Association between inflammation and epithelial damage-restitution processes in allergic airways in vivo

1997 ◽  
Vol 27 (11) ◽  
pp. 1344-1355 ◽  
Author(s):  
J. S. ERJEFALT ◽  
M. KORSGREN ◽  
M. C. NILSSON ◽  
F. SUNDLER ◽  
C. G. A. PERSSON
Keyword(s):  
Eye ◽  
2021 ◽  
Author(s):  
Huping Wu ◽  
Lan Li ◽  
Shunrong Luo ◽  
Xie Fang ◽  
Xumin Shang ◽  
...  

Abstract Objectives To evaluate the safety and efficacy of repeated corneal collagen crosslinking assisted by transepithelial double-cycle iontophoresis (DI-CXL) in the management of keratoconus progression after primary CXL. Methods A retrospective analysis was conducted in the patients who underwent repeated CXL between 2016 and 2018. These patients were treated with DI-CXL if keratoconus progression was confirmed after primary CXL. Scoring of ocular pain and corneal epithelial damage, visual acuity, corneal tomography, in vivo corneal confocal microscopy (IVCM) was performed before and at 3, 6, 12, and 24 months after DI-CXL. Results Overall, 21 eyes of 12 patients (mean age 17.3 ± 1.9 years) were included in this study. Before DI-CXL, an average increase of 4.26 D in Kmax was detected in these patients with a mean follow-up interval of (23.0 ± 13.7) months. After DI-CXL, corneal epithelial damage rapidly recovered within days. Visual acuity remained unchanged with follow-up of 24 months. When compared to baseline, significant decreases were observed in Kmax (at 3 months) and K2 (at 3 and 6 months) after DI-CXL. Corneal thickness of thinnest point significantly decreased at 3 months postoperatively. When compared to baseline, no significant differences were found in any of the refractive or tomographic parameters at 12 and 24 months. IVCM revealed trabecular patterned hyperdense tissues after DI-CXL in the anterior stroma at the depth of 200 μm or more. No corneal infiltration or persistent epithelial defect was recorded after DI-CXL. Conclusion DI-CXL is safe and effective as a good alternative in stabilizing keratoconus progression after primary CXL.


2001 ◽  
Vol 120 (5) ◽  
pp. A122 ◽  
Author(s):  
Basak Coruh ◽  
Marco Marini ◽  
Brian D. Weber ◽  
Christopher A. Moskaluk ◽  
Theresa T. Pizarro

1997 ◽  
Vol 27 (11) ◽  
pp. 1344-1355 ◽  
Author(s):  
J. S. ERJEFÄLT ◽  
M. KORSGREN ◽  
M. C. NILSSON ◽  
F. SUNDLER ◽  
C. G. A. PERSSON
Keyword(s):  

2021 ◽  
Author(s):  
Zhen Gao ◽  
Yanjiao Li ◽  
Chao Xu ◽  
Dan Luo ◽  
Qinghua Qiu ◽  
...  

Abstract To investigate the effects of niacin on rumen fermentation, rumen epithelial antioxidant activity, and rumen epithelial cell apoptosis on high concentrate (HC) diets, nine male Hu sheep were randomly divided into: low concentrate diet (LC; concentrate : forage (C:F) = 20:80, high concentrate diet (HC; C:F = 80:20), and HCN diet (HC diet + niacin at 800 mg/kg diet air-dry matter). Compared with the LC group, the HC group had a lower rumen pH, increased volatile fatty acids and lactic acid in the rumen, reduced activity of antioxidant enzymes and total antioxidant capacity, and increased malondialdehyde content in the rumen epithelium (P < 0.05). Rumen epithelial papilla morphology was decreased, and apoptosis-related indicators and serum inflammatory cytokines were increased in the HC group over the LC group (P < 0.05). Compared with the HC diet, the HCN diet increased rumen pH, rumen epithelium antioxidant capacity, and rumen epithelial papilla morphology, decreased rumen lactate content, serum inflammatory cytokines, and apoptosis-related indicators (P < 0.05). Therefore, adding 800 mg/kg niacin helped protect against rumen epithelial damage by avoiding drastic changes in the rumen environment and improved rumen epithelial antioxidant capacity to inhibit rumen epithelial cell apoptosis in sheep on a HC diet.


