Biomedical subjects

C C Chan

Publications and source records attributed to C C Chan.

At least 325 records · Page 18Linked to original sources

PubMed1994

Metal release from high-copper amalgams containing palladium.

BACKGROUND: High-copper amalgam containing palladium has been successfully developed. However, the effect of palladium on the release of corrosion products remains unknown. We studied the effect of palladium addition on the electrochemical properties of amalgams by measuring the amount of the elements released from the experimental Pd-containing amalgams into Ringer's solution. METHODS: A series of specimens of high-copper amalgams containing different concentrations of palladium, from 0.42 w% to 3.33 w% in the final amalgam, fabricated from a blend of traditional amalgam alloy and copper-silver-palladium ternary alloy, were subjected to free corrosion in Ringer's solution at 37 degrees C for 3 months. Aliquots of 10 microL of electrolyte were removed serially with time, and the concentrations of Ag, Sn, Cu, Pd and Zn were evaluated by graphite furnace atomic absorption technique. In addition, dissolved Hg was evaluated by cold vapor atomic absorption technique in the same aliquotes. Various kinds of commercial amalgam including traditional (Spheraloy), high-copper blends (Dispersalloy and Valiant-Ph.D.) and high-copper spherical (Valiant) were employed as controls. RESULTS: Ag and Sn cations released from the amalgams containing palladium were similar in concentration to those released from the commercial amalgams. The concentrations of released Cu and Hg cations decreased as a function of increased Pd concentration in the experimental amalgams. Averaging an order of magnitude of released Cu and Hg cations less than commercial controls for amalgam containing 1.7 w% Pd. Detection of Pd was essentially below the resolution of the technique and Zn was only detected in case of Dispersalloy. CONCLUSIONS: Pd addition to high-copper amalgam alloy reduces the release of mercury and copper from the Pd-containing amalgam.

Copper↗

PubMed1993

Cloning and expression of rat prostaglandin endoperoxide synthase (cyclooxygenase)-2 cDNA.

Rat prostaglandin endoperoxidase synthase-2 (PGHS-2) cDNA was cloned from rat calvarial osteoblasts total RNA by RT-PCR. The primary sequence of rat PGHS-2 had 98% and 92% identity to the mouse and human enzymes, respectively. Transfection of the rat PGHS-2 cDNA into COS 7 cells, followed by the addition of 20 microM arachidonic acid, resulted in a dramatic increase in PGE2 released from these cells. The amount of PGE2 produced was comparable to that obtained from cells similarly transfected with human PGHS-1 cDNA. In the rat paw carrageenin-oedema inflammatory model, the injected paw had elevated levels of PGHS-2 mRNA compared to the control paw. In a rat pyrexia model, injection of the pyrogen lipopolysaccharide, resulted in elevated levels of PGHS-2 mRNA in the brain. These results suggest that PGHS-2 expression plays a role both in inflammation and fever.

Amino Acid Sequence↗

PubMed1993

Monoclonal antibodies against ICAM-1 (CD54) and LFA-1 (CD11a/CD18) inhibit experimental autoimmune uveitis.

Cell adhesion molecules are surface proteins important for cell migration and adhesion and are strongly expressed in eyes with inflammation. We studied the expression of two cell adhesion molecules: intercellular adhesion molecule-1 (ICAM-1, CD54) and lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18) in mice with experimental autoimmune uveitis. B10.A mice were immunized with interphotoreceptor retinoid-binding protein and eyes were serially examined for expression of cell adhesion molecules using immunohistochemical staining. ICAM-1 was expressed on the vascular endothelium of the ciliary body and retina by 7 days after immunization, and LFA-1 was first expressed on some infiltrating inflammatory cells 9 days after immunization. Clear histologic evidence of ocular inflammation did not occur until 11 days after immunization. We then studied the effect of monoclonal antibodies against ICAM-1 and LFA-1 on the development of experimental autoimmune uveitis. Three groups of mice were immunized and treated for 21 days with daily intraperitoneal injections of rat monoclonal antibody against murine ICAM-1 or LFA-1 or with rat IgG as control. Ocular inflammation, graded clinically by examination of the fundus 14 and 21 days after immunization, was significantly decreased in animals treated with anti-ICAM-1 (P < 0.01 at Days 14 and 21) and with anti-LFA-1 antibody (P < 0.01 at Days 14 and 21). The intraocular inflammation graded histologically was also decreased in mice treated with anti-ICAM-1 and anti-LFA-1 antibody. This difference in the histologic grade of inflammation was statistically significant (P < 0.02) between mice treated with anti-ICAM-1 antibody and control mice and approached statistical significance (P < 0.10) in mice treated with anti-LFA-1 antibody compared to the control mice. Proliferative responses to lipopolysaccharide, PPD, and interphotoreceptor binding protein of lymphocytes obtained from the draining lymph nodes of mice treated with the antibodies were lower than those from the control mice, suggesting that cell-cell binding was impaired in treated mice. These data show that ICAM-1 is expressed in the eye before histologic evidence of inflammation, and that monoclonal antibodies against ICAM-1 and LFA-1 are effective in inhibiting experimental autoimmune uveitis in mice.

