Endothelin inhibition improves cerebral blood flow and is neuroprotective in pneumococcal meningitis

Pfister, Luz Andrea; Tureen, Jay H.; Shaw, Sydney; Christen, Stephan; Ferriero, Donna M.; Täuber, Martin G.; Leib, Stephen L.

doi:10.1002/1531-8249(200003)47:3<329::aid-ana8>3.0.co;2-r

Cited by 75 publications

(23 citation statements)

References 37 publications

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“…Nursing Sprague-Dawley rat pups were infected on postnatal day 11 (n ϭ 142) by intracisternal injection with 10 L of saline containing an inoculum of log 10 6.5 Ϯ 0.6 cfu/mL Streptococcus pneumoniae (17,19,24,25). Uninfected animals (n ϭ 62) were injected intracisternally with 10 L of sterile, pyrogen free saline.…”

Section: Model Of Meningitismentioning

confidence: 99%

“…After dehydration, sections were Nissl stained with cresyl violet and coverslips were fixed with Entellan® (Merck, Darmstadt, Germany). Neuronal injury in the dentate gyrus was evaluated as described previously (24). Apoptosis in the granule cell layer of the hippocampus, defined as cells showing markedly shrunken, condensed or fragmented nuclei (Fig.…”

Section: Model Of Meningitismentioning

confidence: 99%

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Dexamethasone Aggravates Hippocampal Apoptosis and Learning Deficiency in Pneumococcal Meningitis in Infant Rats

et al. 2003

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Section: Model Of Meningitismentioning

confidence: 99%

Section: Model Of Meningitismentioning

confidence: 99%

Dexamethasone Aggravates Hippocampal Apoptosis and Learning Deficiency in Pneumococcal Meningitis in Infant Rats

et al. 2003

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“…The vasoconstrictive effects of endothelins may contribute to ischemic neuronal injury, because an endothelin antagonist (bosentan) significantly reduced neuronal injury in experimental meningitis. The protective effect of bosetan was independent of an effect on nitric oxide production (121). These results should be confirmed in further experiments, especially because bosetan treatment was associated with a substantial increase in spontaneous deaths, even though the increase in mortality did not reach statistical significance.…”

Section: Conserve Cellular Function (I) Blood-brain Barrier and Incrmentioning

confidence: 69%

“…Release of vasoconstrictive agents, such as the endothelins, and vasodilatory agents, such as nitric oxide, causes loss of autoregulation of cerebral perfusion pressure. In the face of systemic hypotension, these events further decrease cerebral perfusion (121).…”

Section: Endothelium Of the Blood-brain Barriermentioning

confidence: 99%

Reprogramming the Host Response in Bacterial Meningitis: How Best To Improve Outcome?

et al. 2003

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Despite effective antibiotic therapy, bacterial meningitis is still associated with high morbidity and mortality in both children and adults. Animal studies have shown that the host inflammatory response induced by bacterial products in the subarachnoid space is associated with central nervous system injury. Thus, attenuation of inflammation early in the disease process might improve the outcome. The feasibility of such an approach is demonstrated by the reduction in neurologic sequelae achieved with adjuvant dexamethasone therapy. Increased understanding of the pathways of inflammation and neuronal damage has suggested rational new targets to modulate the host response in bacterial meningitis, but prediction of which agents would be optimal has been difficult. This review compares the future promise of benefit from the use of diverse adjuvant agents. It appears unlikely that inhibition of a single proinflammatory mediator will prove useful in clinical practice, but several avenues to reprogram a wider array of mediators simultaneously are encouraging. Particularly promising are efforts to adjust combinations of cytokines, to inhibit neuronal apoptosis and to enhance brain repair

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“…This finding showed yet again how M. canis might influence ME in ways that differ from those of classic neuropathogens (82). For example, increased ET-1 levels during acute pneumococcal sepsis promote meningitis through vasoconstriction, resulting in cerebral ischemia (81,83). Brain endothelial cells, microglia, astrocytes, and neurons are other sources of ET-1 (78,84).…”

Section: Discussionmentioning

confidence: 91%

Cellular Microbiology of Mycoplasma canis

et al. 2016

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M ycoplasma canis infects many mammalian hosts but is usually thought of as a commensal or opportunistic cofactor in respiratory or urogenital tract diseases of dogs (1). We found unexpectedly that M. canis was also detectable by culture or PCR in a majority of brain tissue specimens in a retrospective case-control study of canine granulomatous meningoencephalitis (ME) (GME) and necrotizing ME (NME) (2). The presence of M. canis in brain tissue was associated with both GME and NME (both P Ͻ 0.05, as determined by a 2 test). The clinical signs of this common idiopathic neurological disease of dogs include seizures, proprioceptive deficits, circling, and blindness. Immunosuppressive therapy may be palliative, but the syndrome is progressive and uniformly fatal (3). The extensive search for a presumed viral cause of canine GME and NME has been fruitless (4).In humans, bacterial meningitis and encephalitis are multifactorial lethal infections with often severe sequelae for survivors. New detection methods have shown that the variety of bacteria associated with human ME is much more extensive than usually appreciated (5-9). Additional animal models of bacterial ME are necessary to study this broader spectrum of pathogens (10). Since a possible association between M. canis and canine ME was discovered, our objective has been to help fill the void of basic knowledge about the organism's virulence factors, the host responses that it elicits, and its potential roles in pathogenesis. Our working hypotheses were that M. canis is capable of evoking host cell responses that favor dissemination from mucosal surfaces to secondary sites of infection, possibly in a strain-dependent fashion, and also that, regardless of how it might reach those sites, the presence of M. canis there modulates inflammation and direct injury to host cells. Understanding this potential can be expected to help evaluate the cause of canine ME and other diseases.(Portions of these data were presented in abstract form at Congresses of the International Organization for Mycoplasmology [90,91].) MATERIALS AND METHODSMycoplasma strains and cultivation. Strain PG14 T of M. canis (ATCC 19525) was first isolated from the throat of a normal dog (11). Strains UF31, UF33, LV, 5, 26, Cal, and Mara were first isolated from vaginal swabs of dogs without ME (12). Strains UFG1, UFG2, UFG3, and UFG4 were isolated from frozen brain tissues from cases of canine NME (2). Mycoplasma cynos strain H-831 T (ATCC 27544) was first isolated from the lung of a dog with pneumonia (13). Mycoplasma arginini strain G230 T , Mycoplasma bovigenitalium strain PG11 T , Mycoplasma edwardii strain PG24 T , Mycoplasma maculosum strain Skotti B, Mycoplasma molare strain H542 T , Mycoplasma opalescens strain MH5408 T , and Mycoplasma spumans strain PG13T , representing other species that have been isolated from dogs (1), were obtained from The Mollicutes Collection. All strains were propagated under standard conditions (14) in ATCC 988 medium supplemented with fetal bovine serum (FBS) and glu...

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Endothelin inhibition improves cerebral blood flow and is neuroprotective in pneumococcal meningitis

Cited by 75 publications

References 37 publications

Dexamethasone Aggravates Hippocampal Apoptosis and Learning Deficiency in Pneumococcal Meningitis in Infant Rats

Dexamethasone Aggravates Hippocampal Apoptosis and Learning Deficiency in Pneumococcal Meningitis in Infant Rats

Reprogramming the Host Response in Bacterial Meningitis: How Best To Improve Outcome?

Cellular Microbiology of Mycoplasma canis

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