Purpose: The main objectives of the present study were to detect the antimicrobial susceptibility and molecular characteristics of Klebsiella pneumoniae isolated from different hosts and to investigate the possibility of K. pneumoniae transmission between animals and humans. Materials and methods: A total of 189 nonduplicate K. pneumoniae isolates were collected from hospitals and four species of animals in Henan Province, China. The disk diffusion method was used for antimicrobial susceptibility testing, and resistance and virulence genes were screened by polymerase chain reaction (PCR). The molecular types were identified through multilocus sequence typing (MLST), and the hypermucoviscous (HMV) phenotype was identified using the “string-forming test”. Pearson’s parameters were used to determine the potential link among the molecular types and resistance and virulence genes of all K. pneumoniae strains. Results: The resistance rates of the 189 K. pneumoniae isolates against 15 antibiotics ranged from 11.6% to 77.8%. The highest multidrug resistance rate was detected in the pig strains (93.6%), followed by the human strains (90.4%), chicken strains (88.9%), cow strains (52.0%) and sheep strains (50.0%). Forty-eight (25.4%) K. pneumoniae strains presented the HMV phenotype. entB, fimH-1 and mrkD were the most prevalent of the detected virulence genes, and magA and rmpA were the least prevalent genes in all the isolates. The MLST analysis revealed 24 unique sequence types (STs) among from the 189 isolates. ST11, ST235 and ST258 were common STs among the five isolates of host origin. ST258 exhibited significantly positive correlations with blaNDM, magA and the HMV phenotype and a negative correlation with qnrB. Conclusion: K. pneumoniae strains from different hosts, including humans and animals, have common molecular types and similar phenotypes, and these strains can potentially be transmitted between humans and animals.

Background: Recent studies have more focused on gut microbial alteration in tuberculosis (TB) patients. However, no detailed study on gut fungi modification has been reported till now. So, current research explores the characteristics of gut microbiota (bacteria)- and mycobiota (fungi)-dysbiosis in TB patients and also assesses the correlation between the gut microbiome and serum cytokines. It may help to screen the potential diagnostic biomarker for TB. Results: The results show that the alpha diversity of the gut microbiome (including bacteria and fungi) decreased and altered the gut microbiome composition of TB patients. The bacterial genera Bacteroides and Prevotella were significantly increased, and Blautia and Bifidobacterium decreased in the TB patients group. The fungi genus Saccharomyces was increased while decreased levels of Aspergillus in TB patients. It indicates that gut microbial equilibrium between bacteria and fungi has been altered in TB patients. The fungal-to-bacterial species ratio was significantly decreased, and the bacterial-fungal trans-kingdom interactions have been reduced in TB patients. A set model including Bacteroides, Blautia, Eubacterium_hallii_group, Apiotrichum, Penicillium, and Saccharomyces may provide a better TB diagnostics option than using single bacterial or fungi sets. Also, gut microbial dysbiosis has a strong correlation with the alteration of IL-17 and IFN-γ. Conclusions: Our results demonstrate that TB patients exhibit the gut bacterial and fungal dysbiosis. In the clinics, some gut microbes may be considered as potential biomarkers for auxiliary TB diagnosis.

Gut microbiota dysbiosis is associated with certain psychiatric disorders through the “microbiota-gut-brain” axis. Here, we revealed that alcohol consumption induced the colonic microbiota dysbiosis, increased intestinal permeability, and altered the serum metabolic phenotype in rats, and there was a strong correlation between gut microbiota dysbiosis and serum metabolite disorders.

Bacteria communicate with their surroundings through diverse secretory systems, and the recently discovered Type VI Secretion System (T6SS) has gained significant attention. Klebsiella pneumoniae (K. pneumoniae), an opportunistic pathogen known for causing severe infections in both hospital and animal settings, possesses this intriguing T6SS. This system equips K. pneumoniae with a formidable armory of protein-based weaponry, enabling the delivery of toxins into neighboring cells, thus granting a substantial competitive advantage. Remarkably, the T6SS has also been associated with K. pneumoniae’s ability to form biofilms and acquire resistance against antibiotics. However, the precise effects of the T6SS on K. pneumoniae’s functions remain inadequately studied, despite research efforts to understand the intricacies of these mechanisms. This comprehensive review aims to provide an overview of the current knowledge regarding the biological functions and regulatory mechanisms of the T6SS in K. pneumoniae.

