行特征.方法 收集北京市35家哨点医院就诊的急性呼吸道感染病例的病原学标本,检测HPIV-1、HPIV-2、HPIV-3、HPIV-4和其他常见呼吸道病毒.结果 2020年1月至2023年2月北京市HPIVs总体阳性率为3.22％(486/15 106),HPIVs阳性率在2020年最低(1.65％,70/4234),随后逐年增加,2022年阳性率达5.61％(214/3817),2023年1-2月阳性率2.54％(27/1062).HPIVs流行高峰在秋季.此外,HPIVs在2022年10月的阳性率(23.05％,74/321)高于 2020-2023 年间的任何月份.2020-2023 年以 HPIV-3 流行为主(2.11％,318/15 106),其次是 HPIV-1(0.73％,111/15 106)、HPIV-2(0.24％,36/15 106)和 HPIV-4(0.15％,22/15 106).但 2022 年之后,HPIV-1 的阳性率大幅降低,HPIV-2 阳性率明显升高.HPIVs 高发人群为 0～5 岁(8.50％,176/2070),6～17 岁(4.10％,49/1195)和 60 岁以上(2.82％,147/5214).0～5岁人群易感HPIV-3重症肺炎(8.51％,12/141).结论 2020-2023年北京市HPIVs流行强度在初期明显被抑制,后期逐渐回升;流行高峰被推迟,这种特征性改变,可能影响未来的HPIVs流行.

Ethnopharmacological relevance: Ulcerative colitis (UC) is a chronic relapsing intestinal disease with complex pathogenesis. The increasing morbidity and mortality of UC become a global public health threat. Baitouweng decoction (BD), a formulated prescription of Traditional Chinese Medicine, has been applied to cure UC for many centuries. However, the therapeutic efficacy and working mechanisms of this medicine are not well studied. Aim of study: In this study we determined whether Pulsatillae radix, one of four ingredients in BD, had a therapeutic effect on colitis. And explore the underlying mechanism of Pulsatilla chinensis (Bunge) Regel radix in the improvement of DSS-induced colitis in mice model. Methods: The active compounds of Pulsatilla chinensis was identified by UPLC. The composition of the mice's cecum microbiota was determined by 16S rRNA sequencing. And gene expression profile of colon was detected by transcriptome. Results: The results showed that Pulsatillae radix significantly improved the clinical symptom, prevented the shorten of colon length, and decreased the diseased activity index (DAI) in an 3 % DSS-induced ulcerative colitis mouse model. We found that Pulsatillae radix reversed the dysbiosis of gut microbiota as evidenced by increase in the relative abundance of Bacteroidetes, Deferribacteres, and Proteobacteria phyla and decrease in Firmicutes, as well as by decrease in the genera levels of Bacteroides, Parabacteroides, Prevotella, Mucispirillum, Coprococcus, Oscillospira, and Escherichia. The results of transcriptome showed Pulsatillae radix administration led to 128 genes up-regulation, and 122 genes down-regulation, up-regulate NOD-like receptor signaling pathway, down-regulate Cytokine-cytokine receptor interaction, and TNF and IL-17 signaling pathways. Conclusion: in this study, we demonstrate Pulsatillae radix alleviates DSS-induced colitis probably via modulating gut microbiota and inflammatory signaling pathway in DSS-induced colitis mouse model.

Slow transit constipation (STC) is a prevalent gastrointestinal condition with slow transit, and some probiotics can effectively relieve constipation, but the exact mechanisms have not been fully understood. In this study, we evaluate the impact of Lactiplantibacillus plantarum GUANKE (GUANKE) on diphenoxylate-induced slow transit constipation and speculate on the underlying mechanisms in a mouse model. Administration of L. plantarum GUANKE alleviated constipation indexes, including defecation time, fecal output and water content, and gastrointestinal transit ratio. In addition, GUANKE restored the protein expression of constipation-related intestinal factors (aquaporins (AQPs) and interstitial Cajal cells (ICCs)) in colon tissues measured using immunofluorescence staining; regulated the neurotransmitters and hormones, such as increased levels of 5-hydroxytryptamine, substance P, and motilin; and decreased levels of vasoactive intestinal peptide and nitric oxide in serum, as measured by an ELISA. 16S rRNA and correlation analysis of feces indicated that GUANKE administration effectively reduced constipation-induced Prevotella enrichment and suggested a potential contribution of Prevotella to diphenoxylate-induced STC in mice. GUANKE had no effect on short-chain fatty acids (SCFAs) in cecum content. This study revealed that GUANKE may alleviate constipation in mice through regulating intestinal neurotransmitter and hormone release and altering specific bacterial taxa, rather than by affecting SCFAs and the diversity of microbiota in the gut. Further research is needed to confirm if the findings observed in this study will be consistent in other animal studies or clinical trials.