| Backgroud:Nasal inverted papilloma is a benign tumor,but it have characteristics of postoperative recurrence、a locally aggressive pattern of growth、occasionally malignant alteration, these characteristics bring challenges to the clinical treatment. Many people made a lot of speculation and research to the pathogenesis of NIP, but the specific mechanism is still uncertain. Many papers reported the infection of human papilloma virus was associated with NIP, also had the research conclusion on the contrary,after it was put forward to be the cause of NIP firstly in the 1880 s,but so far, it is unclear whether the infection of HPV is the cause of nasal inverted papilloma.There are close relationships between the immune system and microbial infection、inflammation、tumor. TGF-β is the main regulator of epithelial proliferation 、 immunity and angiogenesis;IL-10 is a multifunctional cytokine, it inhibited the T cell’s proliferation、the production of cytokine and the immune reaction;IFN-γ plays an important role in facilitating CTL-mediated immune effector function, through induction of multiple genes associated with MHC class I antigen presentation, and also contributes to the elimination of HPV infection.This paper investigate the relationship between the nasal inverted papillomaon and TGF-β、IL-10、IFN-γ、HPV infection, we hope to find the mechanism of the occurrence and development of nasal inverted papilloma.Objective : To understand the human papillomavirus infection and expression of immune factors of TGF-β, IL-10, IFN-γ in nasal inverted papilloma and nasal squamouscell carcinoma. To explore the relationship between human papilloma virus infection, TGF-β, IL-10, IFN-γ and nasal inverted papilloma. To explore the relationship between human papilloma virus infection, TGF-β, IL-10, IFN-γ and nasal squamous cell carcinoma.Methods:Collected 30 cases of NIP(including 7 cases ofrecurrent NIP, 23 cases), 19 cases of NSCC, NP that admitted to the First Affiliated Hospital of Fujian Medical University From 2011.4 to 2014.8.Using in situ hybridization(ISH) to detect the infection of HPV6/11, HPV16/18.Using immunohistochemical technique(En Vision) to detect the expression of TGF-β, IL-10, IFN-γ.Results:The HPV infection rates of 30 cases of NIP, 23 cases of NSCC are 43.33%, 52.17%.19 cases of NP were not infected with HPV. There were 9 cases of HPV infection in 23 cases non recurrent NIP(39.13%).3 cases of HPV infection in 7 cases recurrent NIP(42.86%). There is significant differences in the infection rate of HPV between NIP and NP, between NSCC and NP(P<0.05). HPV infection rate showed no significant difference in between NIP and NSCC, between recurrent NIP and nonrecurrent NIP(P>0.05). TGF-β, IL-10, IFN-γ are expressed in NSCC, NIP and NP. TGF-β’s expression has significant differences in NIP, NSCC and NP(H=44.32 P< 0.0001).NIP’s expression of TGF-β is more than in NP’s and NSCC’s. There is no significant difference in TGF-β’s expression between NSCC and NP. IL-10’s expression has significant differences in NIP, NSCC and NP(F=5.850, P=0.0045). NIP’s expression of IL-10 lower than the NP’s. There is no significant difference in IL-10’s expression between NIP and NSCC. There is no significant difference in IL-10’s expression between NSCC and NP. IFN-γ’s expression hasn’t significant differences in NIP, NSCC and NP(H=1.718, P=0.4237). There was no correlation between the expression of TGF-β, IL-10, IFN-γand HPV infection in NIP and NSCC(P>0.05).Conclusion : There is significant differences in the infection rate of HPV in NIP, NSCC, NP group. HPV infection is partly related the pathogenesis of NIP, NSCC. The relationship of between HPV infection and NIP’s malignant alteration is not clear. HPV infection is not related to NIP’s relapse. Abnormal expression TGF-β and IL-10 may be involved in the pathogenesis of NIP. There is no relationshipbetween IFN-γ and the NIP’s pathogenesis and development. HPV infection have no related with the expression of TGF-β、IL-10、IFN-γ in NIP and NSCC. |
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