Frontiers in Microbiology最新文献

Helicobacter pylori (H. pylori) infection affects around half of the global population and is a globally highly prevalent pathogen that is closely linked not only to gastrointestinal diseases such as chronic atrophic gastritis, functional dyspepsia and peptic ulcer but also to the development and progression of a variety of extra-gastrointestinal diseases. Numerous studies have shown the correlation between H. pylori infection and iron-deficiency anemia (IDA). The prevalence of H. pylori infection is higher in individuals with IDA, and the hemoglobin level of patients with IDA can be increased to different degrees or even returned to normal following active H. pylori eradication. However, this conclusion is still controversial. In this paper, a comprehensive literature search was conducted using the PubMed/MEDLINE/Web of Science database, combining the following terms: "Helicobacter pylori," "Helicobacter pylori infection," "iron deficiency anemia," "iron deficiency," "iron absorption," "iron malabsorption," "serum iron," "hemoglobin," "pathogenesis," "mechanism," and "eradication therapy." Through extensive literature searches, the correlation between H. pylori infection and IDA, its potential mechanism, and the efficacy of H. pylori eradication therapy in IDA patients have been comprehensively discussed. We conclude that the majority of existing studies have confirmed the correlation between H. pylori infection and IDA, indicating that patients with H. pylori infection are more likely to develop IDA and that the prevalence of H. pylori infection is higher in individuals with IDA. Compared with iron supplementation alone, combining H. pylori eradication with iron supplementation is more effective in treating IDA, particularly in unexplained or refractory IDA cases. These findings provide valuable insights for clinicians managing patients with unexplained or refractory IDA.

Purpose: Herpes simplex encephalitis (HSE) ranks among the most common causes of severe viral encephalitis. It leads to meningitis or encephalitis, with patients frequently encountering adverse outcomes. In this study, we utilized metagenomic next-generation sequencing (mNGS) to rapidly and accurately detect and identify the HSV pathogen directly from cerebrospinal fluid (CSF) samples, aiming to achieve a definitive diagnosis for encephalitis patients.

Methods: From 2018 to 2023, we prospectively identified and enrolled 28 patients diagnosed with HSE at Hengshui People's Hospital. CSF samples were subjected to mNGS to facilitate the diagnosis and characterization of HSE in this cohort. We compiled the clinical characteristics, supplementary examinations, and outcomes of HSE patients, with prognosis assessed using the Glasgow Outcome Scale (GOS) scores at discharge, 1 month post-discharge, and 3 months thereafter.

Results: In this cohort of 28 patients, 12 were females and 16 males, with a mean age of 41.82 ± 18.23. HSE manifested with a variety of clinical symptoms, the most prevalent being headaches (67.9%), fever exceeding 38°C (60.7%), and altered consciousness (60.7%). Seizures (42.9%), vomiting (35.7%), and speech deficits (35.7%) were frequently observed, with a minority of patients displaying personality changes (28.6%). CSF analysis revealed pleocytosis and a mild increase in protein levels. Magnetic resonance imaging (MRI) abnormalities (28.6%) were primarily confined to the frontal and temporal lobes as well as limbic regions, with no indications of cerebral hemorrhage. Half of the patients exhibited Electroencephalogram (EEG) changes suggestive of encephalitis. HSE was confirmed through mNGS analysis of CSF within 3 days of admission. All patients received empirical treatment with ganciclovir, with 46.4% undergoing hormonotherapy and 32.1% receiving immunoglobulin therapy. At the three-month follow-up, 32.1% had GOS scores <5.

Conclusion: HSE often presents with nonspecific signs of encephalitis, and it's not easy for traditional CNS examinations to confirm the diagnosis. mNGS serves as a cutting-edge diagnostic tool for the rapid and precise identification of HSE, facilitating timely clinical diagnosis and intervention to prevent the progression of the disease.

