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Microbiology Research Scope |
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Microbiology research encompasses the study of all microscopic entities including unicellular and multicellular life forms, and non-cellular or acellular particles. When microbes form symbiotic relationships with hosts, either both species benefit from the host-microbe interaction, classified as mutualism, or is described as commensalism where only one species benefits. Conversely in parasitism one species, the parasite, benefits at the expense of the other, the host, often resulting in an infection and/or disease.
Microbial DiseasesMedical microbiology focuses on pathogenic microbes, which represent about 1% or less of all microorganisms. Microbiology as an area of research is closely intertwined with immunology, particularly in the study of host-pathogen interactions in infectious diseases. Microbial pathogen structures commonly referred to as pathogen-associated molecular patterns (PAMPs) are first recognized by cells of the innate immune system through a broad range of pattern recognition receptors (PRRs). Microbial VirulenceMicrobial pathogens induce tissue damage by their unique invasive phenotypes and virulence factors. Bacteria produce endotoxins (e.g., lipopolysaccharide or LPS) and exotoxins (e.g., Botulinum toxin and Clostridium difficile toxin A and B). LPS is a predominant component of the Gram-negative bacterial outer membrane containing a toxic lipid component, Lipid A, which triggers a generalized inflammatory response. In contrast, exotoxins are proteins produced predominantly by Gram-positive bacteria that act upon specific cellular receptors leading to cell damage.
Virus virulence determinants are encoded by both structural and non-structural proteins. Virulence factors act through different mechanisms to modulate virus-host interactions, including the regulation of viral replication, attachment, cell entry, and transmissibility. Additionally, virulence factors may modulate the host’s immune system allowing viruses to remain undetected. This is best exemplified by the immune-modulating factors produced by large DNA viruses such as poxviruses and herpes viruses which either inhibit or mimic host’s cytokines, chemokines, and proteases.
Human MicrobiotaThe human microbiota is expansive, consisting of trillions of microorganisms inhabiting different organs and tissues throughout our bodies. By definition, the genes associated with the community of microbes (bacteria, virus, fungi and more) inhabiting symbiotically the human body, conform the microbiome. Among human organs, the gastrointestinal tract and gut mucosa represent the most populated niche for microbiota-host interactions. The gastrointestinal tract is primarily populated by Firmicutes and Bacteroidetes species. The microbiota, through interactions with the gut epithelium, is implicated in the regulation of metabolic processes and immune responses.
Microbial activity in the gut generates a wide range of metabolites including indoles, folate, secondary bile acids and neurotransmitters such as serotonin and GABA. Microbiota derived metabolites such as short chain fatty acids (e.g., acetic, propionic and butyric acid), interact with cellular receptors in the gut epithelium inducing the release of peptides involved in glucose metabolism.
Gut microbiota dysbiosis, resulting from poor diet (high-fat and low-fiber) and/or antibiotic use, is associated with abnormal metabolite levels, increased LPS, and decreased tight junction integrity. Reduced tight junction integrity, allows LPS leakage across the gut epithelial barrier, which contributes to chronic inflammation of the liver and adipose tissue. Additionally, dysbiosis is associated with reduced levels of short chain fatty acids, which normally interact with G-protein coupled receptors such as GPR-41 in the gut epithelium to promote the release of glucagon-like peptide-1 (GLP1). Reduced release of GLP1 by enteroendocrine L cells, disrupts glucose homeostasis and promotes inflammation. Diagram from Metabolic Syndrome Signaling Poster , published in its original form in a collaborative between Dr. Robert H. Lustig, Dr. Alejandro Gugliucci and Bio-Techne Corporation Read Our Blogs on Microbiology Topics Select References A., R., M.J., K., F., V., G.P., T., & M.R., H. (2014). Clostridium difficile infection: Molecular pathogenesis and novel therapeutics. Expert Review of Anti-Infective Therapy. https://doi.org/10.1586/14787210.2014.866515 Alejo, A., Ruiz-Argüello, M. B., Ho, Y., Smith, V. P., Saraiva, M., & Alcami, A. (2006). A chemokine-binding domain in the tumor necrosis factor receptor from variola (smallpox) virus. Proceedings of the National Academy of Sciences of the United States of America, 103(15), 5995–6000. https://doi.org/10.1073/pnas.0510462103 Wang, B., Yao, M., Lv, L., Ling, Z., & Li, L. (2017). The Human Microbiota in Health and Disease. Engineering. https://doi.org/10.1016/J.ENG.2017.01.008 Cryan, J. (2018). 37. THE GUT MICROBIOME: A KEY REGULATOR OF NEURODEVELOPMENT AND BEHAVIOUR. Schizophrenia Bulletin. https://doi.org/10.1093/schbul/sby014.152 Dabke, K., Hendrick, G., & Devkota, S. (2019). The gut microbiome and metabolic syndrome. Journal of Clinical Investigation. https://doi.org/10.1172/JCI129194 Farhana, A., & Khan, Y. S. (2020). Biochemistry, Lipopolysaccharide. In StatPearls. Freundt, E. C., & Lenardo, M. J. (2005). Interfering with interferons: Hepatitis C virus counters innate immunity. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.0509221102 Mogensen, T. H. (2009). Pathogen recognition and inflammatory signaling in innate immune defenses. Clinical Microbiology Reviews. https://doi.org/10.1128/CMR.00046-08 Su, C., Zhan, G., & Zheng, C. (2016). Evasion of host antiviral innate immunity by HSV-1, an update. Virology journal, 13, 38. https://doi.org/10.1186/s12985-016-0495-5 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4782282/ |
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![Specificity of the F. Tularensis LPS Antibody (FB11) [NB110-7999] was evaluated by testing various bacterial strains and results show that mAb FB11 recognizes the O-antigen moiety of LPS.](https://images.novusbio.com/design/francisella-tularensis-lps-antibody-250px.jpg "Francisella Tularensisurase LPS Western Blot")