1997 ◽  
Vol 27 (12) ◽  
pp. 1458-1470 ◽  
Author(s):  
J. S. ERJEFALT ◽  
M. KORSGREN ◽  
M. C. NTLSSON ◽  
F. SUNDLER ◽  
C. G. A. PERSSON
Keyword(s):  

Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1515
Author(s):  
Shota Shimizu ◽  
Shinri Sato ◽  
Hiroko Taniguchi ◽  
Eisuke Shimizu ◽  
Jingliang He ◽  
...  

Graft-versus-host disease (GVHD) is a major complication after hematopoietic stem cell transplantation (HSCT), and ocular GVHD can cause severe dry eye disease that can lead to visual impairment. Epithelial damage, vascular invasion, corneal fibrosis, and corneal perforation may occur in severe cases. It is generally accepted that inflammatory cells such as dendritic cells and T cells contribute to this pathological condition. However, it is still unknown what pathological condition occurs on the ocular surface after HSCT, and when. We therefore observed the dynamics of inflammatory cells in the cornea of chronic GVHD (cGVHD) model mice from 1 to 4 weeks after bone marrow transplantation (BMT) by in vivo confocal microscopy (IVCM) and considered the relationship with the pathophysiology of ocular GVHD (tear volume, corneal epithelial damage). In the allogeneic group, neovascularization occurred in all eyes at 1 week after BMT, although almost all vessels disappeared at 2 weeks after BMT. In addition, we revealed that infiltration of globular cells, and tortuosity and branching of nerves in the cornea occurred in both cGVHD mice and human cGVHD patients. Thus, we consider that cGVHD mouse model study by IVCM reproduces the state of ocular GVHD and may contribute to elucidating the pathological mechanism for ocular GVHD.


1997 ◽  
Vol 27 (12) ◽  
pp. 1458-1470 ◽  
Author(s):  
J. S. ERJEFÄLT ◽  
M. KORSGREN ◽  
M. C. NTLSSON ◽  
F. SUNDLER ◽  
C. G. A. PERSSON
Keyword(s):  

2002 ◽  
Vol 92 (4) ◽  
pp. 1750-1761 ◽  
Author(s):  
G. P. Lambert ◽  
C. V. Gisolfi ◽  
D. J. Berg ◽  
P. L. Moseley ◽  
L. W. Oberley ◽  
...  

The purpose of this study was to characterize intestinal permeability changes over a range of physiologically relevant body temperatures in vivo and in vitro. Initially, FITC-dextran (4,000 Da), a large fluorescent molecule, was loaded into the small intestine of anesthetized rats. The rats were then maintained at ∼37°C or heated over 90 min to a core body temperature of ∼41, ∼41.5, or ∼42.5°C. Permeability was greater in the 42.5°C group compared with the 37, 41, or 41.5°C groups. Histological analysis revealed intestinal epithelial damage in heated groups. Everted intestinal sacs were then used to further characterize hyperthermia-induced intestinal permeability and to study the potential role of oxidative and nitrosative stress. Increased permeability to 4,000-Da FITC-dextran in both small intestinal and colonic sacs was observed at a temperature of 41.5–42°C compared with 37°C, along with widespread intestinal epithelial damage. Administration of antioxidant enzyme mimics or a nitric oxide synthase inhibitor did not reduce permeability due to heat stress, and tissue concentrations of a lipid peroxidation product were not altered by heat stress, suggesting that oxidative and nitrosative stress were not likely mediators of this phenomenon in vitro. In conclusion, hyperthermia produced increased permeability and marked intestinal epithelial damage both in vivo and in vitro, suggesting that thermal disruption of epithelial membranes contributes to the intestinal barrier dysfunction manifested with heat stress.


