You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1 Heather Armstrong + 3055 word(s) 3055 2021-02-25 08:02:33 |
2 update layout and reference Rita Xu -1595 word(s) 1460 2021-03-05 05:33:30 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Armstrong, H. Diet, Microbes, and Metabolites. Encyclopedia. Available online: https://encyclopedia.pub/entry/7755 (accessed on 16 December 2025).
Armstrong H. Diet, Microbes, and Metabolites. Encyclopedia. Available at: https://encyclopedia.pub/entry/7755. Accessed December 16, 2025.
Armstrong, Heather. "Diet, Microbes, and Metabolites" Encyclopedia, https://encyclopedia.pub/entry/7755 (accessed December 16, 2025).
Armstrong, H. (2021, March 04). Diet, Microbes, and Metabolites. In Encyclopedia. https://encyclopedia.pub/entry/7755
Armstrong, Heather. "Diet, Microbes, and Metabolites." Encyclopedia. Web. 04 March, 2021.
Diet, Microbes, and Metabolites
Edit
This entry is adapted from the peer-reviewed paper 10.3390/cancers13040767

Many studies performed to date have implicated select microbes and dietary factors in a variety of cancers, yet the complexity of both these diseases and the relationship between these factors has limited the ability to translate findings into therapies and preventative guidelines.

cancer diet nutrition microbes misconceptions risk factors

1. Introduction

Although cancer development is known to be complex and related, in many cases, to a diverse array of factors (genetic and environmental), with well-described impacts of longitudinal exposures, there are still critical gaps in the knowledge of what some of these exposures are and how they impact cancer biology. Diet has long been considered a critical and, importantly, modifiable factor in many different biological processes, including cancer. Recent advances in measuring dietary intake and its effect on biological processes (e.g., using metabolomics), and especially the interaction between diet and gut microbes, have opened the way to a myriad of papers implicating diet, the gut microbiome, and related metabolites in the pathogenesis, course, and response to therapy of major cancers. A better definition of how diet is related to cancer biology is especially attractive, as diet is rarely utilized in cancer therapy or prevention and it can provide a safe alternative for intervention in a variety of other chronic conditions [1][2][3][4][5]. However, the potential for diet to affect cancer development and progression remains to be fully elucidated. We focus on diet−microbiome interactions in this setting, as not only do dietary factors and nutrition have profound effects on the health of host cells, but they also affect the human microbiome [6], which in turn is closely linked to cancer.

These observations are especially relevant to the gut: emerging evidence continues to demonstrate that nutritional states directly drive intestinal adaptation, resulting in altered signaling mechanisms within adult intestinal stem cells relevant to intestinal tumour formation [7][8][9][10]. Some correlations to chronic conditions, such as inflammatory diseases, may help inspire future research. The link between inflammation and concomitant tumour development in cancers was first suggested by Virchow in 1863 [11][12], and today roughly 20% of cancers are thought to directly result from chronic inflammation [13]. Likely one of the most well studied examples to date is the link between inflammatory bowel diseases (IBD) and colorectal cancer (CRC) [14][15][16][17]. Notably, select dietary factors including saturated fats, red meat, and refined carbohydrates have been suggested to display pro-inflammatory properties and diet has been shown to play a key role in up to 40% of all cancers [18][19][20][21]. These dietary factors are further involved in modulating the gut microbiome, which in turn is involved in regulating both gut physiology and immune response [22][23][24]. This model of IBD−CRC has further demonstrated the critical role of microbes in inflammatory pathways due to their ability to modulate inflammatory cytokines (e.g., tumour necrosis factor (TNF), interleukin (IL)-1, IL-6), which are similarly dysregulated in both IBD and CRC [25][26][27][28]. While dietary factors have clear effects on organs of the intestinal tract, absorption of these factors results in systemic effects on a number of organ systems, which have been implicated in the progression of a variety of cancers, as detailed in later sections (Figure 1).

Figure 1. Cancer promoting and preventative interactions of dietary factors and organ systems. Intake of dietary factors, as demonstrated only by more recent research studies, can affect cancer progression through positive (green) or negative (red) effects on organ systems, as indicated. Details are further highlighted in Table 1.