β-Carotene, a high value-added natural pigment, is currently produced industrially in Blakeslea trispora. Although photoinduced carotenoid synthesis has been identified in some filamentous fungi, there are still relatively few studies focusing on B. trispora and its potential mechanisms. In this study, an integrated strategy-including correlation analysis of gene expression, bioinformatics analysis, protein interaction, and RNA interference-was adopted to elucidate photoinduced β-carotene synthesis in B. trispora. Light wavelength, intensity, and irradiation duration stimulated the transcription of photoreceptors [btwc-1 (a, b, c) and btwc-2 (a, b, c, d)] and carotenoid structural genes (carB and carRA). The transcription of photoreceptor genes showed significant or high correlation with carotenoid structural genes under continuous or short-term, high-intensity blue light irradiation. To elucidate the role of photoreceptors in carotenoid synthesis, the interaction between BTWC-1 and BTWC-2 was predicted. Furthermore, Glutathione S-Transferase (GST) pull-down assays showed that only BTWC-1C and BTWC-2A could interact to form complexes. Inhibition of btwc-2a expression under dark conditions did not affect β-carotene accumulation or the transcription of carB and carRA, but did reduce these parameters under blue light irradiation, indicating that btwc-2a mediates photoinduced β-carotene synthesis in B. trispora.

Long photoperiods are often characterized by enhanced oxidative stress-induced damage to skeletal muscle, reduced melatonin (MT) levels and intestinal microbiota dysfunction in broilers. In this study, we aimed to investigate the association of breast muscle morphology with melatonin levels and the cecal microbiota of broilers under different photoperiods. A total of 216 healthy 5-day-old Arbor Acres (AA) male broilers were randomly assigned to 12 L:12D, 18 L:6D and 24 L:0D photoperiods for 4 weeks (L = hours of light, D = hours of darkness). The concentration of inflammatory factors and MT concentrations was measured using ELISA kits, whereas breast muscle morphology was examined through the hematoxylin (H) and eosin (E) staining, and microbiota composition was identified through 16 s rRNA analysis. Extended light exposure significantly improved the growth rate of broilers, but significantly decreased feed efficiency (FE). Furthermore, it upregulated the concentration of IL-1β, IL-6 and TNF-α and induced an abnormal breast muscle morphology. Extended light exposure significantly decreased MT levels in the hypothalamus, cecum and breast muscle, while triggering the cecal microbiota composition disorder. Specifically, there was significant alteration to the dominant bacterial phylum, following exposure to long photoperiods, with the abundance of Firmicutes decreasing and the abundance of Bacteroidota increasing. Notably, the relative abundance of Lactobacillus showed a positive correlation with MT levels and a negative correlation with inflammatory cytokines. In conclusion, the present findings indicated that extended light exposure reduced the MT levels, which were related to disturbed cecal microbiota, damaging breast muscle morphology and inducing breast muscle inflammation in broilers.

Background: Invasive candidiasis (IC) is an increasingly common, expensive, and potentially fatal infection. However, IC caused by multiple Candida species is rarely reported in China. Herein, we revealed a complex IC caused by multiple Candida species, comprising the rare C. norvegensis, C. albicans, C. glabrata, and C. tropicalis. The resistance mechanism of azole and echinocandin resistance were explored further.

Methods: The isolates were confirmed using internal transcribed spacer (ITS) sequencing. The resistance mechanisms were investigated using PCR-based sequencing, quantitative real-time reverse transcription PCR, and rhodamine 6G efflux quantification.

Results: Antifungal susceptibility testing showed this complex infection was associated with cross-resistance to azole and echinocandin drugs. For C. glabrata, the acquired echinocandin resistance was likely caused by a novel mutational pattern (1,3-beta-D-glucan synthase subunits FKS1-S629P and FKS2-W1497stop) while the acquired azole resistance in C. glabrata RJ05 was related to complex mechanisms including enhanced efflux activity, pleiotropic drug resistance 1 (PDR1) mutation, and increased expression of Candida drug resistance 1 (CDR1) and CDR2. Additionally, the azole resistance of C. tropicalis was caused by two lanosterol 14-alpha demethylase (ERG11) mutations: Y132F and S154F.

Conclusion: Our study revealed a case of clinically complex, multiple Candida invasive infections, further uncovering the resistance mechanisms to azoles and echinocandins. These findings provide valuable references for the diagnosis and treatment of invasive candidiasis (IC) in clinical practice.

