Colonization resistance

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Colonization resistance is the mechanism whereby the human microbiome protects itself against incursion by new and often harmful microorganisms. [1] [2]

Colonization resistance was first identified in 1967, and it was initially referred to as antibiotic associated susceptibility. It was observed that animals being treated with the antibiotic streptomycin were susceptible to Salmonella enterica at doses 10,000 fold lower than the standard minimal infectious dose. [3] This led to investigations about the mechanisms utilized by endogenous microbial populations that conferred protection against exogenous pathogens attempting to colonize the gut flora.

It has been observed that colonization resistance can occur within the host in a 'direct' or 'indirect' manner. [4] The former refers to particular components of the microbiota directly competing with exogenous pathogens for nutritional niches (e.g. E. coli directly competes with Citrobacter rodentium for carbohydrates in the intestinal lumen [5] ) or by producing growth inhibitors (e.g. Bacteroides thuringiensis can secrete bacteriocin that directly targets spore-forming Clostridium difficile , thus inhibiting its growth through an unknown mechanism), [6] that directly inhibits the colonizing pathogen. Indirect colonization resistance is thought to be mediated through the induction of immune responses in the host that concomitantly inhibit the colonizing pathogen. An example of this has been observed with B. thetaiotaomicron, which can induce the host to produce antimicrobial C-type lectins REGIIIγ and REGIIIβ, both anti-microbial peptides that target gram-positive bacteria. [7]

Scientists found that gut infections increase its microbiota's resistance to subsequent infections, that taurine is used in as a nutrient to nourish and train the microbiota for this by potentiating its production of sulfide and that the exogenous supply of taurine can induce this microbiota alteration. [8] [9]

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The human microbiome is the aggregate of all microbiota that reside on or within human tissues and biofluids along with the corresponding anatomical sites in which they reside, including the gastrointestinal tract, skin, mammary glands, seminal fluid, uterus, ovarian follicles, lung, saliva, oral mucosa, conjunctiva, and the biliary tract. Types of human microbiota include bacteria, archaea, fungi, protists, and viruses. Though micro-animals can also live on the human body, they are typically excluded from this definition. In the context of genomics, the term human microbiome is sometimes used to refer to the collective genomes of resident microorganisms; however, the term human metagenome has the same meaning.

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<span class="mw-page-title-main">Gut microbiota</span> Community of microorganisms in the gut

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<span class="mw-page-title-main">Fecal microbiota transplant</span> Process of transplantation of fecal bacteria from a healthy individual into a recipient

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<i>Clostridioides difficile</i> Species of bacteria

Clostridioides difficile is a bacterium known for causing serious diarrheal infections, and may also cause colon cancer. It is known also as C. difficile, or C. diff, and is a Gram-positive species of spore-forming bacteria. Clostridioides spp. are anaerobic, motile bacteria, ubiquitous in nature and especially prevalent in soil. Its vegetative cells are rod-shaped, pleomorphic, and occur in pairs or short chains. Under the microscope, they appear as long, irregular cells with a bulge at their terminal ends. Under Gram staining, C. difficile cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen. C. difficile is catalase- and superoxide dismutase-negative, and produces up to three types of toxins: enterotoxin A, cytotoxin B and Clostridioides difficile transferase. Under stress conditions, the bacteria produce spores that are able to tolerate extreme conditions that the active bacteria cannot tolerate.

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<span class="mw-page-title-main">Janelle Ayres</span> American immunologist

Janelle S. Ayres is an American immunologist and microbiologist, member of the NOMIS Center for Immunobiology and Microbial Pathogenesis and Helen McLoraine Developmental Chair at the Salk Institute for Biological Sciences. Her research focuses on the relation of host-pathogen interactions with the microbiome.

Eric P. Skaar is an American microbiologist, the Ernest W. Goodpasture Professor of Pathology, Microbiology and Immunology at Vanderbilt University Medical Center, and a University Distinguished Professor at Vanderbilt University.