2. Impact of Select Dietary Factors on Cancer Biology

While diet is considered an environmental exposure, it is difficult to measure accurately in humans for several reasons. In contrast to cigarette smoking, for example, which can be expressed as pack-years, food contains thousands of molecules, is not easily quantified, varies geographically, and humans are notoriously inaccurate in reporting consumption [29]. Although it would probably be best to define dietary exposures using food patterns [30], most current research has focused on specific nutrients. A series of recent review articles highlighting the studies examining cancer in relation to specific dietary patterns labelled Mediterranean [31], Western, Ketogenic [32], or other such common dietary patterns [33], demonstrate that the nutrients or food groups that are specific to these diets appear to underscore potential mechanisms behind the positive or negative effects correlated with these diets. This section will present some examples of links between these specific nutrients and cancer (Figure 1).

2.1. Protective Effects of Vitamins

Vitamins A, C, and D have been demonstrated to play an anticarcinogenic role in a range of studies [34]. A recent meta-analysis of random controlled trials concluded that Vitamin D significantly reduced mortality (13%) but did not have an impact on cancer incidence, with the exception of colorectal and ovarian cancers [35]. Furthermore, vitamin A has been shown to play a significant role in cell proliferation and differentiation [36] and studies demonstrate an inverse relationship between vitamin A and bladder, colorectal, and liver cancers [37][38][39]. These studies suggest that the effects of vitamins may occur through enhanced DNA repair, antioxidant effects, or immunomodulation of host cells [40][41]. The in-depth role of vitamins has previously been well reported in relation to cancer [42][43].

2.2. Sodium and Potassium

Sodium and potassium have long been thought to play a role in the development of cancer as, for example, patients with decreased potassium levels, or hypokalemia (<3.5mmol/L), associated with cell aging, obesity, alcoholism, and stress, display increased rates of cancer; in contrast patients with hyperkalemia (>5.3 mmol/L) and diseases associated with increased potassium levels, such as Parkinson and Addison disease, display reduced cancer rates [34]. The concentrations of sodium and potassium also interestingly play a role in regulating the effects of calcium, resulting in a series of varied results in studies investigating the tumorigenicity of calcium [34]. Furthermore, almost 50% of cancer patients have been shown to display hyponatremia (<135 mmol/L sodium), although this may also be secondary to the cancer itself [44].

2.3. Food Preservatives Linked to Cancer

The sodium salt of propionic acid, sodium propionate, is often used as a food preservative in bakery products and has been shown to exert an antitumour effect through the mitogen-associated protein kinase (MAPK) signalling pathway in breast cancer xenograft models. [45] This example illustrates the complexity between food preservatives, microbes, and cancer, as most are observed to be negatively associated. Nitrates have also been well-described to be associated with colorectal cancer [46], while sorbate and benzoate correlate with the occurrence of breast cancer [47]. Processed foods and the use of food preservatives have dramatically increased over the last few decades and many have attempted to link this with increases in cancer [48]. Food preservatives are a diverse group of ingredients and therefore we have decided to only highlight a few in this review. Most studies focus on negative associations between preservatives and cancer, but to balance the literature, we choose to describe here some studies that display protective effects.

2.4. Not All Additives Are Bad: Potentially Beneficial Chemical Food Components

Capsaicin has long been thought to display anti-inflammatory, antioxidant, anti-proliferative, metabolic, and cardioprotective effects and, interestingly, has been shown to affect microbes within the gut too [49]. Decursin, an extract from the Angelica gigas root, has been shown to display potent anticancer activity in cell line models of lung and colon cancer, along with Lewis lung carcinoma allograft mouse models of tumour growth [50]. A recent study has shown the capacity of decursin to promote HIF-1α degradation within the proteasome, therefore improving T cell activation and antitumour effects within the tumour microenvironment [50].

A subset of dietary fibres, collectively known as β-glucans, are found in a variety of food groups, from mushrooms and other fungi, to wheat, oats, and barley. Interestingly, raw and roasted barley rich in β-glucan has been shown to provide chemoprotective effects via inhibition of growth and promotion of apoptotic pathways [51]. Similar studies examining the effects of raw and roasted oat flakes, following fermentation with human fecal microbes, demonstrated that the fermentation supernatants, with reduce pH and increased butyrate, significantly decreased growth and increased apoptosis of colon adenoma cells [52]. These findings suggest that food products, mostly made of specific grain β-glucans, harbour chemoprotective potential.