Animals↗

PubMed1993

Suppression of S-antigen-induced experimental autoimmune uveoretinitis in Lewis rats by oral administration with CGS-13080, a thromboxane synthetase inhibitor.

Oral administration of CGS-13080 [imidazo (1, 5-alpha) pyridine-5-hexanoic acid], a thromboxane synthetase inhibitor, has been reported to cause a marked reduction in serum thromboxane B2 concentration in humans and animals. Since thromboxane metabolites play an important role in ocular inflammation, the effect of oral CGS-13080 in the development of experimental autoimmune uveoretinitis in Lewis rats has been investigated. Females were immunized with bovine S-antigen (S-Ag). Treatment was started on day 0 of immunization. Animals were divided into three groups. The control group was fed a standard pellet diet, while the treated groups were fed the standard diet supplemented with either a low dose (0.8 g per 10 kg pellet) or a high dose (1.6 g per 10 kg pellet) of CGS 13080. From day 10 after immunization, the eyes of these rats were examined daily for clinical evidence of experimental autoimmune uveoretinitis. On day 14, the eyes were collected for histologic study. The cellular immune responses were evaluated on the draining inguinal lymph nodes. Blood samples were also collected for the measurement of anti-S-Ag antibody production, thromboxane B2 and prostaglandin A2 levels. Clinical disease developed in 73.3% of the control rat group, 30.0% of the low-dose treated group and 17.6% of the high-dose group. The average histologic grade was 1.9 in the control group, 0.65 in low-dose group and 0.32 in high-dose group. Lymphocyte proliferation to S-Ag paralleled the clinical disease scores. Average stimulation indices were 10.9 in the controls, 7.5 in the low-dose group and 2.2 in the high-dose group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Recruitment of antigen-nonspecific cells plays a pivotal role in the pathogenesis of a T cell-mediated organ-specific autoimmune disease, experimental autoimmune uveoretinitis.

Experimental autoimmune uveoretinitis (EAU) is a prototypic T cell-mediated autoimmune disease, whose target tissue is the neural retina, that is used as a model for a number of human blinding ocular diseases of a presumed autoimmune nature. EAU in rats can be induced by adoptive transfer of small numbers of retinal antigen-specific CD4+ T cell lines. Although recruitment mechanisms were assumed to play a role in the immunopathogenesis of uveitis, there is no direct evidence that would permit assessment of the importance of recruited non-antigen-specific T cells in retinal autoimmunity. In the present study, we addressed this question by using congenitally athymic Lewis rats (LEW.rnu/rnu), that are deficient in functional endogenous T cells, but are otherwise syngeneic with the euthymic Lewis rats that develop characteristically severe EAU. The uveitogenic stimulus was delivered in the form of phenotypically and functionally homogeneous pathogenic T cell lines, specific to the major pathogenic epitope of either the intracellular photoreceptor protein, S-Ag, or the extracellular photoreceptor matrix protein, IRBP. Depending on the T cell line used, EAU in athymic rats was either drastically reduced in severity (IRBP), or essentially absent (S-Ag). Susceptibility was restored when the athymic animals were reconstituted with immunocompetent T cells from syngeneic euthymic donors. While the intraocular infiltrate in euthymic rats was predominantly lymphocytic, with smaller numbers of monocyte/macrophages and even fewer neutrophils, the sparse infiltrate in athymics was largely monocytic, and with a relatively high proportion of neutrophils and eosinophils. Reconstituted animals had an intermediate histological picture with respect to the infiltrating cell types and disease severity. Our data are consistent with the interpretation that recruitment of naive T cells constitutes an amplification mechanism that is central to the expression and pathogenesis of uveitis. The extent of dependence on this phenomenon appears to be influenced by the antigenic specificity of the T cell line, and could be connected to the 'accessibility' of the target antigen in vivo.

