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Chronic Inflammation-Related HPV: A Driving Force Speeds Oropharyngeal Carcinogenesis.

Liu X, Ma X, Lei Z, Feng H, Wang S, Cen X, Gao S, Jiang Y, Jiang J, Chen Q, Tang Y, Tang Y, Liang X - PLoS ONE (2015)

Bottom Line: Oropharyngeal squamous cell carcinoma (OPSCC) has been known to be a highly aggressive disease associated with human papilloma virus (HPV) infection.The positive rate of HPV 16 was progressively improved with the malignant progression of oral mucous (P<0.05).Thus, a combination of HPV infection and inflammation expression might become a helpful biomedical marker to predict oropharyngeal carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology (Sichuan University), Chengdu, China.

ABSTRACT
Oropharyngeal squamous cell carcinoma (OPSCC) has been known to be a highly aggressive disease associated with human papilloma virus (HPV) infection. To investigate the relationship between HPV and chronic inflammation in oropharyngeal carcinogenesis, we collected 140 oral mucous fresh specimens including 50 OPSCC patients, 50 cancer in situ, 30 precancerous lesions, and 10 normal oral mucous. Our data demonstrated that there was a significantly higher proportion of severe chronic inflammation in dysplastic epithelia in comparison with that in normal tissues (P<0.001). The positive rate of HPV 16 was parallel with the chronic inflammation degrees from mild to severe inflammation (P<0.05). The positive rate of HPV 16 was progressively improved with the malignant progression of oral mucous (P<0.05). In addition, CD11b+ LIN- HLA-DR-CD33+ MDSCs were a critical cell population that mediates inflammation response and immune suppression in HPV-positive OPSCC. These indicated that persistent chronic inflammation-related HPV infection might drive oropharyngeal carcinogenesis and MDSCs might pay an important role during this process. Thus, a combination of HPV infection and inflammation expression might become a helpful biomedical marker to predict oropharyngeal carcinogenesis.

No MeSH data available.


Related in: MedlinePlus

Schematic diagram of persistent chronic inflammation-related HPV infection response contributes to oropharyngeal carcinogenesis.
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pone.0133681.g004: Schematic diagram of persistent chronic inflammation-related HPV infection response contributes to oropharyngeal carcinogenesis.

Mentions: The observed association between chronic inflammation and HPV infection may be explained through the direct effects of some microorganisms, such as bacteria. Samoff et al [50] have shown that concurrent infection with Chlamydia trachomatis could enhance the persistence of cervical HPV infection and the risk of cervical cancer. Yilmaz et al [51]reported that bacteria that infected oral mucous successfully colonized and persisted in the oral mucous. These data indicated that HPV might be triggered in the microenvironment of the chronic inflammation caused by microorganisms. However, Abd Warif et al[52] reported that the expression of HPV 16 E7 in epidermis of the K14E7 mouse could lead to hyperplasia and chronic inflammation. This seems that the chronic inflammation might be caused by HPV, supporting our findings that the higher level of MDSCs presented in dysplastic tissues and HPV-positive OPSCC compared to the normal tissues. Thus, we cannot exclude the dual modulation possibility of the chronic inflammation and HPV infection, and much work should be further done. On the hand, the stimulation of inflammation and immune might pay a critical role in HPV infection. The malignant transformation of oral epithelium would be a consequence of the immune response like MDSCs, macrophage and T-cell activation and cytokine release [53, 54]. The microbial activation of inflammation and immune cells has been shown to contribute to the transformation of malignancy through DNA damage, peroxidation of lipids, or posttranslational modification of proteins [55]. In addition, the relationship between chronic inflammation and HPV infection in oral and oropharyngeal is biologically plausible. The HPV infects exclusively the basal cells of the oral epithelium, replicates in the basal cell and obtains the access through breaks in the oral mucosa (Fig 4). Mucosal damage, microulcerations, and consequent epithelial proliferation mediated by some microorganisms and inflammatory cytokines create an ideal environment for initial HPV infection and its persistence, which leads to increased risk of HPV transmission and oropharyngeal carcinogenesis[56–58].


