The Intracellular Neutral SH-Dependent Protease Associated with Inflammatory Reactions

Hayash, Hideo

doi:10.1016/s0074-7696(08)60952-3

Cited by 72 publications

(17 citation statements)

References 110 publications

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“…In SeV-infected mice treated with CO once and CY twice, much active inflammatory protease and leucoegresin would have increased the hyper-sensitivity reaction due to severe pneumonia [14,15]. Periarteritis nodosa-or panarteritis nodosa-like lesions and an increase in vascular permeability are caused by intracellular neutral SH-dependent protease I and II, and vasoexin induced by activated neutral SH-protease, respectively, and these are induced by allergic inflammatory lesions [14].…”

Section: Discussionmentioning

confidence: 99%

“…Periarteritis nodosa-or panarteritis nodosa-like lesions and an increase in vascular permeability are caused by intracellular neutral SH-dependent protease I and II, and vasoexin induced by activated neutral SH-protease, respectively, and these are induced by allergic inflammatory lesions [14]. Most important is that these histopathological findings are signs of a delayed hypersensitivity reaction [15,41].…”

Section: Discussionmentioning

confidence: 99%

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Differential Invasion by Sendai Virus of Abdominal Parenchymal Organs and Brain Tissues in Cortisone- and Cyclophosphamide-Based Immunosuppressed Mice

Miyamae

2005

The Journal of Veterinary Medical Science

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ABSTRACT. Pneumotropic virus invasion of parenchymal organs in mice with immunosuppressants is worth studying from an etiopathogenetic viewpoint as an animal model of a compromised host. This study analyzed the invasion by Sendai virus (SeV) of mouse organs in immunosuppressive states induced by cortisone (CO) and cyclophosphamide (CY). After subcutaneous inoculation of CO or CY, or both, in mice infected intra-nasally with SeV, the SeV invasion was investigated by detecting viremia and viral antigen in organs. SeV Nagoya strain and one treatment of CO or CY caused viremia at 18 hr or 3 d, respectively, with infection in tracheal lymph nodes, but not in untreated mice. SeV invaded hepatocytes and splenolymphocytes on days10 and 5-10, respectively, after infection. CO or CY treatment, three times, induced viral invasion of brain tissues or serious respiratory infection, respectively, but progressive invasion of abdominal parenchymal organs was not different between treated groups. One CO and two CY treatments intensified viral invasion into many organs, maintaining seronegativity. Cerebral blood vessels had the highest incidence of viral antigen in the brain. Astroglial sheets, choroid plexuses, pia maters, and ventricular epithelia tested positive; test-positive neurons were few. SeV MN strain caused progressive invasion of the brain with gliosis and neuronophagy. Blood-brain barrier disruption was caused by virulence of the MN strain. Half the infected mice in two groups treated with CO once and CY twice succumbed to delayed hypersensitivity, suggested by cerebromicrovascular nodulation. KEY WORDS: blood-brain barrier disruption, cortisone, cyclophosphamide, Sendai virus, viremia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Differential Invasion by Sendai Virus of Abdominal Parenchymal Organs and Brain Tissues in Cortisone- and Cyclophosphamide-Based Immunosuppressed Mice

Miyamae

2005

The Journal of Veterinary Medical Science

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“…Criteria for determining the role of a mediator(s) in inflammation are : (1) presence of the mediator at sites of inflammation, (2) reproduction of inflammatory responses by the mediator, and (3) inhibition of inflammatory responses by the specific inhibitor (Hayashi, 1975). Based on these factors, we investigated the role of TNFα and IL-1β in LPS-induced uveitis, using homologous reagents.…”

Section: Discussionmentioning

confidence: 99%

Involvement of TNF α, IL-1β and IL-1 Receptor Antagonist in LPS-induced Rabbit Uveitis

Matsukawa

Ohkawara

et al. 1998

Experimental Eye Research

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“…The inflammatory response consists of two phases, a fluid phase and a cellular phase [1]. The fluid phase is initiated by transient vasoconstriction followed by dilation of arterioles, capillaries, and venules, during which blood flow and permeability to plasma proteins is increased.…”

Section: Introductionmentioning

confidence: 99%

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Yamashiro

Kamohara

Yoshimura

1999

Journal of Leukocyte Biology

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The Intracellular Neutral SH-Dependent Protease Associated with Inflammatory Reactions

Cited by 72 publications

References 110 publications

Differential Invasion by Sendai Virus of Abdominal Parenchymal Organs and Brain Tissues in Cortisone- and Cyclophosphamide-Based Immunosuppressed Mice

Differential Invasion by Sendai Virus of Abdominal Parenchymal Organs and Brain Tissues in Cortisone- and Cyclophosphamide-Based Immunosuppressed Mice

Involvement of TNF α, IL-1β and IL-1 Receptor Antagonist in LPS-induced Rabbit Uveitis

MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

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