Animals↗

PubMed1993

Intraocular lymphoma. Clinical and histopathologic diagnosis.

BACKGROUND: Intraocular lymphoma is associated with significant morbidity and mortality, but early diagnosis and treatment may improve prognosis. METHODS: The diagnostic features of 12 cases of intraocular lymphoma diagnosed at the National Eye Institute between 1984 and 1992 were retrospectively reviewed. RESULTS: A pathologic diagnosis of large B-cell lymphoma was made on vitrectomy specimens in ten patients, cerebral spinal fluid in one, and on an enucleation specimen in one. The mean time from onset of symptoms to diagnosis was 21.4 months (range, 1-66 months). All 12 patients were given a final diagnosis of non-Hodgkin's lymphoma of the central nervous system (NHL-CNS), based on the epidemiology, pathology, and clinical course of their tumors. Although an initial vitrectomy was negative for malignant cells in three of ten patients, a repeat vitrectomy specimen subsequently showed intraocular lymphoma. Results of examination of the cerebrospinal fluid (CSF) showed malignant cells in 5 of 11 patients, although malignant cells were only identified after repeat examination of additional samples of CSF in three of these patients. Malignant cells often are difficult to identify, and an experienced cytopathologist was critical in making the correct diagnosis. In addition, corticosteroids are lympholytic to the lymphoma cells, and they appeared to decrease the viability of tumor cells obtained in samples of vitreous and CSF. CONCLUSION: The prompt, appropriate handling of specimens and review by an experienced cytopathologist are critical to the diagnosis of intraocular lymphoma. Malignant cells often are present in the cerebral spinal fluid at the time that ocular lymphoma is diagnosed. Nevertheless, multiple vitrectomies and lumbar punctures may be necessary before the correct diagnosis is made.

Adult↗

PubMed1993

The role of chorioretinal biopsy in the management of posterior uveitis.

BACKGROUND: The ideal management of intraocular inflammation may require a tissue diagnosis. Diagnostic vitrectomy is a well-established method for acquiring such tissue. However, in some patients, the diagnostic pathology is limited to the choroid and retina and vitrectomy may yield no useful information. In such cases, a more aggressive surgical approach to obtain tissue may be useful. METHODS: The authors performed chorioretinal biopsies on seven patients with progressive chorioretinal lesions of unknown etiology. Indications for biopsy included: (1) macular-threatening lesions unresponsive to therapy, (2) suspicion of malignancy, or (3) suspicion of an infectious etiology. In all cases, it was expected that the results would alter therapy or other aspects of clinical care. Preoperative visual acuity was 20/200 or worse in each eye biopsied with one or more peripheral chorioretinal lesions present. Biopsy specimens were divided into three parts and submitted for light and electron microscopy, immunohistochemistry, and tissue culture. RESULTS: On the basis of the biopsy findings, a diagnosis of multifocal choroiditis and subretinal fibrosis was rendered in three eyes, sarcoidosis in two eyes, and viral retinitis in two eyes. Therapy was changed in five patients. Final visual acuity was unchanged or improved in five eyes. Complications included the progression of lens opacity in all eyes and the development of phthisis in one eye that was extensively diseased preoperatively. CONCLUSION: Chorioretinal biopsy may provide useful information for determining the diagnosis and guiding the subsequent management of patients with progressive chorioretinal lesions of unknown etiology.

Adult↗

PubMed1993

Student's exposure to volatile organic compounds while commuting by motorcycle and bus in Taipei City.

This study examined student's exposure to volatile organic compounds (VOCs) while commuting by bus and motorcycle in Taipei, Taiwan in the winter of 1992. A total of 19 target C5-C10 VOCs on three most frequently used commuting routes were collected on Tenax-GC adsorbent tubes. The VOCs were desorbed by thermal desorption method and analyzed by GC-MS. The most abundant VOC exposure experienced by commuters was to toluene. Several alkylated benzenes, such as propyl benzenes, ethyl-methyl-benzenes and trimethyl-benzenes, were relatively abundant on the roads in Taipei. The mean benzene concentration measured in buses was 173 micrograms/m3 and motorcycles. On the average, the commuters in Taipei experienced about three to eight times higher VOC concentrations than the commuters in Los Angeles, California. Higher VOC concentrations were measured on motorcycles than in buses. The VOC concentrations were not significantly different between morning and afternoon commutes, nor among the three commuting routes. VOC concentrations measured in classroom at three schools in downtown Taipei did not vary significantly on each sampling day. However, at each school the in-classroom VOC concentrations varied significantly over the six consecutive sampling days. The VOC concentrations measured on the roads were about five times higher than those measured in the school classrooms in the city. Moderate to high correlations were found among most of the measurements of the 19 VOCs. The survey questionnaire indicated that daily commuting time ranged from 45 minutes for elementary school students to 95 minutes for vocational school students.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

