Defense mechanisms of IFN-γ and LPS-primed murine microglia against Acanthamoeba castellanii infection

Benedetto, N; Rossano, Fabio; Gorga, F; Folgore, A; Rao, María A.; Carratelli, Caterina Romano

doi:10.1016/s1567-5769(03)00047-x

Cited by 20 publications

(16 citation statements)

References 24 publications

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“…Murine microglia activated with either recombinant prolactin or LPS plus IFN-␥ produce synergistic amebastatic activity; infection with Acanthamoeba castellani in vitro stimulates TNF-␣, IL-6, and IL-1␤ production (33,34). More specifically, TNF-␣-and IFN-␥-activated microglia have amebicidal activity, whereas those activated by IL-6 and IL-1␤ with or without IFN-␥ have only amebastatic activity (32).…”

Section: Parasitesmentioning

confidence: 99%

Role of Microglia in Central Nervous System Infections

et al. 2004

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The nature of microglia fascinated many prominent researchers in the 19th and early 20th centuries, and in a classic treatise in 1932, Pio del Rio-Hortega formulated a number of concepts regarding the function of these resident macrophages of the brain parenchyma that remain relevant to this day. However, a renaissance of interest in microglia occurred toward the end of the 20th century, fueled by the recognition of their role in neuropathogenesis of infectious agents, such as human immunodeficiency virus type 1, and by what appears to be their participation in other neurodegenerative and neuroinflammatory disorders. During the same period, insights into the physiological and pathological properties of microglia were gained from in vivo and in vitro studies of neurotropic viruses, bacteria, fungi, parasites, and prions, which are reviewed in this article. New concepts that have emerged from these studies include the importance of cytokines and chemokines produced by activated microglia in neurodegenerative and neuroprotective processes and the elegant but astonishingly complex interactions between microglia, astrocytes, lymphocytes, and neurons that underlie these processes. It is proposed that an enhanced understanding of microglia will yield improved therapies of central nervous system infections, since such therapies are, by and large, sorely needed

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Section: Parasitesmentioning

confidence: 99%

Role of Microglia in Central Nervous System Infections

et al. 2004

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“…In order to culture primary neural cells that contained a variety of neurons and glial cells, a mixed neuron-glia (MNG) culture was prepared using the slightly modified method described in previous studies [21,22]. Briefly, the whole brains of neonatal Sprague-Dawley rats (n= 8) at 1 day or 2 day old were stripped of meninges, mechanically dissociated, and filtered through 70-μm nylon mesh to recover dissociated cells.…”

Section: Culture and Identification Of Microgliamentioning

confidence: 99%

Microglia and cyclooxygenase-2: Possible therapeutic targets of progesterone for stroke

Jiang

Cui

Wang

et al. 2011

International Immunopharmacology

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“…IFN-␥ is a multifunctional Th1 cytokine involved in brain inflammation and the pathogenesis of various brain diseases (34,35) and has been shown to participate in the immune response in the brain through activating microglial cells (36,37). IFN-␥ has been demonstrated to enhance the anticryptococcal activity of murine microglial cells in vitro by inducing MHC class II expression and NO production (37)(38)(39).…”

Section: Ifn-␥ Signaling Is Required For the Protection Induced By Anmentioning

confidence: 99%

Protection from Direct Cerebral Cryptococcus Infection by Interferon-γ-Dependent Activation of Microglial Cells

Zhou

Gault

Kozel

et al. 2007

The Journal of Immunology

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The brain represents a significant barrier for protective immune responses in both infectious disease and cancer. We have recently demonstrated that immunotherapy with anti-CD40 and IL-2 can protect mice against disseminated Cryptococcus infection. We now applied this immunotherapy using a direct cerebral cryptococcosis model to study direct effects in the brain. Administration of anti-CD40 and IL-2 significantly prolonged the survival time of mice infected intracerebrally with Cryptococcus neoformans. The protection was correlated with activation of microglial cells indicated by the up-regulation of MHC II expression on brain CD45lowCD11b+ cells. CD4+ T cells were not required for either the microglial cell activation or anticryptococcal efficacy induced by this immunotherapy. Experiments with IFN-γ knockout mice and IFN-γR knockout mice demonstrated that IFN-γ was critical for both microglial cell activation and the anticryptococcal efficacy induced by anti-CD40/IL-2. Interestingly, while peripheral IFN-γ production and microglial cell activation were observed early after treatment, negligible IFN-γ was detected locally in the brain. These studies indicate that immunotherapy using anti-CD40 and IL-2 can augment host immunity directly in the brain against C. neoformans infection and that IFN-γ is essential for this effect.

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Defense mechanisms of IFN-γ and LPS-primed murine microglia against Acanthamoeba castellanii infection

Cited by 20 publications

References 24 publications

Role of Microglia in Central Nervous System Infections

Role of Microglia in Central Nervous System Infections

Microglia and cyclooxygenase-2: Possible therapeutic targets of progesterone for stroke

Protection from Direct Cerebral Cryptococcus Infection by Interferon-γ-Dependent Activation of Microglial Cells

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