The flower buds of adaptogenic plants, typically found in Chinese traditional medicines, including Gardenia jasminoides, Sophorae japonica, and Lonicerae japonicae, demonstrated a significant effect on reducing polyp burden, along with lowering expression of oncogenic signaling molecules in mice [53]. These changes were associated with a reduction in pathobiont microbes including Helicobacter pylori, along with an increase in beneficial microbes, including the key short chain fatty acid (SCFA) producers, Akkermansia, Barnesiella, Coprococcus, Lachnoclostridium, and Ruminococcus [53]. A diet high in seaweed has been linked with promotion of Bacteroides plebeius, which is involved in the breakdown of the seaweed Sargassum wightii to polysaccharides (SWP1 and SWP2); this significantly reduces cell proliferation and induces apoptosis in human breast cancer cell lines [54][55]. Seaweeds’ health benefits have been associated with the polyphenols, polysaccharides, sterols, and bioactive molecules that have been shown to play a role in anti-inflammatory and anticancer effects [56].

References

  1. Grammatikopoulou, M.G.; Goulis, D.G.; Gkiouras, K.; Nigdelis, M.P.; Papageorgiou, S.T.; Papamitsou, T.; Forbes, A.; Bogdanos, D.P. Low FODMAP Diet for Functional Gastrointestinal Symptoms in Quiescent Inflammatory Bowel Disease: A Systematic Review of Randomized Controlled Trials. Nutrients 2020, 12, 3648.
  2. Anupama, P.H.; Prasad, N.; Nzana, V.B.; Tiwari, J.P.; Mathew, M.; Abraham, G. Dietary Management in Slowing Down the Progression of CKDu. Indian J. Nephrol. 2020, 30, 256–260.
  3. Rubio, C.; Luna, R.; Rosiles, A.; Rubio-Osornio, M. Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Wnt Pathway and KATP Channels. Neurol. 2020, 11, 584298.
  4. McAuliffe, S.; Ray, S.; Fallon, E.; Bradfield, J.; Eden, T.; Kohlmeier, M. Dietary micronutrients in the wake of COVID-19: An appraisal of evidence with a focus on high-risk groups and preventative healthcare. BMJ Nutr. Prev. Health 2020, 3, 93–99.
  5. Lombardi, R.; Iuculano, F.; Pallini, G.; Fargion, S.; Fracanzani, A.L. Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease. J. Mol. Sci. 2020, 21, 8761.
  6. Armstrong, H.; Bording-Jorgensen, M.; Dijk, S.; Wine, E. The Complex Interplay between Chronic Inflammation, the Microbiome, and Cancer: Understanding Disease Progression and What We Can Do to Prevent It. Cancers (Basel) 2018, 10, 83.
  7. Alonso, S.; Yilmaz, O.H. Nutritional Regulation of Intestinal Stem Cells. Rev. Nutr. 2018, 38, 273–301.
  8. Cangelosi, A.L.; Yilmaz, O.H. High fat diet and stem cells: Linking diet to intestinal tumor formation. Cell Cycle 2016, 15, 1657–1658.
  9. Calibasi-Kocal, G.; Mashinchian, O.; Basbinar, Y.; Ellidokuz, E.; Cheng, C.-W.; Yilmaz, OH. Nutritional Control of Intestinal Stem Cells in Homeostasis and Tumorigenesis. Trends Endocrinol. Metab. 2020, 32, 30221–30226.
  10. Hou, Y.; Wei, W.; Guan, X.; Liu, Y.; Bian, G.; He, D.; Fan, Q.; Cai, X.; Zhang, Y.; Wang, G.; et al. A diet-microbial metabolism feedforward loop modulates intestinal stem cell renewal in the stressed gut. Commun. 2021, 12, 271.
  11. Balkwill, F.; Mantovani, A. Inflammation and cancer: Back to Virchow? Lancet 2001, 357, 539–545.
