Human gut-microbiome explorations have enriched our understanding of microbial colonization, maturation, and dysbiosis in health-and-disease subsets. The enormous metabolic potential of gut microbes and their role in the maintenance of human health is emerging, with new avenues to use them as therapeutic agents to overcome human disorders. Microbiome therapeutics are aimed at engineering the gut microbiome using additive, subtractive, or modulatory therapy with an application of native or engineered microbes, antibiotics, bacteriophages, and bacteriocins. This approach could overcome the limitation of conventional therapeutics by providing personalized, harmonized, reliable, and sustainable treatment. Its huge economic potential has been shown in the global therapeutics market. Despite the therapeutic and economical potential, microbiome therapeutics is still in the developing stage and is facing various technical and administrative issues that require research attention. This review aims to address the current knowledge and landscape of microbiome therapeutics, provides an overview of existing health-and-disease applications, and discusses the potential future directions of microbiome modulations.

Osmotolerance is one of the critical factors for successful survival and colonization of microbes in saline environments. Nonetheless, information about these osmotolerance mechanisms is still inadequate. Exploration of the saline soil microbiome for its community structure and novel genetic elements is likely to provide information on the mechanisms involved in osmoadaptation. The present study explores the saline soil microbiome for its native structure and novel genetic elements involved in osmoadaptation. 16S rRNA gene sequence analysis has indicated the dominance of halophilic/halotolerant phylotypes affiliated to Proteobacteria, Actinobacteria, Gemmatimonadetes, Bacteroidetes, Firmicutes, and Acidobacteria. A functional metagenomics approach led to the identification of osmotolerant clones SSR1, SSR4, SSR6, SSR2 harboring BCAA_ABCtp, GSDH, STK_Pknb, and duf3445 genes. Furthermore, transposon mutagenesis, genetic, physiological and functional studies in close association has confirmed the role of these genes in osmotolerance. Enhancement in host osmotolerance possibly though the cytosolic accumulation of amino acids, reducing equivalents and osmolytes involving BCAA-ABCtp, GSDH, and STKc_PknB. Decoding of the genetic elements prevalent within these microbes can be exploited either as such for ameliorating soils or their genetically modified forms can assist crops to resist and survive in saline environment.

The human gut microbiome is a stratified and resilient ecosystem co-inhabited by a diverse and dynamic pool of microorganisms. Microbial selection, establishment, and colonization are modulated through a complex molecular network of host-microbial interactions. These molecular bioprocesses ensure the taxonomic composition of the mature human gut microbiome. The human gut microbiome plays a vital role in host health; otherwise, any microbial dysbiosis could predispose to the onset of physiological and metabolic disorder/s. Focussed research are being carried out to identify key molecular agents defining gut homeostasis. These molecules hold the potential to develop effective therapeutic solutions for microbial dysbiosis-associated human disorders. Of these, Hypoxia-inducible factor-1α (HIF-1α) is a central player in host-microbial crosstalk to maintain gut homeostasis. Human gut microbial metabolites regulate its cellular stability, which in turn regulates various cellular processes required for the stable gut microbiome. In the present review, an effort has been made to summarize the key role of HIF-1α to maintain gut homeostasis. - Explain the molecular process of host microbial molecular interactions. - Establish the explicit role of HIF-1α in intestinal epithelial integrity and gut health. - Regulation of HIF-1α by human gut commensals and vice a versa. - Regulation of the host immune response for survival and colonization of human gut commensal.

Studying respiratory illness-specific microbial signatures and their interaction with other micro-residents could provide a better understanding of lung microbial ecology. Each respiratory illness has a specific disease etiology, however, so far no study has revealed disease—specific microbial markers. The present study was designed to determine disease-specific microbial features and their interactions with other residents in chronic obstructive pulmonary diseases (stable and exacerbated), sarcoidosis, and interstitial lung diseases. Broncho-alveolar lavage samples (n = 43) were analyzed by SSU rRNA gene sequencing to study the alveolar microbiome in these diseases. A predominance of Proteobacteria followed by Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria was observed in all the disease subsets. Shannon diversity was significantly higher in stable COPD when compared to exacerbated chronic obstructive pulmonary disease (ECOPD) (p = 0.0061), and ILD patient samples (p = 0.037). The lung microbiome of the patients with stable COPD was more diverse in comparison to ECOPD and ILD patients (p < 0.001). Lefse analysis identified 40 disease—differentiating microbial features (LDA score (log10) > 4). Species network analysis indicated a significant correlation (p < 0.05) of diseases specific microbial signature with other lung microbiome members. The current study strengthens the proposed hypothesis that each respiratory illness has unique microbial signatures. These microbial signatures could be used as diagnostic markers to differentiate among various respiratory illnesses.