Fecal microbiota transplantation (FMT) represents a therapeutic approach that directly regulates the gut microbiota of recipients, normalizes its composition and reaping therapeutic rewards. Currently, in addition to its general application in treating Clostridium difficile (C. difficile) infection (CDI), FMT treatment has also been extended to the fields of other gastrointestinal diseases, infections, gut-liver or gut-brain axis disorders, metabolic diseases and cancer, etc. Prior to FMT, rigorous donor screening is essential to reduce the occurrence of adverse events. In addition, it is imperative to evaluate whether the recipient can safely and effectively undergo FMT treatment. However, the efficacy of FMT is influenced by the complex interactions between the gut microbiota of donor and recipient, the degree of donor microbiota engraftment is not necessarily positively related with the success rate of FMT. Furthermore, an increasing number of novel factors affecting FMT outcomes are being identified in recent clinical trials and animal experiments, broadening our understanding of FMT treatment. This article provides a comprehensive review of the application scenarios of FMT, the factors influencing the safety and efficacy of FMT from the aspects of both the donors and the recipients, and summarizes how these emerging novel regulatory factors can be combined to predict the clinical outcomes of patients undergoing FMT.

Introduction: Ulcerative colitis (UC) is characterized by chronic inflammation and ulceration in colonic mucosa, accompanied by a defective epithelial barrier. Proteus mirabilis (P. mirabilis) bacterium is a putative intestinal pathogen with invasive ability, yet its role in UC inflammation and gut barrier disruption is unclear. This study aims to investigate its epidemiological presence, pathogenic roles and preventive strategy during UC inflammation.

Method: P. mirabilis culture and PCR amplification of the P. mirabilis-specific ureR gene were used to detect fecal P. mirabilis and determine its prevalence in UC and control stool specimens. P. mirabilis isolated from UC stool specimens was gavaged into dextran sulfate sodium (DSS)-treated mice. Inflammation and the mucus layer of colons were assessed through histological examination and cytokine quantification. Bacteriophages were screened and used to eliminate P. mirabilis in colitis animals.

Results and discussion: The fecal P. mirabilis bacteria were detected by PCR amplification of P. mirabilis-specific ureR gene. Of 41 UC patients, 65.9% patients were P. mirabilis positive, which was significantly higher than the controls. Administration of P. mirabilis aggravated DSS-induced colitis symptom and mucosal inflammation in mice. Interestingly, the colonic mucus layer, an essential component of the epithelial barrier, of the animals was dramatically disrupted, which was consistent with the alteration of human UC colon. The disrupted mucus layer was mediated by the down-regulation of IL-18 in intestinal epithelium. Importantly, a bacteriophage cocktail targeting P. mirabilis could restore the mucus barrier and alleviate the enteric inflammation. Thus, our results suggest that P. mirabilis is a UC pathobiont bacterium, which exacerbates the severity of UC inflammation owing to down-regulation of mucin production and IL-18 expression. Bacteriophage-mediated elimination of P. mirabilis may be effective in limiting UC inflammation.

Introduction: Galacto-oligosaccharides (GOS) are beneficial for alleviating lactose intolerance (LI). GOS have the ability to modify the composition of the intestinal microbiota. The development of intestinal diseases could be influenced by the composition of the gut microbiota. Nevertheless, it remains unclear whether gut microbiota exerts an effect when GOS alleviate LI, whether alterations in composition of the intestinal microbiota influence inflammatory response and lactose digestion.

Methods: We first investigated the effects of GOS on mice with established lactose intolerance. Next, we demonstrated that prophylactic supplementation with GOS also conferred similar benefits.

Results: The results showed that GOS enhanced anti-inflammatory, antioxidant, and gut barrier function. We observed that GOS mediated a change in the gut microbiome by increasing the abundance of Lactobacillus. GOS pre-supplementation reduced incident LI, enhanced anti-inflammatory, antioxidant, and gut barrier function, and markedly altered the gut microbiome by significantly enriching Bifidobacterium. Collectively, the alleviation of LI by GOS suggests an intimate involvement of probiotics.

Discussion: This study demonstrates that GOS ameliorated LI in a gut microbiota-dependent manner. Our findings provide novel evidence that GOS substitute for lactase and serve as a potential modulator of the gut microbiota for the prevention of LI.