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Baral, B.

Publications and source records attributed to Baral, B..

5 recordsLinked to original sources

Efficient colonic colonization by Campylobacter jejuni requires the heme receptor ChuA

Previous research demonstrated that Campylobacter jejuni encodes a heme utilization system that facilitates heme-dependent growth under iron-limiting conditions and that transcription of this system is induced during human infection. Despite these observations, it remained unknown whether the heme transport system is required for colonization and disease in a susceptible host. To address this, we created individual non-polar deletion mutants of each component of the heme transport system and examined their ability to promote heme-dependent growth and iron uptake. From this work, we found that only the heme receptor, ChuA, was required for heme-dependent growth and iron acquisition, which supports the earlier work of another group. Further, we examined whether intestinal colonization, immune activation, and pathology were altered during infection with these mutants. After establishing that elevated heme and chuABCD expression occur during C. jejuni infection of IL-10-/- mice, we found that a mutant of the heme receptor, ChuA, exhibited significantly reduced colonization of the colon. In addition, we found that neutrophil and circulating monocyte recruitment were significantly reduced in the colon during infection with the ChuA mutant, but that populations of self-maintaining tissue macrophages remained high. Loss of ChuA reduced colonic colonization and was accompanied by diminished innate immune cell recruitment and intestinal pathology. Together, these findings identify ChuA-dependent heme acquisition as a key determinant of efficient colonic colonization and the associated inflammatory disease.

microbiology↗

Niche-specific metabolic signatures in non-typeable Haemophilus influenzae

Non-typeable Haemophilus influenzae (NTHi) is a prominent opportunistic pathogen relevant to chronic respiratory diseases. NTHis metabolic diversity enables its survival in a wide range of environmental conditions within the host. As such, deeper research into the metabolic pathways of NTHi may open an avenue for novel therapies aimed at combating NTHi-associated respiratory diseases. Draft genome sequences from nine NTHi clinical strains from three isolation sites - ear (ear sample, ES), pharynx (pharynx sample, PS), and lower respiratory tract (Lungs) - were analyzed and annotated using RAST, PROKKA, KEGG KAAS, and antiSMASH. Pathway module coverage per-strain was computed and summarized by per-group for significant annotated metabolites. Metabolites were analyzed by LC/HRMS, identified by Metaboscape, and statistically compared using MetaboAnalyst and R software. Gene content across the tested NTHi strains was largely conserved, with limited core-genome SNP variation. Gene annotation for metabolite-related pathways revealed that all nine strains possessed largely similar sets of metabolic pathway genes, despite minor nucleotide-level differences, indicating broadly comparable metabolic capacities. In contrast, metabolomics data revealed differential metabolic profiles among the body-site groups. In a principal component analysis (PCA), the ES group was significantly separated from both the PS and Lung groups, which overlapped considerably. Detailed metabolite analyses showed that inosine, hypoxanthine, and uracil were highly significant in the ES group compared to the PS and Lung groups. For the first time, our study sheds light on the extent of metabolic differences associated with NTHi inhabiting diverse host niches. The observed metabolic differences suggest that NTHi may modulate its metabolism in a site-specific manner that is affected by environmental factors. These findings add to our understanding of how NTHi metabolism contributes to site-specific colonization. Author summaryHaemophilus influenzae is widely recognized as a causative agent of meningitis and pneumonia. In particular, H. influenzae strains with a polysaccharide capsule--known as H. influenzae type b (Hib)--were historically a major cause of invasive disease. However, Hib has been largely eradicated following implementation of the Hib vaccine. Nonetheless, there are H. influenzae strains that lack this capsule and are therefore not targeted by the vaccine. These are known as non-typeable H. influenzae (NTHi). Following the decline of Hib, NTHi has rapidly occupied the ecological niche in the lower respiratory tract, becoming the most prominent pathogen in patients with chronic respiratory infections--particularly in those with chronic obstructive pulmonary disease (COPD), where it frequently triggers exacerbations. Importantly, NTHi is also a common component of the normal microbiome in healthy individuals, typically residing in the upper respiratory tract without causing disease. In our study, we investigated the metabolic characteristics of NTHi isolates obtained from different body sites in patients to better understand what distinguishes strains capable of colonizing specific anatomical niches. We successfully identified several distinct metabolic features associated with NTHi strains from the ear, pharynx, and lung. These findings may serve as a foundation for future research into patient-tailored biomarkers and targeted therapies, ultimately aiming to eradicate NTHi in chronic lung infections.

microbiology↗

Epstein-Barr virus and Helicobacter pylori Coinfection Drives Gut and Brain Barrier Dysfunction

