Month: April 2020

(1) Dharmendra Kashyap, Budhadev Baral, and Tarun Prakash Verma in their research article “Oral rinses in growth inhibition and treatment of Helicobacter pylori infection” assert that oral rinses will reduce the H. pylori in the oral cavity and help to control its migration from oral to the gastric compartment. (2) Kashyap, Baral, and Verma provide evidence that oral rinses are efficient in growth inhibition of H. pylori via the down-regulation of virulence factor gene CagA by the use of oral rinses. (3) The purpose of this research article is to evaluate the effect of various oral rinses on isolated H. pylori from different anatomical locations. (4) The authors focus their study towards other researchers in the field as they specify that there is a need for a detailed study about the molecular pathways modulated by the oral rinses and will open various bactericidal combinations for treatment and eradication of H. pylori infection. 

Jha HC, Kashyap D, Baral B, Verma TP, Sonkar C, Chatterji D, Jain AK. 2020. Oral rinses in growth inhibition and treatment of Helicobacter pylori infection.

Any alteration in the gut microbial community is linked to a number of intestinal conditions, including cancer, obesity and a variety of bowel disorders. Depending on how the following behavior causes an alteration, away from or towards a “normal, healthy” community, the potential health impacts may be beneficial, detrimental, or neutral.

Excessive laxative use: Laxative use can influence phyla level of gut microbiota. Drago discusses bowel preparation for colonoscopy and found a significant decrease in Firmicutes abundance and an increase in Proteobacteria immediately after colon cleansing (1). One month after the colonoscopy, the Proteobacteria had decreased two and a half fold and Streptococcaceae had increased fourfold compared with samples before the cleansing and colonoscopy (1). This can lead to microbial dysbiosis through the change of number, diversity, and proportions of microorganisms within the gut, a detrimental health impact.

Probiotic use: Probiotics can increase the diversity, number, and potentially alter the proportion of the gut microbial community which could be both beneficial, as it fosters a bacterial environment, or detrimental, as changing the numbers or proportions of bacteria could lead to microbial imbalance. Probiotics are mainly used for restoring gut microbiota (2).

Consuming fermented foods: Some fermented foods have live or active cultures which may promote microbial community diversity if microbes make it to the intestines and are not killed by the acidity of the stomach. 

Other diet (nutritional therapy), exercise and environment: D’Argenio provides a case study that supports the hypothesis that nutritional therapy may modify the fecal microflora (3). By altering diet and exercise, the microbial community may differ in number of the specific microbial populations that contribute to obesity which would result in beneficial health impacts (2). Microbiota of people in a long-stay care environment were significantly less diverse and correlated with increased frailty compared to individuals living in the community (2). Less exercise and restricted diets may promote less diverse communities which may lead to detrimental health impacts. 

Birth: Guinane and Cotter discuss that infants contain low levels of microbes so the delivery method, feeding type and antibiotic, prebiotic, and probiotic use can significantly vary the number and diversity of microbes in the GI tract (2). 

References

1. Dʼargenio V, Precone V, Casaburi G, Miele E, Martinelli M, Staiano A, Salvatore F, Sacchetti L. 2013. An Altered Gut Microbiome Profile in a Child Affected by Crohnʼs Disease Normalized After Nutritional Therapy. American Journal of Gastroenterology 108:851–852.

• Guinane CM, Cotter PD. 2013. Role of the gut microbiota in health and chronic gastrointestinal disease: understanding a hidden metabolic organ. Therapeutic Advances in Gastroenterology 6:295–308.