Initiation and promotion of colonic aberrant crypt foci in rats by 5-hydroxymethyl-2-furaldehyde in thermolyzed sucrose.

We have previously shown that thermolyzed sucrose in the diet promotes the growth of aberrant crypt foci (ACF) in the rat. HPLC analysis of the light caramel colored product showed that it contained 1% 5-hydroxymethyl-2-furaldehyde (HMF), confirmed by mass and NMR spectroscopy. To determine whether HMF was responsible for the promotion of ACF by thermolyzed sucrose, 45 F344 female rats were initiated with the colon carcinogen azoxymethane (AOM), and a week later were randomized to four groups receiving AIN-76 diets containing untreated sucrose, 20% thermolyzed sucrose, 20% butanol extracted thermolyzed sucrose (HMF free) or 1% HMF. Thermolyzed sucrose in the diet led to larger ACF as previously observed. Thermolyzed sucrose extracted to remove HMF, did not affect ACF size, but 1% HMF added to the diet led to a larger ACF both with relation to average size and number of ACF of larger sizes (P < 0.05). To determine whether HMF had initiating effects, 172 female F344 rats were given water, HMF (at doses to 300 mg/kg) or AOM (5 mg/kg) by gavage twice and the total number of ACF was scored 30 days later. The results demonstrated that HMF induces ACF in a dose-dependent manner (P < 0.02), though the effect was much weaker than that of AOM. We conclude that sugar heated under household cooking conditions may act as both an initiator and a promoter of colon cancer because of the presence of HMF.

Animals↗

PubMed1993

Anterior corneal dystrophy with dyscollagenosis (Reis-Bücklers type?).

Anterior corneal dystrophies involving Bowman's membrane and anterior stroma include several subtypes of uncertain etiology: the Reis-Bückler, Thiel-Behnke, Grayson-Wilbrandt, and "honeycomb" dystrophies. The clinical and pathologic features of these dystrophies overlap to such a degree that they may represent variations of the same entity. Typically, they all present symptoms beginning in childhood, have a dominant pattern of heredity, and manifest painful, recurrent corneal erosions. Some cases have also been interpreted as representing macular and granular dystrophy. In the present report, we describe a pedigree of affected patients whose corneal dystrophy shared many of the clinical and pathologic features of the Reis-Bücklers and allied subtypes but which differ from all in causing visual symptoms late in life and with minimal signs of recurrent erosion. Histopathology revealed a thickening of the anterior stroma by the addition of a partially disorganized and degenerating tissue in which collagen Type III (fetal or repair collagen) is intermixed with the normal (mature) Type I collagen in the entire stroma. This is accompanied by irregular swelling of the basal epithelial cells and hyperplasia of the basement membrane (collagen Type IV, laminin and fibronectin), suggesting an aberrant influence of the epithelium on collagen synthesis.

Aged↗

PubMed1993

Expression of cell adhesion molecules in corneal graft failure.

Corneal graft failure is frequently mediated by uncontrolled inflammatory disease. We studied the expression of cell adhesion molecules in seven penetrating keratoplasty specimens with graft failure and in a normal eye bank cornea using immunohistochemical staining and monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1, CD54), lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and major histocompatibility complex (MHC) class II antigen (HLA-DR). ICAM-1 and HLA-DR were expressed on keratocytes and the corneal endothelium in six of the seven specimens. ICAM-1 expression was strongest in the corneas with the most severe inflammation (corneal allograft rejection and severe intraocular inflammation). LFA-1 is a counter-receptor for ICAM-1, and infiltration with leukocytes expressing either the alpha or beta chain of LFA-1 was found in areas of ICAM-1 expression in four of the seven corneas. In contrast, E-selectin was expressed in the stroma in only two specimens, and VCAM-1 in one specimen. Expression of cell adhesion molecules or MHC class II antigen were not detected in the normal eye bank cornea. These data suggest that ICAM-1 expression may play an important role in the development of corneal graft failure. Furthermore, monoclonal antibodies to block ICAM-1 or its ligands may inhibit the development of corneal inflammation.

