Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has shown that splenic macrophages derived from herpes simplex virus (HSV)-resistant C57BL/6 mice undergo a persistent HSV infection which is characterized by the continuous release of infectious virus particles from a small subpopulation of infected cells. Treatment of persistently infected macrophages for 2 weeks with lipopolysaccharide (LPS) resulted in an increase of HSV yield and in virus-induced cytopathic effects. HSV was also reactivated by treatment of macrophage cultures with lipid A or tumour necrosis factor (TNF). Like macrophages of C57BL/6 origin, cells from LPS-hyporesponsive C3H/HeJ mice could be persistently infected with HSV. These cells were resistant to LPS-induced virus reactivation. The results show that macrophages derived from C57BL/6 mice are rendered susceptible to lytic HSV infection by treatment with LPS or TNF. Thus, these substances may interfere with persistent HSV infection which can be established due to genetically controlled properties of the host.
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PMID:Stimulation of macrophages by endotoxin results in the reactivation of a persistent herpes simplex virus infection. 216 12

C3H/He and BALB/c mice were inoculated with herpes simplex virus (HSV) by corneal or intraperitoneal route. The mouse splenocytes were analyzed to determine the level and mode of cytotoxic T lymphocyte (CTL) induction by a cytotoxicity test, using HSV-infected L929 cells and 3T3 cells as the target cells. To enhance the activities of CTL, mouse splenocytes were restimulated by lipopolysaccharide-induced lymphoblasts (LPS-blasts) infected with HSV before assay. HSV infection by both corneal and intraperitoneal routes induced H-2 restricted T lymphocyte responses specific for HSV. This CTL response became detectable on day 6 in mice with herpetic keratitis and on day 4 with intraperitoneal infection, but 10 days after infection the CTL activities of both groups reached the same level. A high response level persisted as long as 28 days. These results suggest that the protective mechanism in herpetic keratitis is similar to the mechanism in intraperitoneal infection.
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PMID:Immunological studies of herpetic keratitis: induction of cytotoxic T lymphocytes in mouse splenocytes. 387 28

Passively acquired immunity to herpes simplex virus (HSV) was studied in antithymocyte serum (ATS)-treated mice and athymic nude mice to determine whether immunocompetent lymphocytes contribute to the protection observed after transfer of HSV-specific antibody to infected animals. Mice were given three intraperitoneal injections of 0.1 ml of ATS at 24-h intervals. This treatment reduced concanavalin A and lipopolysaccharide stimulation of lymphocytes harvested from these animals by 90% when compared with the stimulation of lymphocytes harvested from untreated animals. It was found that intraperitoneal injection of 0.5 ml of specific antibody 8 h after corneal HSV type 1 infection or subcutaneous HSV type 2 infection did not protect ATS-treated animals from virus infection. Specific antibody passively transferred to ATS-treated animals 8 and 120 h postinfection also failed to protect lymphocyte-depleted animals from HSV. However, ATS-treated animals were protected from HSV infection by passively acquired antibody when lymphocytes harvested from these animals regained 80% of their ability to be stimulated with concanavalin A and lipopolysaccharide. It was also found that specific antibody conferred protection to nude mice infected with HSV only if they were first reconstituted with syngeneic thymus cells 48 h before infection. The results suggest that both antiviral antibody and thymus-derived lymphocytes contribute to the recovery of HSV-infected hosts after passive immunization.
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PMID:Lymphocyte reactivity contributes to protection conferred by specific antibody passively transferred to herpes simplex virus-infected mice. 721 31

We evaluated the in vitro effect of growth hormone (GH), prolactin (PRL) and insulin treatment of human monocytes on Herpes simplex virus type 1 (HSV-1) infection. GH and PRL increased cell susceptibility to infection which was related to a slight TNF-alpha expression and release. Insulin had no significant effect. Cells activated with lipopolysaccharide (LPS) and then treated with PRL showed a lower susceptibility to HSV infection related to a significant increase in TNF-alpha expression and release. On the contrary, GH and insulin increased the susceptibility to infection of activated cells but did not modify TNF-alpha expression with respect to cells treated only with hormones.
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PMID:TNF-alpha expression and herpes simplex infection in human monocytes treated with growth hormone, prolactin and insulin. 969

Several lines of evidence suggest that dendritic cells (DCs), the most potent antigen-presenting cells known, play a role in the immunological control of herpes simplex virus (HSV) infections. HSV infection of DCs induced submaximal maturation, but DCs failed to mature further in response to lipopolysaccharide (LPS). LPS induced interleukin (IL)-12 secretion, and the induction of primary and secondary T cell responses were impaired by infection. Ultimately, DC infection resulted in delayed, asynchronous apoptotic cell death. However, infected DCs induced HSV recall responses in some individuals. Furthermore, soluble factors secreted by DCs after infection induced DC maturation and primed for IL-12 secretion after LPS stimulation. These data support a pathogenetic model of HSV infection, in which initial delay in the generation of immune responses to HSV at peripheral sites is mediated by disruption of DC function but is overcome by bystander DC maturation and cross-presentation of HSV antigens.
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PMID:Herpes simplex virus infection of dendritic cells: balance among activation, inhibition, and immunity. 1255 41