(1/369) Compound-heterozygous mutations in the plasminogen gene predispose to the development of ligneous conjunctivitis.

Homozygous type I plasminogen deficiency has been identified as a cause of ligneous conjunctivitis. In this study, 5 additional patients with ligneous conjunctivitis are examined. Three unrelated patients (1 boy, 1 elderly woman, and 1 man) had plasminogen antigen levels of less than 0.4, less than 0.4, and 2.4 mg/dL, respectively, but had plasminogen functional residual activity of 17%, 18%, and 17%, respectively. These subjects were compound-heterozygotes for different missense mutations in the plasminogen gene: Lys19 --> Glu/Arg513 --> His, Lys19 --> Glu/Arg216 --> His, and Lys19 --> Glu/Leu128 --> Pro, respectively. The other 2 patients, a 14-year-old boy and his 19-year-old sister, who both presented with a severe course of the disease, exhibited plasminogen antigen and functional activity levels below the detection limit (<0.4 mg/dL and <5%, respectively). These subjects were compound-heterozygotes for a deletion mutation (del Lys212) and a splice site mutation in intron Q (Ex17 + 1del-g) in the plasminogen gene. These findings show that certain compound-heterozygous mutations in the plasminogen gene may be associated with ligneous conjunctivitis. Our findings also suggest that the severity of clinical symptoms of ligneous conjunctivitis and its associated complications may depend on the amount of plasminogen functional residual activity.  (+info)

(2/369) Suppression of induction of experimental immune mediated blepharoconjunctivitis by tolerogenic conjugates of the antigen and monomethoxypolyethylene glycol.

AIM: Covalent conjugates consisting of diverse antigens coupled to optimal numbers of monomethoxypolyethylene glycol (mPEG) molecules have been shown to suppress antigen specific antibody formation. In this study, the possibility was examined that the same conjugates might prevent experimental immune mediated blepharoconjunctivitis (EC, formerly EAC) which had been shown to be caused by CD4(+) T cells-that is, to cell mediated immunity. METHODS: 6-8 week old male Lewis rats were used. The test groups of rats received two intravenous injections, each of 300 microg, of a conjugate of ovalbumin mPEG (OVA(mPEG)(11)) in phosphate buffered saline (PBS), 14 and 28 days before the single immunisation with OVA in complete Freund's adjuvant. The rats were challenged 3 weeks later by eye drops containing OVA; 24 hours later they were sacrificed, and their eyes, blood, and lymph nodes were harvested for histological examination and determination of anti-OVA antibody titres and levels of cellular immunity. Two control groups received PBS or OVA in PBS before immunisation. Furthermore, the possibility that OVA(mPEG)(11) may have induced OVA specific suppressor cells was tested by establishing the effects of the co-transfer of splenocytes from OVA(mPEG)(11) treated rats with OVA primed lymph node cells on the manifestations of EC. RESULTS: Either PBS or OVA pretreated rats, which had not received OVA(mPEG)(11), developed high levels of antibodies and cell mediated immune responses to OVA, and application of eye drops led to blepharoconjunctivitis with massive cellular infiltration. In contrast, pretreatment with OVA(mPEG)(11) prevented cellular infiltration into the lids and conjunctivas, as well as the formation of detectable humoral and cellular immunity against OVA. Co-transfer of splenocytes from OVA(mPEG)(11) treated rats with OVA primed lymph node cells suppressed the cellular infiltration on application of OVA on the conjunctiva. CONCLUSIONS: These data indicate that intravenous injection of OVA(mPEG)(11) conjugates suppressed both humoral and cellular immunity by the effects of antigen specific suppressor cells, thus leading to the inhibition of development of EC.  (+info)

(3/369) Expression of gelatinase B in trachomatous conjunctivitis.

BACKGROUND/AIMS: Gelatinase B is a matrix metalloproteinase involved in extracellular matrix (ECM) breakdown often associated with scarring and other pathological disorders. It was investigated whether gelatinase B is involved in the pathogenesis of ECM degradation associated with trachomatous conjunctivitis. METHODS: Conjunctival biopsy specimens obtained from six patients with active trachoma, six patients with active vernal keratoconjunctivitis (VKC), and seven control subjects were studied. Immunohistochemical techniques and a specific monoclonal antibody against human gelatinase B were used, and a monoclonal antibody against macrophage CD68 to identify mononuclear cells with gelatinase B immunoreactivity. In addition, quantitative zymography was used to compare the activity of gelatinase B in conjunctival biopsy specimens from seven patients with active trachoma and seven control subjects. RESULTS: Gelatinase B was detected by immunohistochemistry only in polymorphonuclear cells located in the vascular lumens in three normal conjunctival biopsy specimens. In all trachoma specimens and in five VKC specimens, gelatinase B was localised in monocyte/macrophage cells, positive for the CD68 marker, and in polymorphonuclear cells. The majority of the latter cell type was located in intravascular spaces. Compared with VKC specimens, trachoma specimens showed significantly more immunoreactive gelatinase B monocyte/macrophage cells (52.3 (21.9) v 8.2 (6.4); p <0.001) and polymorphonuclear cells (23.2 (14.2) v 6.3 (5.4); p = 0. 013). Activated macrophages with giant cell morphology clearly stained with the gelatinase B specific monoclonal antibody were observed in trachoma specimens. Zymography revealed that gelatinase B levels in trachoma specimens were significantly higher than the levels found in normal conjunctiva (1739.6 (1078.3) v 609.3 (395.9) scanning units; p = 0.0127). CONCLUSIONS: The increased activity of gelatinase B and numbers of inflammatory cells containing gelatinase B in trachoma specimens suggest that this enzyme plays a part in the pathogenesis of conjunctival scarring in trachoma.  (+info)

(4/369) Expression of CD40 and CD40 ligand in the human conjunctival epithelium.