Chronic Inflammation-Related HPV: A Driving Force Speeds Oropharyngeal Carcinogenesis.

Liu X, Ma X, Lei Z, Feng H, Wang S, Cen X, Gao S, Jiang Y, Jiang J, Chen Q, Tang Y, Tang Y, Liang X - PLoS ONE (2015)

Schematic diagram of persistent chronic inflammation-related HPV infection response contributes to oropharyngeal carcinogenesis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4507986&req=5

pone.0133681.g004: Schematic diagram of persistent chronic inflammation-related HPV infection response contributes to oropharyngeal carcinogenesis.
Mentions: The observed association between chronic inflammation and HPV infection may be explained through the direct effects of some microorganisms, such as bacteria. Samoff et al [50] have shown that concurrent infection with Chlamydia trachomatis could enhance the persistence of cervical HPV infection and the risk of cervical cancer. Yilmaz et al [51]reported that bacteria that infected oral mucous successfully colonized and persisted in the oral mucous. These data indicated that HPV might be triggered in the microenvironment of the chronic inflammation caused by microorganisms. However, Abd Warif et al[52] reported that the expression of HPV 16 E7 in epidermis of the K14E7 mouse could lead to hyperplasia and chronic inflammation. This seems that the chronic inflammation might be caused by HPV, supporting our findings that the higher level of MDSCs presented in dysplastic tissues and HPV-positive OPSCC compared to the normal tissues. Thus, we cannot exclude the dual modulation possibility of the chronic inflammation and HPV infection, and much work should be further done. On the hand, the stimulation of inflammation and immune might pay a critical role in HPV infection. The malignant transformation of oral epithelium would be a consequence of the immune response like MDSCs, macrophage and T-cell activation and cytokine release [53, 54]. The microbial activation of inflammation and immune cells has been shown to contribute to the transformation of malignancy through DNA damage, peroxidation of lipids, or posttranslational modification of proteins [55]. In addition, the relationship between chronic inflammation and HPV infection in oral and oropharyngeal is biologically plausible. The HPV infects exclusively the basal cells of the oral epithelium, replicates in the basal cell and obtains the access through breaks in the oral mucosa (Fig 4). Mucosal damage, microulcerations, and consequent epithelial proliferation mediated by some microorganisms and inflammatory cytokines create an ideal environment for initial HPV infection and its persistence, which leads to increased risk of HPV transmission and oropharyngeal carcinogenesis[56–58].

Bottom Line: Oropharyngeal squamous cell carcinoma (OPSCC) has been known to be a highly aggressive disease associated with human papilloma virus (HPV) infection.The positive rate of HPV 16 was progressively improved with the malignant progression of oral mucous (P<0.05).Thus, a combination of HPV infection and inflammation expression might become a helpful biomedical marker to predict oropharyngeal carcinogenesis.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology (Sichuan University), Chengdu, China.

ABSTRACT
Oropharyngeal squamous cell carcinoma (OPSCC) has been known to be a highly aggressive disease associated with human papilloma virus (HPV) infection. To investigate the relationship between HPV and chronic inflammation in oropharyngeal carcinogenesis, we collected 140 oral mucous fresh specimens including 50 OPSCC patients, 50 cancer in situ, 30 precancerous lesions, and 10 normal oral mucous. Our data demonstrated that there was a significantly higher proportion of severe chronic inflammation in dysplastic epithelia in comparison with that in normal tissues (P<0.001). The positive rate of HPV 16 was parallel with the chronic inflammation degrees from mild to severe inflammation (P<0.05). The positive rate of HPV 16 was progressively improved with the malignant progression of oral mucous (P<0.05). In addition, CD11b+ LIN- HLA-DR-CD33+ MDSCs were a critical cell population that mediates inflammation response and immune suppression in HPV-positive OPSCC. These indicated that persistent chronic inflammation-related HPV infection might drive oropharyngeal carcinogenesis and MDSCs might pay an important role during this process. Thus, a combination of HPV infection and inflammation expression might become a helpful biomedical marker to predict oropharyngeal carcinogenesis.

No MeSH data available.


Related in: MedlinePlus