Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of mucin in the manifestation of Pseudomonas keratitis was studied. Pseudomonas was cultivated in solutions of mucin, in which it grew rapidly and then inoculated into rabbit cornea by needle pricks. When the organism was inoculated as a suspension in saline, infection infrequently occurred as small ring abscesses of short duration around a few sites of inoculation. When the organism was inoculated as a suspension in a solution of gastric mucin, infection was usually observed as severe hypopyon-keratitis with formation of a huge ring abscess. Corneal perforation and panophthalmitis resulted in some cases. It was thus concluded that the pathogenicity of Pseudomonas is definitely increased when it was inoculated into the cornea with mucin solution.
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PMID:The role of mucin on experimental Pseudomonas keratitis in rabbits. 81 95

Adherence of bacteria to the corneal epithelium is the first step in the pathogenesis of corneal infection. Keratitis caused by Pseudomonas aeruginosa usually occurs among the contact lens wearers. Adherence of Pseudomonas aeruginosa to rabbit corneal epithelium, damaged by one week of hard contact lens wear, was examined histologically. The cornea was excised for scanning electron microscopy at 5, 15, 30 and 60 minutes after inoculation of Pseudomonas aeruginosa (0.2 ml, 10(8)CFU/ml). Pseudomonas aeruginosa did not adhere to the intact corneal epithelium, but traumatized cornea provided a site for adherence. In rabbits in which the eyelid was opened by lid retractors, large numbers of organisms were observed adhering to the injured cornea mediated by ocular surface mucin. Thirty minutes after inoculation, the adherent bacteria began to penetrate the epithelial cells and surface mucin by the formation of pockets surrounding the organism.
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PMID:[Adherence of Pseudomonas aeruginosa to the rabbit corneal epithelium]. 211 20

Microbial keratitis with Pseudomonas aeruginosa is the most common corneal infection associated with contact lenses (CLs). Pseudomonas organisms are ubiquitous in nature, and can colonize CLs without a prior breach in lens care or hygiene. Although poor lens care is often found in affected patients, lens contamination and traumatic epithelial defects are more relevant. Hydrophilic lenses, particularly extended wear lenses, have been associated with a greater frequency of Pseudomonas keratitis. The polymer matrix of these lenses is apparently suited to the avid adherence of Pseudomonas organisms. Adherence is promoted by the presence of lens coatings, which begin to accumulate upon lens insertion and whose level mounts over time. Evidence suggests that infection is more common with mucin-coated contaminated CLs than with noncoated contaminated CLs. In general, lens wear can promote bacterial adherence to the ocular surface by shielding the cornea from the wiping action of the eyelids and immune components in tears. Still, experimental models have shown that keratitis develops regularly (84%) only in corneas that have been traumatized. Trauma may arise through lens insertion or removal, deposits or debris entrapment, hypoxia, or toxic reactions to solution preservatives. Extended wear is believed to facilitate the infectious process because of the chronic accumulation of coatings, the chronic exposure of CLs to potentially adherent bacteria, the continuous presence of irritating lens deposits, the prolonged entrapment of debris beneath the lens, and the relative infrequency of lens cleaning and disinfection.
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PMID:Pseudomonas keratitis and contact lens wear: the lens/eye is at fault. 218 78

The adherence of Pseudomonas aeruginosa to extended-wear soft contact lenses (EWSCLs) may be an important initial step in the pathogenesis of EWSCL-associated infectious keratitis. P. aeruginosa tend to adhere more to worn EWSCLs than unworn EWSCLs (P less than 0.05). Normal tear components such as aqueous solutions of albumin, lysozyme, and lactoferrin all significantly enhance adherence of P. aeruginosa to unworn EWSCLs often by as much as 300%. The presence of a 1% solution of sialic acid in the bathing medium significantly reduces the adherence of P. aeruginosa to both unworn and worn lenses. Inhibition of bacterial adherence could also be achieved with the addition of mucin (which contains terminal sialic acid residues in its major sugar chains). Therefore, selective adherence by P. aeruginosa to a specific sugar (sialic acid) may be important in the initial attachment of the bacterium to soft contact lenses.
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PMID:The adherence of Pseudomonas aeruginosa to soft contact lenses. 312 75

