Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative techniques were used to determine the relative concentrations of viable bacteria and polymorphonuclear leukocytes (PMNs) in the corneas of neutropenic and non-neutropenic guinea pigs with experimental bacterial keratitis induced with three strains of Pseudomonas aeruginosa. Neutropenia was produced by whole-body X-irradiation 1 week before infection. Significantly greater numbers of bacteria were present in the cornea of neutropenic animals 48 h after infection than were present in the corneas of non-neutropenic animals. The same was true 24 and 48 h after infecting animals with Staphylococcus aureus. Examination of histological sections showed that fewer PMNs were present in the corneas of infected neutropenic animals than in the corneas of infected non-neutropenic animals. Radiolabeling of PMNs confirmed a significant reduction in PMN concentration in the corneas of infected neutropenic animals. Tears and the corneal epithelium appear to be the most important elements protecting the cornea against local invasion by bacteria. However, once bacterial keratitis is established, PMNs play a role in limiting bacterial multiplication.
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PMID:Experimental bacterial keratitis in neutropenic guinea pigs: polymorphonuclear leukocytes in corneal host defense. 11 62

Corneal infection with herpes simplex virus-1 in immunocompetent mice induces an immunopathologic response termed herpetic stromal keratitis (HSK). The earliest sign of disease is neutrophil infiltration, which lasts for 48 to 72 h and then disappears. However, a secondary neutrophil infiltration, this time more massive, occurs, beginning 8 to 9 days postinfection, a time in which HSK becomes clinically evident. The role of neutrophils in HSK expression was investigated by eliminating such cells using a specific mAb (RB6-8C5). In neutrophil-depleted immunocompetent mice, virus replicated more abundantly, but no effects on HSK expression were observed, possibly because sustained neutropenia could not be maintained. However, using a severe combined immunodeficient mouse model, in which HSK does not occur unless given adoptive transfer of CD4+ T cells, the effects of neutrophil depletion were more pronounced. There were significantly less incidence and severity of HSK in CD4+ T cell-reconstituted severe combined immunodeficient mice that were depleted of neutrophils as compared with controls. Neutrophil-depleted mice displayed moderate to severe periocular skin lesions, progressively became cachetic, and developed signs of encephalitis. Virus was recovered at higher titers and for longer periods from eyes of neutrophil-depleted animals. Brain virus titers were also significantly higher on day 12 postinfection as compared with control animals. These results suggest that herpes simplex virus infection of the cornea rapidly invokes recruitment of neutrophils that may aid in viral clearance, and that neutrophils directly or indirectly serve as agonists in perpetuating a CD4+ T cell-mediated inflammatory reaction.
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PMID:On the essential involvement of neutrophils in the immunopathologic disease: herpetic stromal keratitis. 901 83

We report a case of concurrent orbital cellulitis and endophthalmitis that resulted from endogenous complications of community-acquired Pseudomonas aeruginosa bacteremia in an apparently healthy individual. Pseudomonas pneumonia and extensive focal skin lesions of ecthyma gangrenosum also complicated the condition. The presence of drug-induced neutropenia was a risk factor in this patient. Simultaneous orbital cellulitis and endophthalmitis developed and rapidly progressed. Intravenous, intravitreal, and topical antibiotics were administered along with frequent eye wash with normal saline to dilute copious purulent discharge from a deep subcutaneous abscess of lower eyelid. Because of the exocellular products of Pseudomonas aeruginosa, the sclera and corneal stroma were degraded, resulting in nearly perforated cornea. Tarsoconjunctival flap from the upper eyelid was performed to reconstruct the thinning areas. After the infection was controlled, the patient's ultimate visual acuity was light perception.
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PMID:Orbital cellulitis and endophthalmitis in pseudomonas septicemia. 1908 3

Our studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was undertaken to examine the possible relationship between HO-2 and the recruitment of neutrophils following a corneal surface injury in wild type (WT) and HO-2 knockout (HO-2(-/-)) mice treated with Gr-1 monoclonal antibody to deplete peripheral neutrophils. Epithelial injury was performed by removing the entire corneal epithelium. Infiltration of inflammatory cell into the cornea in response to injury was higher in HO-2(-/-) than in WT. However, the rate of corneal wound closure following neutrophil depletion was markedly inhibited in both WT and HO-2(-/-) mice by 60% and 85%, respectively. Neutropenia induced HO-1 expression in WT but not in HO-2(-/-) mice. Moreover, endothelial cells lacking HO-2 expressed higher levels of the Midkine and VE-cadherin and displayed strong adhesion to neutrophils suggesting that perturbation in endothelial cell function caused by HO-2 depletion underlies the increased infiltration of neutrophils into the HO-2(-/-) cornea. Moreover, the fact that neutropenia worsened epithelial healing of the injured cornea in both WT and HO-2(-/-) mice suggest that cells other than neutrophils contribute to the exaggerated inflammation and impaired wound healing seen in the HO-2 null cornea.
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PMID:The role of neutrophils in corneal wound healing in HO-2 null mice. 2169 50