The Role of α 4 (CD49d) and β 2 (CD18) Integrins in Eosinophil and Neutrophil Migration to Allergic Lung Inflammation in the Brown Norway Rat

The monoclonal antibody OX22 defines a functional split within CD4+ T cells in the rat, with OX22high cells mainly producing interleukin 2 (IL-2) and interferon gamma and responsible for delayed-type hypersensitivity responses, and OX22low cells mainly producing IL-4 and -5 and responsible for providing B cell help. There are reciprocal interactions between OX22high and OX22low cells, and it has been suggested that the OX22low subset has a role in the prevention of autoimmunity. We have used OX22 in vivo to define the role of these subsets in mercuric chloride-induced autoimmunity in the Brown Norway rat. In this model, there is polyclonal B cell activation and animals develop widespread tissue injury. Treatment of thymectomized animals with OX22 led to a profound reduction in the number of OX22high T cells in the peripheral blood. OX22-treated animals consistently developed more severe tissue injury than controls given an irrelevant antibody of the same isotype. Control animals pretreated with broad spectrum antimicrobial drugs showed milder tissue injury, but this protective effect of antimicrobials was lost in OX22-treated animals. Transfer of naive T cells to OX22-treated animals provided protection, but if T cells were depleted in vitro of OX22high cells before transfer, this effect was lost. These data provide evidence for a protective immunoregulatory role for OX22high T cells in mercuric chloride-induced autoimmunity.

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Brown Norway Rat Asthma Model of Diphenylmethane 4,4′-Diisocyanate

Inhalation Toxicology ◽

10.1080/08958370500224631 ◽

2005 ◽

Vol 17 (13) ◽

pp. 729-739 ◽

Cited By ~ 18

Author(s):

Jürgen Pauluhn

Keyword(s):

Brown Norway ◽

Norway Rat ◽

Asthma Model ◽

Brown Norway Rat

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Knockdown of Add3 impairs the myogenic response of renal afferent arterioles and middle cerebral arteries

AJP Renal Physiology ◽

10.1152/ajprenal.00529.2016 ◽

2017 ◽

Vol 312 (6) ◽

pp. F971-F981 ◽

Cited By ~ 18

Author(s):

Fan Fan ◽

Mallikarjuna R. Pabbidi ◽

Ying Ge ◽

Longyang Li ◽

Shaoxun Wang ◽

...

Keyword(s):

Vascular Reactivity ◽

Vascular Dysfunction ◽

Cerebral Arteries ◽

Chromosome 1 ◽

Brown Norway ◽

Myogenic Response ◽

Norway Rat ◽

Vasoconstrictor Response ◽

Brown Norway Rat ◽

Interfering Rna

We have reported that the myogenic response of the renal afferent arteriole (Af-art) and middle cerebral artery (MCA) and autoregulation of renal and cerebral blood flow are impaired in Fawn-Hooded Hypertensive (FHH) rats. Transfer of a region of chromosome 1 containing γ-adducin (Add3) from the Brown Norway rat rescued the vascular dysfunction and the development of renal disease. To examine whether Add3 is a viable candidate gene altering renal and cerebral hemodynamics in FHH rats, we knocked down the expression of Add3 in rat Af-arts and MCAs cultured for 36-h using a 27-mer Dicer-substrate short interfering RNA (DsiRNA). Control Af-arts constricted by 10 ± 1% in response to an elevation in pressure from 60 to 120 mmHg but dilated by 4 ± 3% when treated with Add3 DsiRNA. Add3 DsiRNA had no effect on the vasoconstrictor response of the Af-art to norepinephrine (10−7 M). Add3 DsiRNA had a similar effect on the attenuation of the myogenic response in the MCA. Peak potassium currents were threefold higher in smooth muscle cells isolated from Af-arts or MCAs transfected with Add3 DsiRNA than in nontransfected cells isolated from the same vessels. This is the first study demonstrating that Add3 plays a role in the regulation of potassium channel function and vascular reactivity. It supports the hypothesis that sequence variants in Add3, which we previously identified in FHH rats, may play a causal role in the impaired myogenic response and autoregulation in the renal and cerebral circulation.

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