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1 therapeutic application in the inhibition of corneal inflammation.
2 se model of lipopolysaccharide (LPS)-induced corneal inflammation.
3 gets for inhibition of S. marcescens-induced corneal inflammation.
4 have a potential anti-inflammatory effect on corneal inflammation.
5  effect of topical AZM was studied in murine corneal inflammation.
6  cells was sufficient to mediate LPS-induced corneal inflammation.
7 ing disease leading to loss of vision due to corneal inflammation.
8  effective antagonist of TLR4/MD-2-dependent corneal inflammation.
9 long-term visual morbidity due to persistent corneal inflammation.
10 (-/-) gave rise to significantly less severe corneal inflammation.
11  (MyD88) in a Staphylococcus aureus model of corneal inflammation.
12 enoviral infection associated with prolonged corneal inflammation.
13 dy changes in their expression levels during corneal inflammation.
14 1 significantly suppressed VEGF(164)-induced corneal inflammation.
15 novel therapeutic targets for the control of corneal inflammation.
16 r immune intervention in neutrophil-mediated corneal inflammation.
17 ed cornea may be responsible for UV-mediated corneal inflammation.
18 ne the mechanisms by which IL-2 mediates the corneal inflammation.
19 e seems to be an effective strategy to treat corneal inflammation and angiogenesis.
20 d anti-viral ability), in an animal model of corneal inflammation and angiogenesis.
21 l cases with central tectonic grafts, active corneal inflammation and donor size >/= 9 mm were risk f
22 pithelial PD-L1 amplifies dry eye-associated corneal inflammation and epitheliopathy by increasing th
23 tor type 1 (IL-1R1) in S. marcescens-induced corneal inflammation and infection.
24                   Tbeta4 treatment decreases corneal inflammation and modulates the MMP/TIMP balance
25  spike during tear instability, resulting in corneal inflammation and triggering sensory neurons.
26 ical steroids are frequently used to control corneal inflammation and uveitis or is administered afte
27  addition, parstatin significantly inhibited corneal inflammation and VEGF-induced retinal leukostasi
28 ored daily on a 12-point scale to categorize corneal inflammation and were enucleated for quantitativ
29 ors examined the effect of HO-1 induction on corneal inflammation and wound healing in mice undergoin
30 in an intrinsic lipid circuit that regulates corneal inflammation and wound healing.
31 on, ocular surface disease, glaucoma, active corneal inflammation, anterior synechiae), donor endothe
32 of I-TAC and MIG gene expression at sites of corneal inflammation are more tightly regulated than tha
33  PLY and Freund's adjuvant is able to reduce corneal inflammation associated with pneumococcal kerati
34 o poor bacterial clearance and resolution of corneal inflammation at a later stage.
35   Our results demonstrate that IL-2 mediates corneal inflammation by 1) regulating local IFN-gamma pr
36 ly, these results suggest that IL-6 promotes corneal inflammation by acting in an autocrine-paracrine
37                        S. marcescens induces corneal inflammation by activation of TLR4/MD-2/MyD88 an
38 icone hydrogel contact lens, and we examined corneal inflammation by confocal microscopy and neutroph
39  that IFN-gamma contributes to HSV-1-induced corneal inflammation by facilitating PMN infiltration; t
40  of corneal-derived cytokines in UV-mediated corneal inflammation has not been established.
41                                       Active corneal inflammation (hazard ratio [HR], 2.5; 95% CI, 1.
42      Tobramycin-killed S. marcescens induced corneal inflammation in C57BL/6 mice, which was impaired
43 vestigated mechanisms of TLR9 ligand-induced corneal inflammation in mice after epithelial debridemen
44 eed, we show that much of the HSK-associated corneal inflammation in mice is actually attributable to
45 f the clear corneal surface is a hallmark of corneal inflammation in the human eye, we determined whe
46 ammatory response, we used a murine model of corneal inflammation in which LPS is injected into the c
47 cells that expressed LYVE-1 decreased during corneal inflammation, in conjunction with ingrowth of ly
48                                              Corneal inflammation induced by P. aeruginosa in the pre
49 eceptor 2 (TLR2) is an essential mediator of corneal inflammation induced by the filarial nematode On
50          The current study demonstrates that corneal inflammation induced by Wolbachia or O. volvulus
51 ese findings indicate that S. aureus-induced corneal inflammation is mediated by TLR2 and MyD88 in re
52 ly how antibody treatment prevents excessive corneal inflammation is not known.
53 opic cytokine is an essential participant in corneal inflammation is unclear.
54 ratitis (HSK), a CD4(+) T(H)1 cell-dependent corneal inflammation, is demonstrated.
55 rthermore, given our findings on LPS-induced corneal inflammation, it is likely that IFN-gamma-induce
56              To further investigate IL-33 in corneal inflammation, it was overexpressed in Mvarphi (R
57                                              Corneal inflammation (keratitis) is a major cause of vis
58                                Consistently, corneal inflammation resulted in reduced expression of v
59                      In additional models of corneal inflammation, Slurp1 expression was abrogated wi
60      IL-1 mediates mechanisms of immunity in corneal inflammation that subvert the normal eye's immun
61 nificantly diminishes P. aeruginosa-mediated corneal inflammation through multiple mechanisms.
62  this factor may provide novel therapies for corneal inflammation, transplant rejection, and other ly
63                                              Corneal inflammation was induced by thermal cautery in B
64 determine whether these KSPGs have a role in corneal inflammation, we examined Kera(-/-) and Lum(-/-)
65 corrected visual acuity, surface defects and corneal inflammation were also assessed.
66 tem may constitute a novel strategy to treat corneal inflammation while accelerating wound repair aft

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