• Dʼargenio V, Precone V, Casaburi G, Miele E, Martinelli M, Staiano A, Salvatore F, Sacchetti L. 2013. An Altered Gut Microbiome Profile in a Child Affected by Crohnʼs Disease Normalized After Nutritional Therapy. American Journal of Gastroenterology 108:851–852

According to the World Health Organization there are over 100 strains of the Human Papilloma Virus; a small subset of these strains are known to have carcinogenic properties. HPV strains 16 and 18 are known to cause cervical and oral cancers. Other strains that are known to cause cancers are 33, 35, 39, 51, 52, 56, 58, and 59. In 2006, the vaccine Gardisil became available for females aged 9-26. The vaccine protects against HPV strains 6,11,16, and 18 (strains 6 and 11 most commonly cause genital warts). Though the vaccine spurred much controversy it is now also recommended that young males complete the vaccination series as HPV is a leading cause of cancers in the mouth and throat. Based on the article “Viruses and Human Cancer: From Detection to Cause”, I believe that a new vaccination would best serve to protect against other strains that are known to be “probably carcinogenic to humans”  such as 33, 35, 39, 51, 52, 56, 58, and 59. By expanding the variety of strains that could be prevented via vaccination the rates of cancer related to HPV would hopefully decrease. This would also be more cost effective than creating vaccines for all of the strains. Ideally all young women and men would get the vaccine before they engage in any form of sexual intercourse so that they gain immunity before they are exposed to any HPV strains. Recommendations from the CDC for the timing of the HPV vaccine include two doses spaced apart by six months starting at age 11-12 for both boys and girls. I would agree with the logic to give the vaccination early to help prevent any future risk for cancer. The article by Sarid and Gao states that the “onset of cancer typically occurs decades after initial infection with a potentially transforming virus”. With the use of both vaccination and regular medical screenings, including cervical exams, the rates of cancer caused by the Human Papilloma Virus can be decreased. 

References

Human papillomavirus (HPV) and cervical cancer. (n.d.). Retrieved from https://www.who.int/news-room/fact-sheets/detail/human-papillomavirus-(hpv)-and-cervical-cancer

Sarid, R., & Gao, S.-J. (2011). Viruses and human cancer: From detection to causality. Cancer Letters, 305(2), 218–227. doi: 10.1016/j.canlet.2010.09.011

Prompt: List as many human non-infectious diseases that you can think of that are influenced by microorganisms.  

Irritable Bowel, Crohn’s, MS, Cancers, Parkinson’s, Alzheimer’s, Autoimmune diseases, Heart disease

While I do not know the interaction of microorganisms with these noncommunicable diseases, it would make sense that microbes would influence or play an integral role in these diseases and many more. Specifically, I am aware that there are certain super-strain gut bacteria that produce harmful amounts of alcohol. While this may be very uncommon, these excessive alcohol-producing bacteria may affect cells. Heavy alcohol intake is associated with an increased risk of colorectal cancer because of carcinogenic agents in alcohol (Cogliano et al., Gong et al.). Alcohol may delay DNA repair or antagonize metabolism of methyl groups, contributing to abnormal DNA methylation which may increase risks of CRC via loss of control of protooncogene activity (Chan et al., Ferrari et al.). Carcinogens can also promote mutations in cell signaling pathways.

References

Chan, A.T. & Giovannucci, E.L. (2010). Primary prevention of colorectal cancer. Gastroenterology, 138, 2029-2043.

Cogliano, V.J., Baan, R., Straif, K., Grosse, Y., Lauby-Secretan, B., El Ghissassi, F., … & Wild, C.P. (2011). Preventable exposures associated with human cancers. DOI:10.1093/jnci/djr483

Ferrari, P., Jenab, M., Norat, T., Moskal, A., Slimani, N., Olsen, A., … & Riboli, E. (2007). Lifetime and baseline alcohol intake and risk of colon and rectal cancers in the European Prospective Investigation into Cancer and Nutrition (EPIC). International Journal of Cancer, 121, 2065-2072. DOI:10.1002/ijc.22966

Gong, J., Hutter, C.M., Newcomb, P.A., Ulrich, C.M., Bien, S.A., Campbell, P.T., … Peters, U. (2016). Genome-wide interaction analyses between genetic variants and alcohol consumption and smoking for risk of colorectal cancer. PLOS Genetics. DOI:10.1371/journal.pgen.1006296