Multiple alcohol dehydrogenases but no functional acetaldehyde dehydrogenase causing excessive acetaldehyde production from ethanol by oral streptococci

Pavlova, Sylvia I.; Jin, Ling; Gasparovich, Stephen R.; Lin, Tao

doi:10.1099/mic.0.066258-0

Cited by 55 publications

(53 citation statements)

References 47 publications

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“…Among six alcohol dehydrogenases in S. pneumoniae type 2 D39, only SPD_1834 (AdhE) was strongly induced by ethanol (15). AdhE has 98% identity with Streptococcus gordonii AdhE (AcdH), which uses only ethanol as its substrate (45). Moreover, a BLAST search revealed that SPD_0265 has 93% identity with S. gordonii AdhA, which preferentially catalyzes 1-propanol (45).…”

Section: Discussionmentioning

confidence: 99%

“…SPD_1126 (GenBank) seems to function as a threonine dehydrogenase in amino acid transport and metabolism. SPD_1636 has 85% identity with S. gordonii AdhB, which preferentially catalyzes 1-butanol (45). On the other hand, SPD_1865 (GenBank) seems to function in propanoate metabolism and as a formaldehyde dehydrogenaselike ADH.…”

Section: Discussionmentioning

confidence: 99%

“…AdhE has 98% identity with Streptococcus gordonii AdhE (AcdH), which uses only ethanol as its substrate (45). Moreover, a BLAST search revealed that SPD_0265 has 93% identity with S. gordonii AdhA, which preferentially catalyzes 1-propanol (45). SPD_1126 (GenBank) seems to function as a threonine dehydrogenase in amino acid transport and metabolism.…”

Section: Discussionmentioning

confidence: 99%

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Ethanol-Induced Alcohol Dehydrogenase E (AdhE) Potentiates Pneumolysin in Streptococcus pneumoniae

et al. 2015

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Alcohol impairs the host immune system, rendering the host more vulnerable to infection. Therefore, alcoholics are at increased risk of acquiring serious bacterial infections caused by Streptococcus pneumoniae, including pneumonia. Nevertheless, how alcohol affects pneumococcal virulence remains unclear. Here, we showed that the S. pneumoniae type 2 D39 strain is ethanol tolerant and that alcohol upregulates alcohol dehydrogenase E (AdhE) and potentiates pneumolysin (Ply). Hemolytic activity, colonization, and virulence of S. pneumoniae, as well as host cell myeloperoxidase activity, proinflammatory cytokine secretion, and inflammation, were significantly attenuated in adhE mutant bacteria (⌬adhE strain) compared to D39 wild-type bacteria. Therefore, AdhE might act as a pneumococcal virulence factor. Moreover, in the presence of ethanol, S. pneumoniae AdhE produced acetaldehyde and NADH, which subsequently led Rex (redox-sensing transcriptional repressor) to dissociate from the adhE promoter. An increase in AdhE level under the ethanol condition conferred an increase in Ply and H 2 O 2 levels. Consistently, S. pneumoniae D39 caused higher cytotoxicity to RAW 264.7 cells than the ⌬adhE strain under the ethanol stress condition, and ethanol-fed mice (alcoholic mice) were more susceptible to infection with the D39 wild-type bacteria than with the ⌬adhE strain. Taken together, these data indicate that AdhE increases Ply under the ethanol stress condition, thus potentiating pneumococcal virulence.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Ethanol-Induced Alcohol Dehydrogenase E (AdhE) Potentiates Pneumolysin in Streptococcus pneumoniae

et al. 2015

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“…Although >700 bacterial species inhabit the oral cavity (105), only the prevalence of several aerobic Gram-positive bacteria and yeast have been proved to play a leading role in acetaldehyde production (106). This phenomenon may due to the increased ADH activity, which has been confirmed in Streptococcus gordonii V2016 (107), Neisseria (108) and Streptococcus salivarius (109), the prevalence of aerobic Gram-positive bacteria and yeast are important in acetaldehyde production (109), due to their increased ADH activity.…”

Section: Interactions Between Alcohol Consumption and The Correspondimentioning

confidence: 99%

Alcohol consumption and corresponding factors: A novel perspective on the risk factors of esophageal cancer

