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)

Hartley guinea pigs injected subconjunctivally with Onchocerca lienalis (OL) microfilariae (Mf) develop punctate corneal opacities resembling the punctate keratitis of human onchocerciasis. Antibody production and antigen-induced proliferative responses were studied in conjunctival-associated lymphoid tissues (CALT), spleens (SL) and peripheral blood lymphocytes (PBL) from experimentally infected guinea pigs. Cultured single cell suspensions of CALT, SL and PBL were assayed for IgG1, IgG2, IgA and IgE antibody production. IgG1, IgG2, and IgA Onchocerca-specific antibodies were found in culture supernatants of CALT, SL and PBL. When initiated 10 days after a challenge injection of OL, CALT cultures produced antibody levels equal to or less than those produced by the corresponding SL cultures. When initiated 66 days after the last injection of Mf, CALT cultures produced significantly more antibody than the corresponding SL cultures. Blastogenic responses to OL Mf antigen were observed in peripheral and splenic lymphocytes of OL-infected guinea pigs. Animals given subconjunctival injections of Mf followed by treatment with a microfilaricide had greater responses to OL antigen than those given Mf alone, while responses to phytomitogens were similar in drug-treated and non-treated animals. The CALT was locally immunologically responsive against the subconjunctivally injected OL Mf, with the capacity for localized memory responses. The local immunologic responses to conjunctival Onchocerca microfilariae may play a significant role in the immunopathological reactions of ocular onchocerciasis.
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PMID:Experimental ocular onchocerciasis: local and systemic antibody and cell-mediated immune responses. 225 38

Pentostatin (2'-deoxycoformycin, DCF) was administered to 17 patients with a variety of lymphoid neoplasms, both T- and B-cell, that were refractory to conventional treatments. Several responses and 2 complete remissions occurred. Toxic effects were less severe than previously described: this may be attributable to relatively low doses of DCF or to precautions taken to prevent tumour lysis syndrome. DCF appears valuable as a second-line treatment in non-Hodgkin's lymphomas and as initial treatment in T-cell chronic lymphocytic leukaemia and mycosis fungoides. Although myelosuppression is mild, immunosuppression and superinfection are potential hazards of treatment with DCF. The ocular toxicity of DCF, previously described as conjunctivitis, appears to be a keratitis of moderate severity which requires further study.
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PMID:Effectiveness of pentostatin (2'-deoxycoformycin) in refractory lymphoid neoplasms. 660 39

Our study was designed to investigate the mechanism of the stromal reaction in experimental ocular infection of murine eyes with herpes simplex virus (HSV). Severe stromal keratitis with scarring occurred in BALB/c mice after infection of the scarified cornea but similar reactions did not occur in athymic mice. However, if athymic mice were given adoptive transfers of lymphoid cells, a severe necrotizing and ulcerative keratitis accompanied by scarring resulted. The lesion progressed more quickly in recipients of lymphoid cells specifically immune to HSV and containing cytotoxic T-lymphocyte activity. In such mice, necrosis and ulceration were marked on the sixth day after transfer compared with 9-12 days for those given nonimmune cells. Removal of T-lymphocytes from the immune lymphoid population by treatment with specific antiserum and complement abrogated the adoptive transfer of the stromal reaction. Our results further demonstrate that stromal keratitis represents a host immunopathologic response to HSV infection in which T-lymphocytes are essential participants. Multiple mechanisms of T-cell immunopathology appear to be operating, including a reaction mediated by cytotoxic T-lymphocytes.
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PMID:Role of T-lymphocytes in the pathogenesis of herpetic stromal keratitis. 661 24

Malignant catarrhal fever (MCF) in cattle is generally associated with a short clinical course and a high case fatality rate (90-95%). The lesions in cattle that survive acute MCF for a prolonged period or appear to recover have not been documented. In a naturally occurring outbreak of MCF in a herd of beef cattle in Wyoming, 7 of 84 yearling heifers (8.3% of replacement herd) and 2 of 230 cows (0.9% of cow herd) developed clinical signs of pyrexia, mucopurulent discharge, bilateral keratitis, and weight loss following contact with ewes that had lambed 34-62 days earlier. Six of 9 affected cattle were examined postmortem following clinical signs (CS) that developed 2-150 days earlier. Three cattle with CS for < or = 39 days had lesions of regional lymphadenopathy and widespread severe segmental lymphoid arteritis-phlebitis that were typical of acute MCF, and proliferative intimal lesions were present in a small proportion of arteries at days 20 and 39 of CS. By contrast, 3 cattle that survived to 90, 105, and 150 days after clinical onset had distinctive arterial lesions in multiple organs, characterized by proliferative concentric fibrointimal plaques, disrupted inner elastic lamina, focally atrophic tunica media, and vasculitis of variable severity. Immunohistochemical and ultrastructural examination of intimal plaques identified the predominant cellular component to be smooth muscle cells with a contractile phenotype. No viral structures were seen. Serologic studies, using a competitive inhibition enzyme-linked immunosorbent assay (CI-ELISA) that detects antibody to an epitope broadly conserved among isolates of the MCF virus, found that 2 chronically affected cattle were serologically positive between days 42 and 100 of CS, with seroconversion in 1 animal between days 52 and 73 of CS. Seroprevalence was 7.9% in the 76 remaining healthy animals of the replacement heifer herd and 40% (75% in adult sheep and 4% in lambs) in the in-contact sheep flock 77 days after onset of CS in the index case. This episode suggests that, in addition to the common and well recognized acute form of MCF in cattle, this viral infection encompasses a disease spectrum that includes chronic disease and partial to "complete" clinical recovery, and in recovered animals chronic obliterative arteriopathy is the preeminent lesion.
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PMID:Chronic generalized obliterative arteriopathy in cattle: a sequel to sheep-associated malignant catarrhal fever. 777 45

