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Microbiology Research Scope

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.



Single celled organisms that lack membrane-bound organelles; with pathogenic bacteria causing infections and disease
Bacteria- Prokaryotic unicellular forms are defined by their lack of organized membrane-enclosed DNA or nuclei and organelles.

Types of Protozoa including amoebas are either free living or can cause disease
Protozoa- Eukaryotic unicellular organisms include free living and parasitic forms.

Unicellular or Multicellular Acellular

Eukaryotic microorganisms that include yeast and molds. Thermally dimorphic fungi infect humans and other mammals
Fungi- Eukaryotic organisms may be unicellular, as exemplified by yeasts, and includes multicellular forms, represented by molds and dimorphic fungi.

Small parasites, having DNA or RNA, capsid, envelope, and membrane proteins; requiring a host to replicate.
Viruses- Non-cellular particles consistent of genetic material (DNA or RNA) and proteins. Viruses infect cells of multicellular and unicellular organisms which serve as hosts for their replication.

Microbial Diseases

Medical 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).

Learn About PAMPs and DAMPs

Microbial Virulence

Microbial 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.

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.

Specificity of Francisella Tularensis LPS Antibody (FB11) [NB110-7999]. Inactivated F. tularensis SCHU S4 (lane 1), SCHU S4 deltawbtI (lacks O-antigen, lane 2), LVS (lane 3), F. tularensis subsp. holarctica (lane 4), subsp. novicida (lane 5), F. philomiragia (lane 6), purified B. pseudomallei LPS (lane 7) and E. coli LPS (lane 8) were separated on 12% SDS-PAGE gels and blotted onto nitrocellulose membranes. The membranes then were probed with mAb FB11. Image collected and cropped by CiteAb from the following publication (//, licensed under a CC-BY licence.

Titration of the recombinant toxin B (TcdB) protein detected by Western Blot

Clostridium difficile toxin B (TcdB) is one of the main exotoxins produced by C. difficile which induces cytotoxicity through the inactivation of GTP binding proteins (Rho, Rac, and Cdc42). Western blot analysis of recombinant C. difficile Toxin B/TcdB (6246-GT). PVDF membrane was probed with 1 µg/mL of Sheep Polyclonal Antibody to C. difficile Toxin B/TcdB Antigen (AF6246) followed by HRP-conjugated Anti-Sheep IgG Secondary Antibody (HAF016). A specific band was detected for Toxin B/TcdB at approximately 75 kDa.

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.


Virus Immunomodulating Protein Immune Evasion Mechanism


Cytokine response modifier (CRMB)

Soluble tumor necrosis factor receptor (TNFR) homologue, binds to chemokines preventing immune cell recruitment.

Hepatitis C Virus (HCV)

Nonstructural protein 3 (NS3)

Serine protease, targets the mitochondrial antiviral signaling protein (MAVS) to inhibit IFN-beta production.

Herpes Simplex Virus (HSV)

UL36 ubiquitin-specific protease (UL36USP)


Kinase US3

Tegument protein with deubiquitinase activity, inhibits INF-beta production.

Inhibits production of IFN thorough TBK1 sequestration.

Serine/threonine kinase, reduces activation of type I IFN.

Human Microbiota

The 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.


Human Gut Microbiota Composition

Predominant phyla

Minor phyla


Liver Disease
Metabolic Syndrome

The human gut microbiota is implicated in the modulation of a wide range of physiological processes including digestion (e.g., processing of indigestible substrates), metabolism (e.g., glucose and lipid homeostasis), immunity (e.g., pathogen exclusion), development (e.g., neuronal, epithelial and immune cells).

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.

A poor diet and/or antibiotic use leads to dysbiosis and results in abnormal metabolite levels, increased LPS, reduced tight junction integrity and short chain fatty acids, interference with glucose homeostasis and causes inflammation.

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

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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.

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) virusProceedings of the National Academy of Sciences of the United States of America103(15), 5995–6000.

Wang, B., Yao, M., Lv, L., Ling, Z., & Li, L. (2017). The Human Microbiota in Health and Disease. Engineering.


Dabke, K., Hendrick, G., & Devkota, S. (2019). The gut microbiome and metabolic syndrome. Journal of Clinical Investigation.

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.

Mogensen, T. H. (2009). Pathogen recognition and inflammatory signaling in innate immune defenses. Clinical Microbiology Reviews.

Su, C., Zhan, G., & Zheng, C. (2016). Evasion of host antiviral innate immunity by HSV-1, an updateVirology journal13, 38.