Trevor Lawley FMedSci is a Faculty member and Group Leader in the Host-Microbiota Interactions Lab at the Wellcome Sanger Institute (WSI). He is also co-founder and Chief Scientific Officer of the biotech company Microbiotica.

The poultry microbiome is an understudied, yet extremely impactful part of the poultry industry. Poultry is defined as any avian species used for production purposes such as food or down feathers. The United States consumes more poultry, specifically broiler meat, than any other type of protein. Worldwide, poultry makes up 33% of consumed meat. This makes poultry extremely valuable and the impact of the poultry microbiome on health and production even more valuable. Antonie van Leeuwenhoek was the first to notice microbes inside animals through stool samples giving light to further research into the gut microbiome. His discovery lead to the ever evolving study of the microbiota and microbiome. The microbiota is the entirety of living organisms including bacteria, viruses, fungi, and archaea in an environment. The microbiome is the combination of the microbiota and the additional activities in that system including metabolites and chemicals in a habitat. Much of the work done to characterize the poultry microbiome has been accomplished over the past decade and was done through the use of 16s rRNA sequencing.

References

  1. ↑ Wilson, Michael (2005). Microbial inhabitants of humans: their ecology and role in health and disease. Cambridge University Press. ISBN   978-0-521-84158-0.
  2. ↑ Trevor Lawley and Alan Walker, "Intestinal colonization resistance", Immunology , volume 38, pages 1-11, 2013.
  3. ↑ Bohnhoff M, Miller CP (1962). "Enhanced Susceptibility to Salmonella Infection in Streptomycin-Treated Mice". Journal of Infectious Diseases. 111 (2): 117–127. doi:10.1093/infdis/111.2.117. PMID   13968487.(subscription required)
  4. ↑ Buffie CG, Pamer EG (2013). "Microbiota-mediated colonization resistance against intestinal pathogens". Nature Reviews Immunology. 13 (11): 790–801. doi:10.1038/nri3535. PMC   4194195 . PMID   24096337.
  5. ↑ Kamada N, Kim YG, Sham HP, Vallance BA, Puente JL, Martens EC, Núñez G (2012). "Regulated virulence controls the ability of a pathogen to compete with the gut microbiota". Science. 336 (6086): 1325–1329. Bibcode:2012Sci...336.1325K. doi:10.1126/science.1222195. PMC   3439148 . PMID   22582016.
  6. ↑ Rea MC, Sit CS, Clayton E, O'Connor PM, Whittal RM, Zheng J, Vederas JC, Ross RP, Hill C (2010). "Thuricin CD, a posttranslationally modified bacteriocin with a narrow spectrum of activity against Clostridium difficile". Proceedings of the National Academy of Sciences of the United States of America. 107 (20): 9352–9357. doi: 10.1073/pnas.0913554107 . PMC   2889069 . PMID   20435915.
  7. ↑ Cash HL, Whitham CV, Behrendt CL, Hooper LV (25 August 2006). "Symbiotic bacteria direct expression of an intestinal bactericidal lectin". Science. 313 (5790): 1126–1130. Bibcode:2006Sci...313.1126C. doi:10.1126/science.1127119. PMC   2716667 . PMID   16931762.
  8. ↑ "NIH scientists identify nutrient that helps prevent bacterial infection". National Institutes of Health (NIH). 15 January 2021. Retrieved 13 February 2021.
  9. ↑ Stacy, Apollo; Andrade-Oliveira, Vinicius; McCulloch, John A.; Hild, Benedikt; Oh, Ji Hoon; Perez-Chaparro, P. Juliana; Sim, Choon K.; Lim, Ai Ing; Link, Verena M.; Enamorado, Michel; Trinchieri, Giorgio; Segre, Julia A.; Rehermann, Barbara; Belkaid, Yasmine (4 February 2021). "Infection trains the host for microbiota-enhanced resistance to pathogens". Cell. 184 (3): 615–627.e17. doi: 10.1016/j.cell.2020.12.011 . ISSN   0092-8674. PMC   8786454 . PMID   33453153.
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