2016

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Abstract. Esophageal cancer is the eighth most common type of cancer in the world, and the sixth most common cause of mortality from cancer. Alcohol consumption is the major risk factor for esophageal cancer, due to the worldwide prevalence and high carcinogenicity of the ethanol metabolite. In epidemiological studies, the efficiency of alcohol intake to enhance the risk of esophageal cancer is altered by daily ethanol consumption, type of alcoholic beverages ingested, time since quitting drinking, age of drinking initiation, differences in population and subtypes of esophageal cancer. Corresponding factors, including gene polymorphisms, tobacco smoking, oral microorganisms and folate deficiency, reveal a synergistic effect in concurrent alcohol users that may lead to an increased risk of developing esophageal cancer. Consequently, esophageal cancer prevention involves multiple aspects, including quitting drinking and smoking, maintaining an adequate oral health and ingesting adequate quantities of folate, particularly in genetically high-risk populations.

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“…Streptococcus spp. express: AdhA, AdhB or AdhE genotypes for metabolism of ETOH with release of acetaldehyde in a protective process similar to Listeria [15,16]. AA in turn contributes to a mutator gene environment that can be characterized indirectly through enhanced expression of markers such as, Annexin A2, a heterotetramer protein.…”

Section: Introductionmentioning

confidence: 99%

Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

2014

J Oral Biol

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Background: Oropharyngeal carcinoma is often associated with human papilloma virus subtype 16 (HPV) infections; however events that lead to HPV entry and carcinoma are poorly understood. We simulated a clinical situation in the laboratory by examining human epithelial and oral keratinocyte (HOK) responses to oral commensal bacteria (Streptococcus spp.) and metabolism of ethyl alcohol (ETOH). These studies led us to conclude that oral bacteria and ethyl alcohol through keratinocyte membrane signals act as co-factors for HPV 16 entry. Methods:We tested ETOH exposure responses of Streptococcus spp., ETOH-sensitive, acetaldehyde (AA) producers: S. mutans (LT11), S. salivarius strain, 109-2 and S. gordonii (V2016; wild type). In comparison to ETOH-resistant, non-producers of AA: S. salivarius strain, 101-7 or S. gordonii (adh ABE mutant). 5×105 per cfu/mL of bacteria were exposed to ETOH (5%,v/v) for 1h and then co-incubated for 3h with epithelial targets: immortalized: 293TT; HPV 16 (HOK/HPV 16B cells), or telomerase: hTERT HOK. Streptococci spp. attachment to epithelial cells and subsequent effects were enumerated with immune cytochemistry; Western immunoblotting, and immunoprecipitation techniques. These methods delineated expressions of syndecans-1, 4; phospho-L-tyrosine epidermal growth factor receptor (EGFR), and furin convertase (FC) with HPV 16 pseudo virus (PsV) entry into 293TT, hTERT HOKs and oral squamous cell carcinoma (SCC-25). To verify these relationships we used inhibitors of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and FC.Results: Streptococcus spp. metabolism of ETOH released AA to trigger HOK expressions of syndecans 1 and 4 and heparin sulfate binding proteins were degraded by heparanase. Following these events enhanced phosphorylated EGFR expression and HPV 16 entry through FC activity were recorded.Conclusions: Some oral Streptococcus spp. response to ETOH mediates epithelial cell susceptibility to HPV 16 entry. This occurs through membrane associated expression changes of proteoglycans and EGFR. Moreover, oral cancer cell differentiation and growth may be dependent upon these associations.

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Multiple alcohol dehydrogenases but no functional acetaldehyde dehydrogenase causing excessive acetaldehyde production from ethanol by oral streptococci

Cited by 55 publications

References 47 publications

Ethanol-Induced Alcohol Dehydrogenase E (AdhE) Potentiates Pneumolysin in Streptococcus pneumoniae

Ethanol-Induced Alcohol Dehydrogenase E (AdhE) Potentiates Pneumolysin in Streptococcus pneumoniae

Alcohol consumption and corresponding factors: A novel perspective on the risk factors of esophageal cancer

Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

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