  12. Schmidt, A.; Weber, O.F. In memoriam of Rudolf virchow: A historical retrospective including aspects of inflammation, infection and neoplasia. Microbiol. 2006, 13, 1–15.
  13. Siegel, R.L.; Miller, K.D.; Jemal, A. Cancer statistics, 2016. CA Cancer J. Clin. 2016, 66, 7–30.
  14. Yi, M.; Xu, J.; Liu, P.; Chang, G.J.; Du, X.L.; Hu, C.Y.; Song, Y.; He, J.; Ren, Y.; Wei, Y.; et al. Comparative analysis of lifestyle factors, screening test use, and clinicopathologic features in association with survival among Asian Americans with colorectal cancer. J. Cancer 2013, 108, 1508–1514.
  15. Tung, J.; Politis, C.E.; Chadder, J.; Han, J.; Niu, J.; Fung, S.; Rahal, R.; Earle, C.C. The north-south and east-west gradient in colorectal cancer risk: A look at the distribution of modifiable risk factors and incidence across Canada. Oncol. 2018, 25, 231–235.
  16. Patel, P.; De, P. Trends in colorectal cancer incidence and related lifestyle risk factors in 15-49-year-olds in Canada, 1969–2010. Cancer Epidemiol. 2016, 42, 90–100.
  17. Wang, X.; Chan, A.T.; Slattery, M.L.; Chang-Claude, J.; Potter, J.D.; Gallinger, S.; Caan, B.; Lampe, J.W.; Newcomb, P.A.; Zubair, N.; et al. Influence of Smoking, Body Mass Index, and Other Factors on the Preventive Effect of Nonsteroidal Anti-Inflammatory Drugs on Colorectal Cancer Risk. Cancer Res. 2018, 78, 4790–4799.
  18. Hardman, W.E. Diet components can suppress inflammation and reduce cancer risk. Res. Pract. 2014, 8, 233–240.
  19. Dumas, J.A.; Bunn, J.Y.; Nickerson, J.; Crain, K.I.; Ebenstein, D.B.; Tarleton, E.K.; Makarewicz, J.; Poynter, M.E.; Kien, C.L. Dietary saturated fat and monounsaturated fat have reversible effects on brain function and the secretion of pro-inflammatory cytokines in young women. Metabolism 2016, 65, 1582–1588.
  20. Lopez-Alarcon, M.; Perichart-Perera, O.; Flores-Huerta, S.; Inda-Icaza, P.; Rodriguez-Cruz, M.; Armenta-Alvarez, A.; Bram-Falcon, M.T.; Mayorga-Ochoa, M. Excessive refined carbohydrates and scarce micronutrients intakes increase inflammatory mediators and insulin resistance in prepubertal and pubertal obese children independently of obesity. Inflamm. 2014, 2014, 849031.
  21. Samraj, A.N.; Pearce, O.M.; Laubli, H.; Crittenden, A.N.; Bergfeld, A.K.; Banda, K.; Gregg, C.J.; Bingman, A.E.; Secrest, P.; Diaz, S.L.; et al. A red meat-derived glycan promotes inflammation and cancer progression. Natl. Acad. Sci. USA 2015, 112, 542–547.
  22. De Filippo, C.; Cavalieri, D.; Di Paola, M.; Ramazzotti, M.; Poullet, J.B.; Massart, S.; Collini, S.; Pieraccini, G.; Lionetti, P. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Natl. Acad. Sci. USA 2010, 107, 14691–14696.
  23. Li, W.; Dowd, S.E.; Scurlock, B.; Acosta-Martinez, V.; Lyte, M. Memory and learning behavior in mice is temporally associated with diet-induced alterations in gut bacteria. Behav. 2009, 96, 557–567.
  24. Armstrong, H.; Alipour, M.; Valcheva, R.; Bording-Jorgensen, M.; Jovel, J.; Zaidi, D.; Shah, P.; Lou, Y.; Ebeling, C.; Mason, A.L.; et al. Host immunoglobulin G selectively identifies pathobionts in pediatric inflammatory bowel diseases. Microbiome 2019, 7, 1–17.
  25. Karlsen, T.H.; Folseraas, T.; Thorburn, D.; Vesterhus, M. Primary sclerosing cholangitis—A comprehensive review. Hepatol. 2017, 67, 1298–1323.
  26. Ong, H.S.; Yim, H.C.H. Microbial Factors in Inflammatory Diseases and Cancers. Exp. Med. Biol. 2017, 1024, 153–174.
