Ocular Toxoplasmosis in an Adult Receiving Long-Term Corticosteroid Therapy

Nicholson, Don H.; Wolchok, Eugene B.

doi:10.1001/archopht.1976.03910030120009

Cited by 110 publications

(47 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Retinal pigment epithelial cells are thought to play an important role in ocular toxoplasmosis. These cells become hypertrophic, migrate to the retina, and appear to contain parasites (45,68,69). It has been suggested that this may represent an attempt at parasite eradication by retinal pigment epithelial cells (45).…”

Section: Discussionmentioning

confidence: 99%

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

et al. 2013

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

et al. 2013

View full text Add to dashboard Cite

“…RPE respond to inflammatory stimuli and secrete molecules such as IL-6, IL-8, GMCSF, nitric oxide and ICAM-1 [16][17][18][19]. Histopathological examination of the eyes of patients with toxoplasma-induced retinochoroiditis revealed the presence of free tachyzoites and tissue cysts in the RPE and the neuroretina [20][21][22]. In our previous studies, we have characterized the replication of T. gondii in human RPE cultures [23] and the secretion of inflammatory molecules upon T. gondii infection [24].…”

Section: Introductionmentioning

confidence: 99%

Transforming growth factor-β expression in human retinal pigment epithelial cells is enhanced by Toxoplasma gondii: a possible role in the immunopathogenesis of retinochoroiditis

Nagineni

Detrick

Hooks

2002

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYRetinochoroiditis caused by Toxoplasma gondii infection results in inflammation and necrosis of the retina. We have used human retinal pigment epithelial cultures (HRPE) as an in vitro model to investigate the role of TGF-b in T. gondii-induced retinochoroiditis. RT-PCR analyses showed enhanced steady state levels of TGF-b1 and TGF-b2 mRNA in T. gondii-infected HRPE. Uninfected HRPE secrete TGF-b1 in a latent form while 10-30% of the secreted TGF-b2 was in the active form. T. gondii infection induced a significant increase (P < 0·01) in total TGF-b1 and TGF-b2 secretion by HRPE. In addition, soluble extracts of T. gondii (ST) stimulated secretion of both TGF-b1 and TGF-b2 significantly (P < 0·01). Interestingly, T. gondii infection as well as ST of the parasites completely inhibited secretion of the active form of TGF-b2. Studies evaluating the effect of TGF-b on T. gondii replication in HRPE revealed that TGF-b enhanced parasite replication. The interactions between host retinal cells and T. gondii may play an active role in the pathogenesis of retinochoroiditis.

show abstract

“…In a rabbit model, injection of tachyzoites into the suprachoroidal space resulted in outer retinal lesions and localized foci of retinal pigment epitheliosis within 48 h. This suggests the crossing of the parasite through the RPE-Bruchs membrane barrier from the choroid to the retina (27). Histopathological examination of the eyes of patients with toxoplasma-induced retinochoroiditis revealed the presence of free tachyzoites and cysts in the RPE and the retina (9,19,24). Hence, studies of the mechanisms of T. gondii replication within retinal cells and the responses of the host cells to parasite invasion would be valuable in understanding the immunopathological basis of retinochoroiditis.…”

mentioning

confidence: 99%

Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

2000

View full text Add to dashboard Cite

We have used human retinal pigment epithelial (HRPE) cultures to investigate the primary cellular responses of retinal resident cells to intracellular Toxoplasma gondii replication. At 4 days postinoculation, when all of the cells were infected, the secretion of interleukin 1␤ (IL-1␤), IL-6, granulocyte-macrophage colonystimulating factor (GM-CSF), and intercellular adhesion molecule 1 (ICAM-1) was augmented by 23-, 10-, 8-, and 5-fold, respectively, over the control. Northern and reverse transcriptase PCR analyses showed significant upregulation of steady-state levels of mRNA for IL-1␤, IL-6, GM-CSF, and ICAM-1. The secretion of these molecules by HRPE cells may play a critical immunoregulatory role in the pathophysiological processes associated with T. gondii-induced retinochoroiditis.Retinochoroiditis caused by Toxoplasma gondii during ocular toxoplasmosis results in inflammation and disorganization of the retina, occasionally leading to severe loss of vision (11,20,23,30). The intensity of damage to the retina and choroid depends on the severity of the infection and the associated inflammatory reaction (11,13,20). Inflammatory cells, predominantly macrophages and lymphocytes, infiltrate the retina, the subretinal space, and the vitreous (6,11,20). In the severe form of T. gondii-induced uveitis, destruction of large segments of the outer retina and pigment epithelium is observed (6, 9, 13, 24). Within the retina, lysosomal and other autolytic enzymes released by inflammatory cells are thought to contribute to the pathogenic mechanisms of retinal tissue damage (6, 11).Retinal pigment epithelium (RPE), an integral part of the neuroretina in the posterior pole of the eye, acts as a barrier between the highly vascularized choroid and the retina with a complex architecture of neuronal cells (2, 31). In addition to its role in the transport of metabolites between retina and choroid, the RPE phagocytose the shed outer segments of retinal rods and cones (2, 31). Many of these activities of the RPE are essential for the structural and functional integrity of the retina and choroid. The RPE, because of its critical location and physiological activities, is constantly subjected to contact with various infectious agents and inflammatory mediators (12,14).Tachyzoites of T. gondii injected into the peritonial cavities of mice were thought to reach the retina via both choroidal and retinal circulation (8,21,26). In a rabbit model, injection of tachyzoites into the suprachoroidal space resulted in outer retinal lesions and localized foci of retinal pigment epitheliosis within 48 h. This suggests the crossing of the parasite through the RPE-Bruchs membrane barrier from the choroid to the retina (27). Histopathological examination of the eyes of patients with toxoplasma-induced retinochoroiditis revealed the presence of free tachyzoites and cysts in the RPE and the retina (9,19,24). Hence, studies of the mechanisms of T. gondii replication within retinal cells and the responses of the host cells to parasite invasion would be ...

show abstract

Ocular Toxoplasmosis in an Adult Receiving Long-Term Corticosteroid Therapy

Cited by 110 publications

References 10 publications

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

CD40 Induces Anti-Toxoplasma gondii Activity in Nonhematopoietic Cells Dependent on Autophagy Proteins

Transforming growth factor-β expression in human retinal pigment epithelial cells is enhanced by Toxoplasma gondii: a possible role in the immunopathogenesis of retinochoroiditis

Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

Contact Info

Product

Resources

About