A field study investigating the occurrence of Mycoplasma gallisepticum (MG) in house finches (Carpodacus mexicanus) was conducted in Maryland and Georgia. Eighty-eight finches were captured and examined grossly and microscopically for MG-related conjunctivitis. Serum samples were obtained for serum plate agglutination (SPA) and hemagglutination inhibition (HI) testing. Swabs from conjunctiva, sinus, and choanal cleft were inoculated into two mycoplasma broth media for culture and polymerase chain reaction (PCR) testing. From Maryland, 12 of 57 birds examined had gross conjunctival lesions. MG was isolated from 9 of the 12 affected birds and from three birds without gross lesions. Fourteen of 22 finches tested by PCR were positive for MG. Sixteen of 38 birds were positive for MG by SPA, and 9 of these had HI titers of 1:40 or 1:80. From Georgia, 3 of 31 finches examined had gross lesions; two of these were both culture and PCR positive for MG. Twelve birds were positive by SPA, and two of these had HI titers of 1:80. Histologic findings in birds with gross conjunctivitis from both locations were characterized by extensive epithelial and lymphoid hyperplasia as well as lymphoplasmacytic inflammation in conjunctival tissues; keratitis was rarely present. The source of MG infection in house finches is unknown, and further research is warranted to determine the prevalence and impact of this newly described disease.
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PMID:Field investigation of Mycoplasma gallisepticum infections in house finches (Carpodacus mexicanus) from Maryland and Georgia. 879 Aug 83

Malignant catarrhal fever (MCF) is traditionally regarded as a disease with a short clinical course, low morbidity and high case fatality rate. Owing to the limitations of the assays used for laboratory diagnosis. It was difficult in characterise the clinical spectrum of sheep-associated MCF, particularly when the cattle recovered from an MCF-like clinical syndrome. Over a period of three years, 11 cattle that survived MCF for up to two-and-a-half years were identified on four premises. A clinical diagnosis of MCF was confirmed by the detection of ovine herpesvirus-2 DNA in peripheral blood leucocytes using a polymerase chain reaction (PCR) assay that detects a specific 238 base-pair fragment of viral genomic DNA. Of the 11 cattle examined, six recovered clinically with the exception of bilateral corneal oedema with stromal keratitis (four animals) and unilateral perforating keratitis (one animal). The 10 animals available for postmortem examination had disseminated subacute to chronic arteriopathy. Recovery was associated with the resolution of the acute lymphoid panarteritis that characterises the acute phase of MCF, and with the development of generalised chronic obliterative arteriosclerosis. Bilateral leucomata were due in part to the focal destruction of corneal endothelium secondary to acute endothelialitis. Formalin-fixed tissues and/or unfixed lymphoid cells from all 11 cattle were positive for sheep-associated MCF by PCR. These observations indicate that recovery and chronic disease are a significant part of the clinical spectrum of MCF and that such cases occur with some frequency in the area studied. The affected cattle remain persistently infected by the putative sheep-associated MCF gammaherpesvirus.
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PMID:Chronic and recovered cases of sheep-associated malignant catarrhal fever in cattle. 953

Herpetic stromal keratitis (HSK), resulting from corneal HSV-1 infection, represents a T cell-mediated immunopathologic lesion. In T cell transgenic mice on a SCID or RAG knockout background, the T cells mediating lesions are unreactive to viral Ags. In these bystander models, animals develop ocular lesions but are unable to control infection. Transfer of HSV-immune cells into a CD8(+) T cell bystander model resulted in clearance of virus from eyes, animals survived, and lesions developed to greater severity. However, the adoptively transferred CD8(+) T cells were not evident in lesions, although they were readily detectable in the lymphoid tissues as well as in the peripheral and CNS. Our results indicate that viral-induced tissue damage can be caused by bystander cells, but these fail to control infection. Immune CD8(+) T cells trigger clearance of virus from the eye, but this appears to result by the T cells acting at sites distal to the cornea. A case is made that CD8(+) T cell control is expressed in the trigeminal ganglion, serving to curtail a source of virus to the cornea.
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PMID:Protective and pathological roles of virus-specific and bystander CD8+ T cells in herpetic stromal keratitis. 1558 85