  27. Maeda, Y.; Takeda, K. Role of Gut Microbiota in Rheumatoid Arthritis. Clin. Med. 2017, 6, 60.
  28. Mellemkjaer, L.; Linet, M.S.; Gridley, G.; Frisch, M.; Moller, H.; Olsen, J.H. Rheumatoid arthritis and cancer risk. J. Cancer 1996, 32, 1753–1757.
  29. Weaver, C.M.; Miller, J.W. Challenges in conducting clinical nutrition research. Rev. 2017, 75, 491–499.
  30. Lichtenstein, A.H.; Petersen, K.; Barger, K.; Hansen, K.E.; Anderson, C.A.M.; Baer, D.J.; Lampe, J.W.; Rasmussen, H.; Matthan, N.R. Perspective: Design and Conduct of Human Nutrition Randomized Controlled Trials. Nutr. 2021, 12, 4–20, doi:10.1093/advances/nmaa109.
  31. Mentella, M.C.; Scaldaferri, F.; Ricci, C.; Gasbarrini, A.; Miggiano, G.A.D. Cancer and Mediterranean Diet: A Review. Nutrients 2019, 11, 2059.
  32. Weber, D.D.; Aminazdeh-Gohari, S.; Kofler, B. Ketogenic diet in cancer therapy. Aging (Albany NY) 2018, 10, 164–165.
  33. Steck, S.E.; Murphy, E.A. Dietary patterns and cancer risk. Rev. Cancer 2020, 20, 125–138.
  34. Jansson, B. Potassium, sodium, and cancer: A review. Environ. Pathol. Toxicol. Oncol. 1996, 15, 65–73.
  35. Keum, N.; Lee, D.H.; Greenwood, D.C.; Manson, J.E.; Giovannucci, E. Vitamin D supplementation and total cancer incidence and mortality: A meta-analysis of randomized controlled trials. Oncol. 2019, 30, 733–743.
  36. Nutting, C.M.; Huddart, R.A. Retinoids in the prevention of bladder cancer. Expert Rev. Anticancer. Ther. 2001, 1, 541–545.
  37. Tang, J.E.; Wang, R.J.; Zhong, H.; Yu, B.; Chen, Y. Vitamin A and risk of bladder cancer: A meta-analysis of epidemiological studies. World J. Surg. Oncol. 2014, 12, 130.
  38. Okayasu, I.; Hana, K.; Nemoto, N.; Yoshida, T.; Saegusa, M.; Yokota-Nakatsuma, A.; Song, S.Y.; Iwata, M. Vitamin A Inhibits Development of Dextran Sulfate Sodium-Induced Colitis and Colon Cancer in a Mouse Model. Res. Int. 2016, 2016, 4874809.
  39. Lan, Q.Y.; Zhang, Y.J.; Liao, G.C.; Zhou, R.F.; Zhou, Z.G.; Chen, Y.M.; Zhu, H.L. The Association between Dietary Vitamin A and Carotenes and the Risk of Primary Liver Cancer: A Case-Control Study. Nutrients 2016, 8, 624.
  40. Fleet, J.C.; DeSmet, M.; Johnson, R.; Li, Y. Vitamin D and cancer: A review of molecular mechanisms. J. 2012, 441, 61–76.
  41. Vissers, M.C.M.; Das, A.B. Potential Mechanisms of Action for Vitamin C in Cancer: Reviewing the Evidence. Physiol. 2018, 9, 809.
  42. Carlberg, C.; Munoz, A. An update on vitamin D signaling and cancer. Cancer Biol. 2020, doi:10.1016/j.semcancer.2020.05.018.
  43. Mamede, A.C.; Tavares, S.D.; Abrantes, A.M.; Trindade, J.; Maia, J.M.; Botelho, M.F. The role of vitamins in cancer: A review. Cancer 2011, 63, 479–494.
  44. Holland-Bill, L.; Christiansen, C.F.; Farkas, D.K.; Donskov, F.; Jorgensen, J.O.L.; Sorensen, H.T. Diagnosis of hyponatremia and increased risk of a subsequent cancer diagnosis: Results from a nationwide population-based cohort study. Acta Oncol. 2018, 57, 522–527.
  45. Park, H.S.; Han, J.H.; Park, J.W.; Lee, D.H.; Jang, K.W.; Lee, M.; Heo, K.S.; Myung, C.S. Sodium propionate exerts anticancer effect in mice bearing breast cancer cell xenograft by regulating JAK2/STAT3/ROS/p38 MAPK signaling. Acta Pharmacol. Sin. 2020, 1–13, doi:10.1038/s41401-020-00522-2.