Antibodies, Monoclonal↗

PubMed1993

Budd-Chiari syndrome: successful treatment by percutaneous transluminal angioplasty.

Budd Chiari syndrome is a rare disorder. It is caused by obstruction of the hepatic veins. The prognosis is usually dismal, except in the rare case where the obstruction is due to either webs in the hepatic veins or membranous obstruction of the inferior vena cava. Such cases, more common in the Orient, can be treated by percutaneous transluminal angioplasty. We report a case of Budd Chiari syndrome, due to a membranous obstruction in the right hepatic vein, successfully treated by percutaneous transluminal angioplasty.

Adolescent↗

PubMed1993

NK2 receptors mediate plasma extravasation in guinea-pig lower airways.

1. Neurokinin (NK) receptor-mediated extravasation has been examined in guinea-pig airways by use of a recently described marker for microvascular protein leakage, 125I-labelled human fibrinogen. 2. Neurokinin A (NKA) caused a dose-dependent increase in plasma [125I]-fibrinogen extravasation in trachea, main bronchi, secondary bronchi and intraparenchymal airways. In contrast, the NK2 selective agonist [beta-Ala8]NKA(4-10) only caused extravasation in the secondary and intraparenchymal airways. 3. The NK2 selective antagonist, SR 48968, caused a dose-dependent inhibition of NKA and [beta-Ala8]NKA(4-10)-induced extravasation of fibrinogen in guinea-pig secondary bronchi and intraparenchymal airways. SR 48968 was without effect on the NKA-induced extravasation in trachea and main bronchi. 4. NKA- or [beta-Ala8]NKA(4-10)-induced plasma extravasation was not modified by pretreatment with histamine H1- or H2-receptor antagonists. 5. It is concluded that NK2 receptors mediate plasma [125I]-fibrinogen extravasation in guinea-pig secondary bronchi and intraparenchymal airways. This effect is direct and does not depend upon histamine released from mast cells.

Animals↗

PubMed1993

Neurokinin receptor mediated plasma extravasation in guinea pig and rat airways: comparison of 125I-labelled human fibrinogen and 99mTc-labelled human serum albumin as markers of leakage.

In the present study we have characterized NK-1 and NK-2 receptor induced microvascular leakage in guinea pig and rat airways, using 125I-labelled human fibrinogen ([125I]FN) versus 99mTc-labelled human serum albumin ([99mTc]HSA) as markers for plasma protein extravasation. Intravenous administration of the selective NK-1 agonist [Sar9, Met(O2)11]SP (1 nmol kg-1) caused a dose-dependent increase of [125I]FN extravasation in guinea pig trachea, main bronchi, secondary bronchi, and intraparenchymal airways. Extravasation of [125I]FN increased by up to 192 (trachea), 284 (main bronchi), 368 (secondary bronchi), and 271% (intraparenchymal bronchi) over control levels in these regions of the airways. Pretreatment of the animals with CP 99,994 and RP 67,580, two NK-1 nonpeptide antagonists, caused a dose-dependent inhibition of [Sar9, Met(O2)11]SP-induced leakage of [125I]FN. [Sar9, Met(O2)11]SP (1 nmol kg-1) did not induce specific leakage of [99mTc]HSA in the intraparenchymal bronchi. Specific NK-2 receptor induced leakage was detected in the lower airways but only when using [125I]FN as a marker. We have also compared the ability of CP 99,994 and RP 67,580 to inhibit [Sar9, Met(O2)11]SP induced extravasation of [125I]FN in rat airways. CP 99,994 was 40-50 (tracheobronchial region) to 75 (lower airways) times more potent in the guinea pig than the rat airways. In contrast, RP 67,580 had higher affinity for rat airways compared with guinea pig airways. The results of this study highlight the superiority of [125I]FN as a sensitive marker of plasma extravasation over [99mTc]HSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1993

Human retinoblastoma cells express alpha B-crystallin in vivo and in vitro.

alpha B-crystallin is a major lens protein that is a member of the heat-shock family of proteins. Using immunohistochemical and northern blot techniques, we now demonstrate its presence in freshly-fixed retinoblastoma tissue. The protein is also abundantly expressed in cultured human retinoblastoma cells (Y-79 NEI, WERI Rb-1) as well as two subcultured Y-79 lines (ATCC and GM01232C). High expression of alpha B-crystallin may be involved in tumor growth and/or be a marker for general oncogenic "stress" in the tumor tissue.

