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HPV and Cancer pp 75–106Cite as

Poly-Microbial Interaction with Human Papilloma Virus Leading to Increased Risk for Head and Neck Squamous Cell Carcinoma and Oral Squamous Cell Carcinomas

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Abstract

750 bacterial taxa reside in the oral pharynx and oral cavity with additional populations of fungi and viruses. This initial microbial presence is independent of host inflammatory response and produces a persistent level of microbial populations. In time a dependent phase characterized by a constant level of inflammatory host responses becomes evident that can overwhelm constitutive mucosa protection to initiate a process of epithelial cell transformation after additional challenges are presented (e.g., oxidative stress, DNA damages). For example, ethyl alcohol products and diets high in glucose are metabolized and increase microbial proliferation and attachment to oral keratinocytes. One result is release of carcinogens such as acetaldehyde. Consequently a loss of epithelial mucosa intercellular attachment and integrity is expected to create more access to basal oral keratinocyte populations by human papilloma virus (HPV) and oral microbes such as Streptococci sp. This interaction increases risk for malignant transformation as HPV subtypes such as 16 initiate oncogenic changes associated with head and neck squamous cell carcinoma (HNSCC). In contrast the oncogenic status for Streptococci sp. is unclear but there are similarities between these two different types of microbes. These include transmission through sexual activity, oropharyngeal colonization, a similar means for attachment using heparan sulfate binding proteins, and a activation of particular differentiation and cell growth regulatory pathways (e.g., EGFr/MAPKp38/PTEN/AKT/JNK/c-fos/myc/HIFs-Cyclin D1-p16-p21waf1/CIPI- p53-Rb). Ultimately, cooperation between Streptococci sp. and HPV 16 results in a loss of differentiation of keratinocytes and malignant transformation particularly in environments that include metabolism of tobacco derived poly-cyclic aromatic hydrocarbons or ethyl alcohol to produce DNA damage (bulky adducts) in basal keratinocyte populations. Expansion of transformed clones of these damaged epithelial cells is associated with migration through basement membrane and underlying stroma. Presence of a robust and complex cooperation between microbes requires consideration as important etiologic factors for HNSCC.

Abstract

Infections by oral bacteria such as Streptococci sp. often occur in head and neck regions because of direct contact and intermittently from sexual activity. Therefore persistent local colonization of oropharynx, hypopharynx, larynx, and other areas of the head and neck can occur because these are also sites for viral infections such as, Human papilloma viruses (HPV). HPV of various subtypes are more likely to result from sexual activity but HPV infection of oncogenic subtypes (e.g., 16) increase risk for head and neck squamous cell carcinoma (HNSCC). Moreover, both types of microorganisms target keratinocytes following changes in environment. Survival and attachment by Streptococci sp. and HPV is a product of binding to oral keratinocyte cell surface heparan sulfate proteoglycan binding proteins (HSGBPs). An initial microbial proliferation phase is independent of host inflammatory response followed by a dependent phase that includes a host response. Presence of microbes induces innate and acquired inflammatory activities because foreign microbial glycoproteins and proteoglycans accumulate. Furthermore, attachment by microbes to oral keratinocytes disrupts normal intercellular attachment, produces aberrant exogenous and endogenous signals (e.g., release of IL-6, IL-8, Transforming growth factors, Tumor necrosis related proteins, etc.) that lead to a loss of mucosa integrity. Access by microorganisms to mucosa basement membrane, stromal tissues, and selective stem cell keratinocyte population results from these events leading to increased transformation with persistent DNA damage of keratinocytes. Environmental factors such as ethyl alcohol (ETOH) that are metabolized by Streptococci sp., other microbes and oral keratinocytes, are responsive to increased levels of metabolized ETOH which produces acetaldehyde (AA), a DNA damaging agent and carcinogen. Eventually malignant clones form and expand to lead to HNSCC or oral squamous cell carcinoma (OSCC).

There is a paucity of studies that describe bacterial interactions with HPV in details that elucidate our understanding of biologic features that lead to a malignant oral keratinocyte phenotype. In this review we provide hypotheses and some preliminary observations that hopefully enhance this understanding of microorganism interaction with HPV infected oral keratinocytes and risk for HNSCC.

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Abbreviations

HPV:

Human Papilloma Virus

HNSCC:

Head & Neck Squamous Cell Carcinoma

HSGBPs:

Heparan Sulfate Proeoglycan Binding Proteins

DNA:

Deoxyribonucleic Acid

ETOH:

Ethyl Alcohol

AA:

Acetaldehyde

OSCC:

Oral Squamous Cell Carcinoma

DB[a,1]P:

Dibenz[a,1]pyrene

ADH:

Alcohol Dehydrogenase

ALDH:

Aldehyde Dehydogenase

HOK:

HOK Human Oral Kenatinocytes

DMEM:

Dulbecco's Modified Eagle's Medium

CCD:

Charge Coupled Device

MDA:

Malondialdehyde

RNA:

Ribonucleic Acid

PDZ:

Post-synaptic Density Proteins

ZO:

Zona Occludens

GTP:

Guanosine Triphosphate

JAMS:

Junctional Adhesion Molecules

PMN:

Polymorphonuclear Leukocytes

LPS:

Lipopolysaccharide

EMT:

Epithelial Mesenchymal Transition

Fc:

Fragment, crystallizable

VEGF:

Vascular Endothelial Growth Factor

FGF:

Fibroblast Growth Factor

BRK:

Baby Rat Kidney

GAG:

Glycosaminoglycan

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  1. College of Dentistry, Department of Oral Medicine and Diagnostic Sciences, University of Illinois at Chicago, 801 South Paulina Street, Chicago, IL, USA

    Joel Schwartz

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    James A. Radosevich

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Schwartz, J. (2012). Poly-Microbial Interaction with Human Papilloma Virus Leading to Increased Risk for Head and Neck Squamous Cell Carcinoma and Oral Squamous Cell Carcinomas. In: Radosevich, J. (eds) HPV and Cancer. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-5437-9_4

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