PURPOSE: CD40 antigen is a membrane receptor that plays a role in the regulation of immune reactions. The expressions of CD40 and CD40 ligand (CD40L) were investigated ex vivo and in vitro in conjunctival epithelial cells, in correlation with HLA DR class H antigen, previously shown to be upregulated in conjunctival inflammatory conditions. METHODS: Impression cytology specimens were collected in 186 patients: 52 normal ones, 65 with keratoconjunctivitis sicca, and 69 with chronic conjunctivitis. Cells were processed for flow cytometry, by using monoclonal antibodies to CD40, CD40L, and HLA DR antigens. Chang conjunctival cells were also used and treated with human recombinant interferon (IFN)-gamma or tumor necrosis factor (TNF)-alpha. CD40, CD40L, and HLA DR expressions were studied by flow cytometry after 24 and 48 hours of treatment. RESULTS: CD40 was found in both normal and pathologic eyes. Quantitation of levels of fluorescence showed a significantly higher expression in pathologic eyes than in normal ones (P < 0.0001). CD40L was variably and inconstantly expressed by conjunctival cells. A strong expression of HLA DR was observed in pathologic eyes, whereas normal eyes showed very low levels (P < 0.0001). Significantly positive correlations were found among CD40, CD40L, and HLA DR levels. Chang conjunctival cells expressed CD40 in basal conditions, whereas CD40L and HLA DR were negative. CD40 expression significantly increased after 24 hours of IFNgamma treatment and after 48 hours' exposure to TNFalpha. These cytokines had no effect on CD40L expression. HLA DR was upregulated after 24 hours of treatment with IFNgamma but remained negative after exposure to TNFalpha. CONCLUSIONS: Human conjunctival epithelial cells normally express CD40 antigen, and, more inconsistently, CD40L. Flow cytometry showed higher expression of these molecules in inflammatory eyes than in normal ones in correlation with class II antigen expression, as well as CD40 and HLA DR upregulation after treatment with proinflammatory cytokines in vitro.  (+info)

(5/369) An investigation of the family background of acute Haemophilus infections of children.

Nose and throat swabs, for culture of Haemophilus influenza type b, and blood samples, for measurement of antibodies specific for that serotype, were collected from members of 28 families from which children had been admitted to hospital with acute H. influenzae type b infections (mainly meningitis or epiglottitis). The patients with meningitis were younger than those with epiglottitis and had more siblings, with a marked predominance of sisters. Investigations within a few days of admission of the affected children to hospital detected carriers of H. influenzae type b (19 altogether) in 13 of the 28 families, including 9 of the 13 families with 3 or more children. Members with raised antibody titres for H. influenzae type b (suggesting the presence of the organism for at least a few weeks) were found in 17 of the 25 families from which blood samples were obtained, including all 11 families with 3 or more children. Most of the patients probably acquired their infections from within their own families, and siblings under 11 years old were of predominant importance both as carriers and as potential sources of the patients' infections. Persistence of the organism within families for up to 6 months was demonstrated. Possible reasons for the difference in age-incidence between haemophilus meningitis and epiglottitis and for the occurrence of the former in babies with older sisters are suggested, and also a possible connection between the results of this survey and the likely value of immunization against H. influenzae type b.  (+info)

(6/369) Simple tests for the diagnosis of picornavirus epidemic conjunctivitis (acute haemorrhagic conjunctivitis).

Simple tests for the study of picornavirus epidemic conjunctivitis are described. The virus was successfully isolated in wells of microtitration plates containing HeLa cell suspension and the isolates were easily identifiable by neutralization in the micrometabolic inhibition test. For the estimation of antibody titre in patients' sera, the latter procedure was found to be as reliable as neutralization in tissue culture tubes. These micromethods would enable virus laboratories not equipped for tissue culture work to study this new ocular disease, which has been endemic in a number of countries since the pandemic outbreak of 1969-72 in Africa, Asia, and Europe (London).  (+info)

(7/369) Untoward effects associated with practolol: demonstration of antibody binding to epithelial tissue.

An antibody which sticks to the intercellular region of xenogenic epidermal tissue has been shown by indirect immunofluorescence to be present in the serum of patients with practolol-induced eye damage. These antibodies and those found in patients with pemphigus were compared for their ability to bind to isolated epidermal cells. Binding was achieved only with the pemphigus antibody, which suggests that it may have a different specificity from the antibody associated with practolol-induced eye damage.  (+info)

(8/369) Recent epidemiological status of feline upper respiratory infections in Japan.

Epidemiology of upper respiratory infections of cats was studied. Nasal, ocular, and oral swabs collected from 111 cats presented at animal hospitals during the past 2.5 years were examined. Twenty-four (21.6%) and 4 (3.6%) cats were diagnosed as feline calicivirus (FCV) infection and feline viral rhinotracheitis, respectively, indicating FCV is more prevalent than feline herpesvirus-1, which revealed a considerable shift from data obtained in 1970s. Cat sera immunized by using vaccines containing either FCV F9 or 255 strains neutralized 42.9% and 66.7% of the FCV isolates, respectively. Chlamydia psittaci, examined by a PCR assay amplifying the ompA gene, was found in 26.9% of 26 diseased cats that typically showed conjunctivitis and rhinitis.  (+info)