Chronic alcohol consumption, an important risk factor for diseases and deaths, can cause intestinal microbiota dysbiosis and increase the infection of some opportunistic pathogens. However, the current studies on the effects of alcohol-induced intestinal microbiota dysbiosis on gut colonization of Klebsiella pneumoniae are still scarce. In the present study, we established a binge-on-chronic alcohol model in mice to identify the characteristics of alcohol-induced intestinal microbiome and metabolite dysbiosis using multi-omics and explored the effects and potential mechanisms of these dysbioses on the intestinal colonization of K. pneumoniae . The results show that chronic alcohol consumption alters the diversity and composition of gut microbiota (including bacteria and fungi), decreases the complexity of the interaction between intestinal bacteria and fungi, disturbs the gut metabolites, and promotes the colonization of K. pneumoniae on the gut of mice. The relevance analyses find that alcohol-induced gut microbiome dysbiosis has a strong correlation with the alteration of secondary bile acids. In vitro results suggest that the high concentration of lithocholic acid, a secondary bile acid, could significantly inhibit the proliferation of K. pneumoniae , and the adhesion of K. pneumoniae to Caco-2 cells. Our results indicate that alcohol-induced microbiome dysbiosis contributes to decreased levels of secondary bile acids, which was one of the main reasons affecting the colonization of K. pneumoniae in mice’s intestines. Some secondary bile acids (e.g., lithocholic acid) might be a potential drug to prevent the colonization and spread of K. pneumoniae . IMPORTANCE: Alcohol is one of the most commonly misused substances in our lives. However, long-term heavy drinking will increase the colonization of some opportunistic pathogens (e.g., Klebsiella pneumoniae ) in the body. Here, we revealed that binge-on-chronic alcohol consumption disrupted the balance between gut bacteria and fungi, induced the gut microbiome and metabolites dysbiosis, and promoted the colonization of K. pneumoniae in the intestine of mice. In particular, alcohol-taking disrupted intestinal bile acid metabolism and reduced the lithocholic acid concentration. However, a high concentration of lithocholic acid can protect against intestinal colonization of K. pneumoniae by inhabiting the bacterial growth and adhesion to the host cell. Hence, regulating the balance of gut microbiota and intestinal bile acid metabolism may be a potential strategy for reducing the risk of K. pneumoniae infection and spread.

Alcohol dependence (AD) is a worldwide epidemic of psychiatric disorders. Gut microbiota dysbiosis may be involved in the development of AD. Recently, the number of studies on the relationship between gut microbiota and alcohol is increasing. However, most previous studies were focused on rodent models and gut microbiota, and the data about the alteration of the gut fungi in AD patients were scarce. Convincing evidence of the gut microbiota’s role in the development of AD is lacking. Here, we investigated the characteristics of gut microbiota (bacterial) and mycobiota (fungal) dysbioses in AD patients and assessed the role of the gut microbiome on the behaviors of rats by fecal microbiota transfer, trying to illuminate the possible microbiota mechanism in AD development. We found that AD patients developed gut microbiota dysbiosis, displayed by the fact that the bacterial genus of Ruminococcaceae significantly decreased and that of Lachnospiraceae increased and the fungal genus of Saccharomyces and Kurtzmaniella obviously increased and that of Candida decreased. Alcohol consumption disturbs the gut equilibrium between bacteria and fungi. The fungal-to-bacterial species ratio was significantly decreased, and the bacterial-fungal trans-kingdom interactions were reduced. By transplanting the gut microbiota from AD patients to rats, we confirmed that the microbiota from AD patients induced the behavioral alterations associated with alcohol dependence in rats, including increased anxiety- and depression-like behaviors, reduced exploratory and recognition memory, and higher alcohol preference. Meanwhile, the microbiota from the AD patient donor upregulated the expression levels of cholecystokinin receptors in the frontal lobe, hippocampus, and cortex in rats, which might be involved in the development of alcohol dependence. Our results demonstrate that AD patients developed gut bacterial and fungal microbiota dysbioses and the gut microbiota may be involved in the development of alcohol addiction by regulating the endogenous cholecystokinin and related receptors’ expression. Our data open new avenues for adjuvant treating AD patients via administrating the intestinal microbiota. IMPORTANCE: Intestinal microbiome dysbiosis is associated with psychiatric disease through the “microbiota-gut-brain” axis. Here, we revealed that there was obvious intestinal microbiome (including bacterial and fungal) dysbiosis in alcohol-dependent patients. Alcohol consumption seriously disturbs the gut equilibrium between bacteria and fungi, reduces the interactions among bacterial-fungal trans-kingdom, and increases intestinal permeability. Gut microbiota should be considered as a whole to study the development of alcohol dependence. The gut microbiome of alcohol-dependent patients increased the anxiety- and depression-like behavior in rats. The gut microbiota dysbiosis may promote the development of alcohol dependence by regulating the endogenous cholecystokinin (CCK) and related receptors. Hence, regulating the balance of gut microbiota and the endogenous CCK may be a potential strategy for reducing the risk of relapse in alcohol addiction patients.