Citation:Lu Y,Yin Y,Gong L.Meibomian gland dysfunction model induced with complete Freund’s adjuvant in C57BL/6 mice.Int J Ophthalmol 2020;13(11):1705-1712,doi:10.18240/ijo.2020.11.04
Meibomian gland dysfunction model induced with complete Freund’s adjuvant in C57BL/6 mice
Received:April 26, 2020  Revised:August 04, 2020
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DOI:10.18240/ijo.2020.11.04
Key Words:meibomian gland dysfunction  complete Freund’s adjuvant  inflammation  acinar atrophy  intense pulsed light
Fund Project:Supported by National Natural Science Foundation of China (No.81700797); Science and Technology Commission of Shanghai Municipality (No.17411961800).
        
AuthorInstitution
Yang Lu Department of Ophthalmology and Vision Science, Eye&ENT Hospital of Fudan University, Shanghai , China
Yue Yin Department of Ophthalmology and Vision Science, Eye&ENT Hospital of Fudan University, Shanghai , China
Lan Gong Department of Ophthalmology and Vision Science, Eye&ENT Hospital of Fudan University, Shanghai , China
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Abstract:
      AIM: To establish a new inflammatory animal model of meibomian gland dysfunction (MGD) in C57BL/6 mice.

    METHODS: C57BL/6 mice were randomly divided into complete Freund’s adjuvant (CFA) group (14 animals, 14 eyes), naphthazolin hydrochloride (NH) group (14 animals, 14 eyes) and control group (14 animals, 14 eyes). In CFA group, CFA was used in eyelid conjunctiva injection; in NH group, NH eye drops were used twice a day; control group was injected with equal dose of saline at the same time point and same site with animals in CFA group. The meibomian gland orifices score (MGOS) was evaluated on a scale of 0 to 3 in the middle five meibomian gland orifices of the upper and lower eyelid using slit lamp. After the successful induction of each animal model, intense pulsed light (IPL) was introduced on each mouse in CFA and NH group. Oil red O (ORO), hematoxylin and eosin (H&E) staining were performed before and after successful induction of CFA, NH and control group.

    RESULTS: At 12wk after CFA injection, inflammatory cell infiltration and fiber necrosis was observed, with acinar density and duct dilatation significantly lower compared with control group. In NH group, the meibomian gland acini were relatively smaller and deformed compared with control group, the number of meibomian gland acini was also slightly lower. No inflammatory cell or fiber necrosis was observed in NH group. After three times of IPL treatment (5/10 mice in each group, and the other 5 mice served as non-IPL control), MGOS was significantly lower in IPL-treated mice in NH group (P<0.01). After three times of IPL treatment, the MGOS of NH group was significantly lower than that in the CFA group (P<0.01).

    CONCLUSION: We develop a novel animal model that studies the role of inflammation in the development of MGD and IPL treatment. This model indicates that persistent inflammatory state may be the cause of MGD and weaken the therapeutic effect of IPL.

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