Alterations of the ocular surface epithelial MUC16 and goblet cell MUC5AC in patients with atopic keratoconjunctivitis.
BACKGROUND
An increased understanding of the ocular surface at cellular level in the conjunctiva and the cornea may help explain the pathogenesis and the subsequent clinical appearance of atopic ocular allergies, which may be potentially blinding.


OBJECTIVE
To investigate the MUC16 and MUC5AC alterations, tear function and the ocular surface disorder in patients with atopic keratoconjunctivitis (AKC).


METHODS
Thirty-six eyes of 18 AKC patients as well as 28 eyes of 14 age- and sex-matched normal subjects were studied. The subjects underwent corneal sensitivity measurements, Schirmer test, tear film break-up time (BUT), fluorescein and Rose-Bengal staining of the ocular surface, conjunctival impression cytology and brush cytology. Impression cytology samples underwent periodic acid schiff and immunohistochemical staining with MUC16 and MUC5AC antibodies. Brush cytology specimens underwent evaluation for inflammatory cell numbers and quantitative real-time polymerase chain reaction (PCR) for MUC16 and MUC5AC mRNA expression.


RESULTS
The mean corneal sensitivity and BUT values were significantly lower in patients with AKC, compared with controls (P < 0.001). Brush cytology specimens from AKC patients revealed significantly higher numbers of inflammatory cells (P < 0.001). Specimens from patient eyes showed positive staining for MUC5AC and MUC16. MUC16 mRNA expression was significantly upregulated with significant downregulation of MUC5AC mRNA expression in eyes with AKC compared with the eyes of control subjects.


CONCLUSIONS
Ocular surface inflammation, decline in corneal sensitivity, tear film instability, changes in conjunctival epithelial MUC5AC and MUC16 mRNA expressions were thought to be important in the pathogenesis of atopic ocular surface disease.
Dogru
M
M
Department of Ophthalmology, Tokyo Dental College Ichikawa General Hospital, Ichikawa, Japan.
Matsumoto
Y
Y
Okada
N
N
Igarashi
A
A
Fukagawa
K
K
Shimazaki
J
J
Tsubota
K
K
Fujishima
H
H
D000293:Adolescent; D000328:Adult; D018394:CA-125 Antigen / Q000096:biosynthesis* / Q000235:genetics; D002648:Child; D003228:Conjunctiva / Q000378:metabolism / Q000473:pathology*; D003233:Conjunctivitis, Allergic / Q000378:metabolism / Q000473:pathology*; D015536:Down-Regulation / Q000235:genetics; D005136:Eye Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D020397:Goblet Cells / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007637:Keratoconjunctivitis / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis* / Q000235:genetics; D008875:Middle Aged; D055271:Mucin 5AC; D009077:Mucins / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D015854:Up-Regulation / Q000235:genetics
D018394:CA-125 Antigen; D005136:Eye Proteins; C451759:MUC16 protein, human; C524678:MUC5AC protein, human; D008565:Membrane Proteins; D055271:Mucin 5AC; D009077:Mucins; D012333:RNA, Messenger