The adherence of microorganisms to contact lenses may be an important initial step in the pathogenesis of contact lens-associated infectious keratitis. Using a strain of Candida albicans whose interaction with various polymers has been well characterized we systematically investigated the adherence of this pathogen to hard hydrophobic and soft hydrophilic extended-wear contact lenses. Yeasts adhere to the hydrophobic lenses in direct proportion to the wetting angle of the lens whereas yeasts adhere to the hydrophilic lenses in direct proportion to the water content of the lens. Tear proteins such as albumin, lactoferrin, and lysozyme in addition to fibronectin enhance yeast adherence to both types of lenses (P less than 0.01). Concanavalin A reduces adherence of yeasts to both lens types (P less than 0.01). Among tear components however, only mucin (0.5%) consistently reduced yeast adherence to both lens types. Hydrophilic extended wear lenses worn for at least 28 days by normal patients consistently had greater adherence of yeasts than unworn lenses of the same type, often as much as ten-fold or greater yeasts/mm2 of lens surface area (P less than 0.05). These investigations indicate that tear components both in solution and adsorbed to the lens surface enhance microorganism adherence to contact lenses.
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PMID:Blocking Candida adherence to contact lenses. 353 31

Mucinlike glycoprotein from tears and conjunctival goblet cell densities were determined in normal subjects and in patients. The results indicated that although there was a statistically significant decrease, a substantial amount of mucinlike glycoprotein was present in tears from patients with ocular cicatricial pemphigoid (OCP), radiation keratitis, and corneal anesthesia. In the same patients, the goblet cell count was profoundly decreased in OCP and radiation keratitis, well out of proportion to the modest fall in mucinlike glycoprotein. This indicated that the tear mucin content shows minimal variation over a great variation in goblet cell density, suggesting that while moderate mucin deficiency may be associated with surface abnormalities, such mucin deficiency may not be the only cause of the ocular surface epithelial problems characteristic of these diseases. In addition, it is proposed that the goblet cell content of the conjunctiva is a sensitive indicator of primary ocular surface disease.
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PMID:Goblet cell density in ocular surface disease. A better indicator than tear mucin. 688 59

To gain access to the corneal epithelium and cause infections keratitis, bacterial pathogens must first interact with ocular surface factors that could affect bacterial adherence. In this study, we demonstrated that the mucus layer, and, in particular, the mucin fraction of mucus, modulated adherence to intact corneal epithelium of Pseudomonas aeruginosa but not that of Staphylococcus aureus or Streptococcus pyogenes. Removal of endogenous mucus from rat or rabbit eyes increased the adherence of P. aeruginosa by 3- to 10-fold. Ocular mucus obtained from rat eyes, porcine stomach mucin, or bovine submaxillary gland mucin inhibited adherence of P. aeruginosa to uninjured corneal epithelium. The mucin fraction of ocular mucus, purified by ultracentrifugation, was found to contain the inhibitory activity, and inhibition was demonstrated at concentrations of mucin as low as 35 micrograms/ml. Ocular mucin was the only material tested that inhibited adherence of P. aeruginosa to an injured cornea. However, the binding of P. aeruginosa to immobilized substrates in vitro did not predict which fraction would possess antiadherence activity: bacteria bound well to whole ocular mucus, mucin, the nonmucin fraction of ocular mucus, and dilute human tears as well as to porcine stomach mucin and bovine submaxillary gland mucin. The effectiveness of the mucin fraction of ocular mucus at inhibiting the binding of P. aeruginosa to the cornea implies that this material is a barrier that protects the surface of the eye from P. aeruginosa adherence.
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PMID:Modulation of Pseudomonas aeruginosa adherence to the corneal surface by mucus. 816 42