  46. Crowe, W.; Elliott, C.T.; Green, B.D. A Review of the In Vivo Evidence Investigating the Role of Nitrite Exposure from Processed Meat Consumption in the Development of Colorectal Cancer. Nutrients 2019, 11, 2673.
  47. Javanmardi, F.; Rahmani, J.; Ghiasi, F.; Gahruie, H.H.; Khaneghah, A.M. The Association between the Preservative Agents in Foods and the Risk of Breast Cancer. Cancer 2019, 71, 1229–1240.
  48. Fiolet, T.; Srour, B.; Sellem, L.; Kesse-Guyot, E.; Alles, B.; Mejean, C.; Deschasaux, M.; Fassier, P.; Latino-Martel, P.; Beslay, M.; et al. Consumption of ultra-processed foods and cancer risk: Results from NutriNet-Sante prospective cohort. BMJ 2018, 360, k322.
  49. Rosca, A.; Lesanu, M.L.; Zahiu, C.D.M.; Voiculescu, S.E.; Paslaru, A.C.; Zagrean, A.-M. Capsaicin and Gut Microbiota in Health and Disease. Molecules 2020, 25, 5681.
  50. Ge, Y.; Yoon, S.H.; Jang, H.; Jeong, J.H.; Lee, Y.M. Decursin promotes HIF-1alpha proteasomal degradation and immune responses in hypoxic tumour microenvironment. Phytomedicine 2020, 78, 153318.
  51. Schlormann, W.; Atanasov, J.; Lorkowski, S.; Dawczynski, C.; Glei, M. Study on chemopreventive effects of raw and roasted beta-glucan-rich waxy winter barley using an in vitro human colon digestion model. Food Funct. 2020, 11, 2626–2638.
  52. Glei, M.; Zetzmann, S.; Lorkowski, S.; Dawczynski, C.; Schlormann, W. Chemopreventive effects of raw and roasted oat flakes after in vitro fermentation with human faecal microbiota. J. Food Sci. Nutr. 2020, 1–13, doi:10.1080/09637486.2020.1772205.
  53. Xia, W.; Khan, I.; Li, X.A.; Huang, G.; Yu, Z.; Leong, W.K.; Han, R.; Ho, L.T.; Wendy Hsiao, W.L. Adaptogenic flower buds exert cancer preventive effects by enhancing the SCFA-producers, strengthening the epithelial tight junction complex and immune responses. Res. 2020, 159, 104809.
  54. Hehemann, J.H.; Correc, G.; Barbeyron, T.; Helbert, W.; Czjzek, M.; Michel, G. Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. Nature 2010, 464, 908–912.
  55. Vaikundamoorthy, R.; Krishnamoorthy, V.; Vilwanathan, R.; Rajendran, R. Structural characterization and anticancer activity (MCF7 and MDA-MB-231) of polysaccharides fractionated from brown seaweed Sargassum wightii. J. Biol. Macromol. 2018, 111, 1229–1237.
  56. Penalver, R.; Lorenzo, J.M.; Ros, G.; Amarowicz, R.; Pateiro, M.; Nieto, G. Seaweeds as a Functional Ingredient for a Healthy Diet. Drugs 2020, 18, 18.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Microbiology
Contributor MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Heather Armstrong
View Times: 663
Revisions: 2 times (View History)
Update Date: 05 Mar 2021
Table of Contents
    Notice
    You are not a member of the advisory board for this topic. If you want to update advisory board member profile, please contact office@encyclopedia.pub.
    OK
    Confirm
    Only members of the Encyclopedia advisory board for this topic are allowed to note entries. Would you like to become an advisory board member of the Encyclopedia?
    Yes
    No
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    There is no comment~
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    ${ selectedItem.replyTextCharacter }/${ selectedItem.replyMaxCharacter }
    Submit
    Cancel
    Confirm
    Are you sure to Delete?
    Yes No
    Academic Video Service
    Feedback