1997 ◽  
Vol 82 (2) ◽  
pp. 621-631 ◽  
Author(s):  
U. M. Wells ◽  
S. Duneclift ◽  
J. G. Widdicombe

Wells, U. M., S. Duneclift, and J. G. Widdicombe.H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin. J. Appl. Physiol. 82(2): 621–631, 1997.—Exogenous hydrogen peroxide (H2O2) causes airway epithelial damage in vitro. We have studied the effects of luminal H2O2in the sheep trachea in vivo on tracheal permeability to low-molecular-weight hydrophilic (technetium-99m-labeled diethylenetriamine pentaacetic acid;99mTc-DTPA) and lipophilic ([14C]antipyrine; [14C]AP) tracers and on the tracheal vascular response to luminal capsaicin, which stimulates afferent nerve endings. A tracheal artery was perfused, and tracheal venous blood was collected. H2O2exposure (10 mM) reduced tracheal potential difference (−42.0 ± 6.4 mV) to zero. It increased arterial and venous flows (56.7 ± 6.1 and 57.3 ± 10.0%, respectively; n = 5, P < 0.01, paired t-test) but not tracheal lymph flow (unstimulated flow 5.0 ± 1.2 μl ⋅ min−1⋅ cm−1, n = 4). During H2O2exposure, permeability to99mTc-DTPA increased from −2.6 to −89.7 × 10−7cm/s ( n = 5, P < 0.05), whereas permeability to [14C]AP (−3,312.6 × 10−7cm/s, n = 4) was not altered significantly (−2,565 × 10−7cm/s). Luminal capsaicin (10 μM) increased tracheal blood flow (10.1 ± 4.1%, n = 5) and decreased venous99mTc-DTPA concentration (−19.7 ± 4.0, P < 0.01), and these effects were significantly greater after epithelial damage (28.1 ± 6.0 and −45.7 ± 4.3%, respectively, P < 0.05, unpaired t-test). Thus H2O2increases the penetration of a hydrophilic tracer into tracheal blood and lymph but has less effect on a lipophilic tracer. It also enhances the effects of luminal capsaicin on blood flow and tracer uptake.


1995 ◽  
Vol 78 (5) ◽  
pp. 1921-1930 ◽  
Author(s):  
U. M. Wells ◽  
A. J. Woods ◽  
Z. Hanafi ◽  
J. G. Widdicombe

Tracheal osmolaity affects blood flow and the flux of a tracer, technetium-99m-labeled diethylenetriamine pentaacetic acid (99mTc-DTPA), from tracheal lumen to venous blood in anesthetized sheep. Hyperosmolar liquids increase blood flow and slightly decrease 99mTc-DTPA flux, whereas hyposmolar liquids have no effect on blood flow and greatly increase 99mTc-DTPA flux. We have now investigated whether epithelial damage induced by exposure of the tracheal lumen to a detergent (0.2% Triton X-100) alters these effects. A tracheal artery was perfused, and tracheal venous blood was collected. The initial tracheal volume was 12.8 +/- 0.7 ml. Triton X-100 greatly increased the permeability coefficient for 99mTc-DTPA from -2.1 x 10(-7) to -240 x 10(-7) cm/s. Hyperosmolar Krebs-Henseleit solution (KH; 739 +/- 6 mosmol/kg) increased arterial (+14.3%) and venous (+21.5%) flows and decreased 99mTc-DTPA output by 51.7%. Water flux into the lumen (+0.3 +/- 0.1 ml) was not significant, and the osmolality decreased by 99 +/- 9 mosmol/kg. Hyposmolar KH (124 +/- 2 mosmol/kg) had no effect on arterial and venous flows (-1.3% for both), and the increase in 99mTc-DTPA output (+8.3%) was small and not significant. The volume decreased by 0.4 +/- 0.1 ml, and the osmolaity increased by 36 +/- 4 mosmol/kg. Thus epithelial damage greatly increases the baseline permeability of the tracheal wall to 99mTc-DTPA. It does not alter the qualitative effects of hypersomolar KH on blood flow and 99mTc-DTPA output but does reduce the effect of hyposmolar KH on 99mTc-DTPA output. The latter effect may be a consequence of the reduced net water movement in response to non-isosmolar solutions after epithelial damage.


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