Biological barriers, including blood-brain barrier (BBB) and gut epithelial barrier, are essential to maintain homeostasis and provide protection against pathogenic stress. Here, we investigated the impact of Helicobacter pylori-Epstein Barr Virus coinfection on gut-brain axis integrity. Our results demonstrate that coinfection induces significant disruptions in tight and adherens junction (TJ and AJ respectively) proteins in gastric epithelial cells, including downregulation of ZO-1 and E-cadherin. The secretome from these coinfected cells significantly compromises the integrity of BBB-derived endothelial cells, including cleavage of VE-cadherin, loss of TJ proteins such as Claudin-5, and enhanced permeability. Furthermore, the sole exposure of mice to coinfected secretome lead to the loss of cerebral VE-cadherin and ZO-1 and the induction of neuroinflammation, characterized by elevated pro-inflammatory cytokines, TNF-, amyloidogenic accumulation, and neurocognitive deficits. The secretome driving such forces potentially carries pathogenic metabolites, host inflammatory cytokines and metabolites that might contribute to disease pathogenesis as observed in this study. Together, our current study provides novel insights into how coinfections contribute to gut-brain axis dysregulation and neurological pathogenesis. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=174 SRC="FIGDIR/small/655045v1_ufig1.gif" ALT="Figure 1"> View larger version (51K): org.highwire.dtl.DTLVardef@138ca23org.highwire.dtl.DTLVardef@15eccc4org.highwire.dtl.DTLVardef@d588c6org.highwire.dtl.DTLVardef@106a485_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG

microbiology↗

Single cell mutant selection for metabolic engineering of actinomycetes

Actinomycetes are important producers of pharmaceuticals and industrial enzymes. However, wild type strains require laborious development prior to industrial usage. Here we present a generally applicable reporter-guided metabolic engineering tool based on random mutagenesis, selective pressure, and single-cell sorting. We developed fluorescence-activated cell sorting (FACS) methodology capable of reproducibly identifying high-performing individual cells from a mutant population directly from liquid cultures. Genome-mining based drug discovery is a promising source of bioactive compounds, which is complicated by the observation that target metabolic pathways may be silent under laboratory conditions. We demonstrate our technology for drug discovery by activating a silent mutaxanthene metabolic pathway in Amycolatopsis. We apply the method for industrial strain development and increase mutaxanthene yields 9-fold to 99 mg l-1 in a second round of mutant selection. Actinomycetes are an important source of catabolic enzymes, where product yields determine industrial viability. We demonstrate 5-fold yield improvement with an industrial cholesterol oxidase ChoD producer Streptomyces lavendulae to 20.4 U g-1 in three rounds. Strain development is traditionally followed by production medium optimization, which is a time-consuming multi-parameter problem that may require hard to source ingredients. Ultra-high throughput screening allowed us to circumvent medium optimization and we identified high ChoD yield production strains directly from mutant libraries grown under preset culture conditions. In summary, the ability to screen tens of millions of mutants in a single cell format offers broad applicability for metabolic engineering of actinomycetes for activation of silent metabolic pathways and to increase yields of proteins and natural products.

bioengineering↗

Helicobacter pylori and Epstein-Barr virus coinfection stimulates the aggressiveness in gastric cancer through the regulation of gankyrin

Persistent coinfection of Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV) promotes aggressive gastric carcinoma. The molecular mechanisms underlying the aggressiveness in H. pylori and EBV coinfected gastric cancer is not well characterized. In the current study, we investigated the molecular mechanism involved in the cooperation of H. pylori and EBV-driven proliferation of gastric epithelial cells. Results showed that the coinfections are significantly more advantageous to the pathogens to create a microenvironment that favors the higher pathogen-associated gene expression. The EBV latent genes EBNA1 and EBNA3C are highly overexpressed in the coinfections compared to individual EBV infection at different time points (12 and 24 hrs). The H. pylori-associated genes 16s rRNA, CagA, and BabA has also been highly overexpressed in coinfections compared to H. pylori alone. Gankyrin is a small protein of 25 KDa involved in multiple biological and physiological processes. The upregulation of gankyrin modulates the various cell signaling pathways, leading to oncogenesis. The gankyrin shows a similar expression pattern as EBNA3C at both transcript and protein levels, suggesting a possible correlation. Further EBV and H. pylori create microenvironments that induce cell transformation and oncogenesis by dysregulation of the cell-cycle regulator, GC marker, cell migration, DNA response, and antiapoptotic genes in infected gastric epithelial cells by enhancing the expression of gankyrin. Our study provides new insights into the molecular mechanism where the interplay between two oncogenic agents (H. pylori and EBV) leads to the enhanced carcinogenic activity of gastric epithelial cells through overexpression of oncoprotein gankyrin. ImportanceIn the present study, we have evaluated the synergistic effect of EBV and H. pylori infection on gastric epithelial cells in various coinfection models. These coinfection models depict the first exposures of gastric epithelial cells with EBV and then the H. pylori. While other coinfection models narrated the first exposures of H. pylori followed by the infection of EBV. This led to an enhanced oncogenic phenotype in gastric epithelial cells. We determined the coinfection of EBV and H. pylori enhanced the expression of oncogenic protein gankyrin. The interplay between EBV and H. pylori promotes the oncogenic properties of AGS cells through the newly discovered oncoprotein gankyrin. EBV and H. pylori mediated upregulation of gankyrin further dysregulates various cancer-associated hallmarks of genes such as cell-migratory, gastric cancer marker, tumor suppressor, DNA damage response, and proapoptotic genes.

microbiology↗