Recent advances in corneal graft technology, including donor tissue retrieval, storage and surgical techniques, have greatly improved the clinical outcome of corneal grafts. Despite these advances, immune mediated corneal graft rejection remains the single most important cause of corneal graft failure. Several host factors have been identified as conferring a "high risk" status to the host. These include: more than two quadrant vascularisation, with associated lymphatics, which augment the afferent and efferent arc of the immune response; herpes simplex keratitis; uveitis; silicone oil keratopathy; previous failed (rejected) grafts; "hot eyes"; young recipient age; and multiple surgical procedures at the time of grafting. Large grafts, by virtue of being closer to the host limbus, with its complement of vessels and antigen-presenting Langerhans cells, also are more susceptible to rejection. The diagnosis of graft rejection is entirely clinical and in its early stages the clinical signs could be subtle. Graft rejection is largely mediated by the major histocompatibility antigens, minor antigens and perhaps blood group ABO antigens and some cornea-specific antigens. Just as rejection is mediated by active immune mediated events, the lack of rejection (tolerance) is also sustained by active immune regulatory mechanisms. The anterior chamber associated immune deviation (ACAID) and probably, conjunctiva associated lymphoid tissue (CALT) induced mucosal tolerance, besides others, play an important role. Although graft rejection can lead to graft failure, most rejections can be readily controlled if appropriate management is commenced at the proper time. Topical steroids are the mainstay of graft rejection management. In the high-risk situations however, systemic steroids, and other immunosuppressive drugs such as cyclosporin and tacrolimus (FK506) are of proven benefit, both for treatment and prevention of rejection.
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PMID:Corneal allograft rejection: risk factors, diagnosis, prevention, and treatment. 1613 Feb 77

Two prominent anti-inflammatory mechanisms involved in controlling HSV-1-induced corneal immunopathology (stromal keratitis or SK) are the production of the cytokine IL-10 and the activity of natural regulatory T cells (nTregs). It is not known whether, under in vivo conditions, IL-10 and nTregs influence the corneal pathology independently or in concert. In the current study using wild-type and IL-10(-/-) animals, we have assessed the activity of nTregs in the absence of IL-10 both under in vitro and in vivo conditions. The IL-10(-/-) animals depleted of nTregs before ocular infection showed more severe SK lesions as compared with the undepleted IL-10(-/-) animals. In addition, nTregs purified from naive WT and IL-10(-/-) animals were equally able to suppress the proliferation and the cytokine production from anti-CD3-stimulated CD4(+)CD25(-) T cells in vitro. Furthermore, intracellular cytokine staining results indicated that nonregulatory cells expressing B220 and CD25 markers were the major IL-10-producing cell types in the lymphoid tissues of HSV-infected mice. In contrast, in the infected corneas, cells with the CD11b(+)Gr1(+) phenotype along with a minor population of Foxp3(-)CD4(+) and a few F4/80(+) cells produced IL-10. Our current investigations indicate that at least two independent anti-inflammatory mechanisms are involved in limiting the corneal lesions in SK, both of which may need to be modulated to control SK therapeutically.
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PMID:IL-10 and natural regulatory T cells: two independent anti-inflammatory mechanisms in herpes simplex virus-induced ocular immunopathology. 1842 53

Ocular HSV-1 infection can result in stromal keratitis, a blinding immunoinflammatory lesion that represents an immunopathological response to the infection. CD4(+) T cells are the main orchestrators, and lesions are more severe if the regulatory T cell (Treg) response is compromised from the onset of infection. Little is known about the role of Foxp3(+)CD4(+) Tregs during ongoing inflammatory reactions, which is the topic of this article. We used DEREG mice and depleted Tregs at different times postinfection. We show that lesions became more severe even when depletion was begun in the clinical phase of the disease. This outcome was explained both by Tregs' influence on the activity of inflammatory effector T cells at the lesion site and by an effect in lymphoid tissues that led to reduced numbers of effectors and less trafficking of T cells and neutrophils to the eye. Our results demonstrate that Tregs can beneficially influence the impact of ongoing tissue-damaging responses to a viral infection and imply that therapies boosting Treg function in the clinical phase hold promise for controlling a lesion that is an important cause of human blindness.
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PMID:On the role of regulatory T cells during viral-induced inflammatory lesions. 2312 53


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