Inhibition of the Tuberculin Reaction in Albino Rats

Henson, Edmond C.; Brunson, Joel G.

doi:10.1159/000230272

Cited by 2 publications

(4 citation statements)

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“…Epi rapidly increases circulating natural killer (NK) cells (24), modulates T-helper (Th) 1 activities (7), mobilizes granulocytes from marginal pools (1), and increases L-selectin expression (20) and LPS-mediated upregulation of TNF-␣ receptors by blood monocytes (11). In rats, Epi administered daily before antigen sensitization and through subsequent antigen challenge inhibits cutaneous tuberculin reactions (12).…”

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confidence: 99%

Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism

Jain

Zhao

Selig

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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. Epinephrine promotes pulmonary angiitis: evidence for a ␤1-adrenoreceptor-mediated mechanism. Am J Physiol Lung Cell Mol Physiol 285: L232-L239, 2003; 10.1152/ajplung.00248.2002 increases lymphocyte traffic to lung. We investigated whether Epi also modulates pulmonary cell-mediated immune responses in vivo. C57BL/6 mice were immunized with hen-egg lysozyme (HEL) on day 0, challenged with HEL intratracheally at day 12, and killed at day 15. Mice received Epi (0.5 mg/kg) subcutaneously during the sensitization phase, days 1-7 (Epi-SP), or the effector phase, days 12-14 (Epi-EP); controls received saline subcutaneously. Epi-SP mice showed increased airway inflammation (P Ͻ 0.03) and pulmonary angiitis (P Ͻ 0.04) characterized by endothelialitis and subendothelial fibrin deposition. Macrophages and granulocytes were increased in perivascular cuffs in situ (P Ͻ 0.001). CD3 ϩ lymphocytes increased in the bronchoalveolar lavage fluid, whereas NK1.1 ϩ and CD4 ϩ CD25 ϩ lymphocytes decreased (all P Ͻ 0.05). Atenolol, a selective ␤1-adrenoreceptor (AR) antagonist, inhibited the increased vascular and airway inflammation and the reduction in CD4 ϩ CD25 ϩ lymphocytes (all P Ͻ 0.05) yielded by Epi, whereas all ␣/␤-AR blockers inhibited airway inflammation. We conclude that Epi-EP selectively promotes vascular inflammation in vivo via a ␤ 1-receptor-mediated mechanism.

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confidence: 99%

Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism

Jain

Zhao

Selig

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Others found that epinephrine decreased the in flammation produced by mild thermal and chemical injury and other forms of injury which do not involve altered intravascular coagulation [8,9]. Epinephrine alone has been shown to produce slight inhibition of the tuberculin reaction in albino rats [3]. This was thought to be caused by the constrictive effect of epinephrine on the peripheral vas culature which inhibited egress of vascular contents into the extravascular spaces.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies showed propiomazinc and epinephrine to be effective in inhibiting the formation of humoral antibody, the Arthus reaction, and tuberculin sensitivity in rabbits, rats, and mice [1][2][3]. The present study utilized guinea pigs which have been shown to be much more resistant than the above species to the anti-inflammatory and immunosuppressive effects of cortisone (and cortisol) and the antimetabolite group of drugs [5].…”

Section: Discussionmentioning

confidence: 99%

“…In these studies, concerned with the formation of humoral antibody and immediate hypersensitivity, leukocyte numbers remained within normal limits in the treated animals. In other studies it was shown that the propiomazinc-epinephrine mixture was effective in preventing the tuberculin reaction in albino rats [3]. Although the drug com bination docs not produce the lympholytic effects accompanying large doses of cortisone (and cortisol) it is thought to possess at least one mechanism of action similar to cortisone (and cortisol) in maintaining the integrity of cellular and subcellular membrane systems [4], and…”

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Inhibition of the Tuberculin Reaction in Guinea Pigs

Henson¹,

Collins²,

Izard³

et al. 1971

Int Arch Allergy Immunol

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Administration of a mixture of propiomazine (a phenothiazine derivative) and epinephrine markedly inhibited development of the tuberculin reaction when given at three different dose levels and by the s.c. or i.p. routes of administration. Inhibition was produced when the animals were treated prior to sensitization or when initiation of treatment was delayed until time of sensitization. Inhibition was also produced by short-term treatment at time of sensitization or at challenge. The mechanisms involved in the synergistic effect produced by the combination of epinephrine and propiomazine are under investigation. The combination is thought to operate by maintaining the integrity of cellular and subcellular membrane systems which causes such cells and tissues to be refractory to noxious stimuli and unreactive to stimulation by antigen. Epinephrine or propiomazine when used alone in actively sensitized guinea pigs resulted in only slight or no inhibition of the tuberculin reaction.

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Inhibition of the Tuberculin Reaction in Albino Rats

Cited by 2 publications

References 9 publications

Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism

Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism

Inhibition of the Tuberculin Reaction in Guinea Pigs

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Inhibition of the Tuberculin Reaction in Albino Rats

Cited by 2 publications

References 9 publications

Epinephrine promotes pulmonary angiitis: evidence for a β1-adrenoreceptor-mediated mechanism

Epinephrine promotes pulmonary angiitis: evidence for a β1-adrenoreceptor-mediated mechanism

Inhibition of the Tuberculin Reaction in Guinea Pigs

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Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism

Epinephrine promotes pulmonary angiitis: evidence for a β₁-adrenoreceptor-mediated mechanism