In summary, this review has provided information concerning the application of histochemical and cytochemical procedures used to detail the normal versus pathological cornea and ocular surface. Specifically, histochemical analysis has been used to study protein and peptide degradation in cornea, to analyze stromal non-collagenous and collagenous fibers and associated extracellular matrix. Cytochemistry of the ocular surface has been used to detail the morphology of corneal and conjunctival mucin. Use of small cationic probes as well as lectin-gold binding was advantageous to quantitatively demonstrate that ocular mucin contains sialylated residues and that the number of these residues significantly changes (increases) with age. These data are important in that the degree of sialylation has been shown to correlate with the ability of bacterial organisms to adhere to and infect the immature in contrast to the mature corneal surface. The use of lectin analysis of diseased ocular tissue also has shown that there are specific alterations in glycoconjugates which occur in the diseased versus normal human cornea. Wound healing in cornea is an important problem which has been studied at length using combined histochemical and biochemical approaches. Results support the hypothesis that apical cell surfaces of the leading edge of a migrating sheet differ from those of the normal epithelium. During wound healing, alpha 6 integrin expression by corneal epithelial cells has been demonstrated, but another protein, syndecan was only seen in non-migrating epithelium which had restratified. The association of immunoglobulins with the ocular surface epithelium of the cornea, their change with age and kinetics of appearance also has been demonstrated using a cytochemical approach. Histochemical procedures have been used to localize Class I and Class II molecules in cornea and conjunctiva. Class II antigen expression has been shown to be absent on corneal endothelium, but it can be induced by treatment with IFN-gamma. These data are of importance in corneal pathology such as that resulting in rejection of corneal transplants. Langerhans cells (Class II, Ia positive) also are not found in normal central cornea. They are localized in the peripheral cornea and are stained histochemically by ADPase, ATPase and by specific anti-Ia and other antisera. Increased numbers of LC have been demonstrated in cornea following various stimuli and in diseases of the cornea including both bacterial and viral induced keratitis.
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PMID:Corneal and ocular surface histochemistry. 845 77

Pseudomonas aeruginosa has emerged as an important causative agent of bacterial keratitis, a rapidly progressive ocular condition that may result in blindness. Secretory mucin forms the main constituent of the precorneal tear film, a three-layer film on the ocular surface protecting the underlying corneal epithelium from potential pathogens. The purpose of the present study was to compare mucin degradation mechanisms between ocular P. aeruginosa strains. Mucin degradation was assessed by agarose electrophoresis, lectin blotting, and size exclusion chromatography. The results indicate that certain P. aeruginosa strains (Paer12, ATCC 15442, 6294, and Paer25) had depleted mucin from the culture supernatant and that this was contingent on the inherent ability of these isolates to produce proteases. Non-protease-producing strains (Paer1 and Paer3) did not appreciably degrade mucin. Further, galactosidase, N-acetylglucosaminidase, and N-acetylgalactosaminidase activities were detected in some strains, suggesting the operation of further mechanisms of mucin degradation by P. aeruginosa. Mucin degradation by P. aeruginosa also seemed to be for the acquisition of nutrients, as a growth advantage was observed in mucin-depleting strains over nondepleting strains in the long term. It is postulated that the degradation of mucin serves to collapse the mucin barrier and its associated network containing antibacterial tear components and to provide energy for sustained bacterial growth.
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PMID:Mucin degradation mechanisms by distinct Pseudomonas aeruginosa isolates in vitro. 1450 Apr 75

The purpose of the study was to investigate the adhesion of Pseudomonas aeruginosa strains with varying pathogenic potential to purified ocular mucin. Bovine conjunctival mucin was purified by three sequential density gradient centrifugation steps. Immobilised mucin was probed with biotin-labelled bacteria isolated from different contact lens events and quantified by densitometry. Bacterial pili were identified by electron microscopy. The results indicate that purified ocular mucin consisted of a polydisperse high molecular weight population containing at least one species of goblet cell origin and was associated with a 97 kDa mucin-associated protein. Three pathogenic P. aeruginosa strains, Paer1 (57.5 +/- 10.8x10(6) CFU ml(-1); contact lens induced acute red eye (CLARE)), 6294 (127.0 +/- 4.7x10(6) CFU ml(-1); microbial keratitis) and Paer25 (60.5 +/- 11.3x10(6) CFU ml(-1); CLARE) exhibited a significantly higher level of adhesion to mucin than the negative control, E. coli (14.3 +/- 9.6x10(6) CFU ml(-1)) (p<0.005). The remaining P. aeruginosa isolates, Paer3 (asymptomatic patient), Paer12 (microbial keratitis) and ATCC 15442 (standard environmental strain) did not significantly differ in their mucin adhesion from the negative control. The majority of bacterial strains tested contained pili; thus differences in mucin adhesion observed could not be solely explained by pili status. In conclusion, P. aeruginosa isolates exhibit differential adhesion patterns to purified ocular mucin. It is proposed that more avid mucin-adhering strains are given the opportunity to adhere and subsequently penetrate the mucous layer of the tear film to initiate pathogenesis.
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PMID:Isolation of conjunctival mucin and differential interaction with Pseudomonas aeruginosa strains of varied pathogenic potential. 1460 58


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