Animals↗

PubMed1993

Treatment of autoimmune uveoretinitis in the rat with rapamycin, an inhibitor of lymphocyte growth factor signal transduction.

Rapamycin (RAPA) is a macrolide antibiotic with unique immunosuppressive properties. RAPA inhibits T-cell function by interfering with IL-2 and IL-4 signal transduction. It does not prevent IL-2 production or IL-2R expression. The efficacy of RAPA in the treatment of autoimmune diseases was evaluated using the experimental autoimmune uveoretinitis (EAU) model. EAU was actively induced in Lewis rats by immunization with S-antigen in Hunter's adjuvant. RAPA and control vehicle were administered by continuous intravenous infusion over a 14 day period by miniosmotic pump. RAPA treatment initiated on the day of immunization or 7 days later was found to efficiently inhibit EAU induction. The minimal effective dose was 0.1 mg/kg/d. EAU inhibition was correlated with reduced number of cells in the immunization site draining lymph nodes, as well as with a shift and lowering of the peak of the lymphocyte proliferative response curve. The anti-S-antigen antibody response was delayed by 3 days under RAPA treatment and the serum levels lowered in a dose dependent manner. An initial body weight loss was observed during the first week of drug administration, but there was a normal weight gain afterward.

Animals↗

PubMed1993

Splenectomy abrogates the induction of oral tolerance in experimental autoimmune uveoretinitis.

Oral administration of uveitogenic antigens inhibits the development of experimental autoimmune uveoretinitis (EAU) and the cellular immune response initiated by these antigens. The mechanism of oral tolerance is not completely clear, but accumulating data indicate that suppressor cells are actively involved in this process. The spleen is known to harbor suppressor cells and their precursors and the present study was aimed at testing the role of this organ in the induction of oral tolerance by S-antigen (S-AG). We report here that: (a) splenectomy abrogated the induction of oral tolerance; unlike in sham operated controls, feeding with S-Ag did not inhibit the development of EAU in splenectomized rats; (b) splenectomized rats responded with higher cellular immune responses than did sham operated controls, but feeding with S-Ag inhibited these responses in both groups of animals; (c) splenectomy also abrogated the adoptive transfer of tolerance: EAU induction was inhibited in sham operated recipients of splenocytes from S-Ag fed donors but not in the splenectomized recipients. The data thus indicate that the spleen plays an important role in the induction of oral tolerance, perhaps by acting as the site for induction and/or amplification of cells with suppressor activity.

Animals↗

PubMed1993

Monoclonal antibody against CD11b/CD18 inhibits endotoxin-induced uveitis.

PURPOSE: To examine the serial expression of cell adhesion molecules in C3H/HeN mice with endotoxin-induced uveitis, and to study the effect of treatment with a monoclonal antibody against Mac-1 on the development of endotoxin-induced uveitis. METHODS: Immunohistochemical staining was used to document the serial expression of Mac-1, intercellular adhesion molecule-1 (ICAM-1), and lymphocyte function-associated antigen-1 (LFA-1) in eyes of C3H/HeN mice with endotoxin-induced uveitis. Then, in two separate experiments, endotoxin-induced uveitis was produced in a total of 48 mice by injecting Salmonella typhimurium endotoxin into one hind footpad. At the time of endotoxin injection, 24 mice received an intraperitoneal injection of anti-Mac-1 antibody and 24 control mice received an intraperitoneal injection of rat IgG. Histopathologic sections of eyes taken 24 hours after endotoxin injection were graded by two masked observers on a scale of 0 to 4. RESULTS: Intercellular adhesion molecule-1 was first expressed on the ciliary body epithelium 6 hr after endotoxin injection and Mac-1 and LFA-1 were expressed on infiltrating inflammatory cells 12 hr after endotoxin injection. Treatment with anti-MAC-1 antibody significantly inhibited the development of ocular inflammation when compared with treatment with control IgG (P < 0.001). CONCLUSION: Intercellular adhesion molecule-1 is expressed in the eye before clinical or histologic signs of inflammation. Furthermore, treatment with antibody against Mac-1 significantly inhibits the development of endotoxin-induced uveitis in mice and suggests that anti-Mac-1 antibody may be useful for treating acute ocular inflammation.

Animals↗