A Case of Pemphigus Vulgaris Improved by Cigarette Smoking

Mehta, Jessica N.; Martin, Ann G.

doi:10.1001/archderm.136.1.15

Cited by 49 publications

(36 citation statements)

References 7 publications

(7 reference statements)

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“…115 Presumably due to its anti-inflammatory properties, 116 smoking is known to be a protective factor against ulcerative colitis, 117 and a few reports described successful treatment of its associated cutaneous manifestation, pyoderma gangrenosum, with nicotine. [118][119][120] Recently, several studies demonstrated the beneficial effects of smoking on pemphigus vulgaris, [121][122][123] likely as a result of nicotineÕs effects on the keratinocyte cholinergic network affected in pemphigus. 124 …”

Section: Protective Effects Of Smokingmentioning

confidence: 99%

Cutaneous Effects of Smoking

et al. 2004

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Section: Protective Effects Of Smokingmentioning

confidence: 99%

Cutaneous Effects of Smoking

et al. 2004

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“…A recently reported case of PV that had improved by cigarette smoking 14 and a study showing successful use of nicotinamide as a steroid-sparing agent in pemphigus, 15 suggested that pharmacological regulation of keratinocyte acetylcholine (ACh) axis may be a novel antiacantholytic therapy for pemphigus because (1) cigarette smoke contains the cholinomimetic agent nicotine and (2) nicotinamide exhibits cholinomimetic effects 16 owing to the stimulation of ACh release 17 and inhibition of acetylcholinesterase (AChE). 18 To determine whether a pharmacologic stimulation of keratinocyte cholinergic receptors can be used as a steroid-sparing regimen in the treatment of pemphigus, we administered pyridostigmine bromide (Mestinon; ICS Pharmaceuticals, Costa Mesa, Calif; 60-mg tablets) to a patient with active PV at the dose of 360 mg/d.…”

Section: Report Of a Casementioning

confidence: 99%

Pemphigus Vulgaris Acantholysis Ameliorated by Cholinergic Agonists

Nguyen¹,

Arredondo²,

Chernyavsky³

et al. 2004

Arch Dermatol

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“…Nicotinamide exhibits cholinomimetic effects (36) due to both stimulation of ACh release (37) and inhibition of acetylcholinesterase (38). Finally, because cigarette smoke contains the cholinomimetic agent nicotine, a reported case of PV that improved due to cigarette smoking (39) further suggested that pharmacologic activation of the keratinocyte ACh axis can facilitate healing of pemphigus erosions. The therapeutic effects of cholinomimetics in PV may stem from their ability to abrogate PV IgG-induced phosphorylation of keratinocyte adhesion molecules, because carbachol and pyridostigmine bromide can decrease by severalfold the PV IgG-dependent phosphorylation of E-cadherin and ␥-catenin (31).…”

mentioning

confidence: 99%

Differential Coupling of M1 Muscarinic and α7 Nicotinic Receptors to Inhibition of Pemphigus Acantholysis

Chernyavsky

Arredondo

Piser

et al. 2008

Journal of Biological Chemistry

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The mechanisms mediating and regulating assembly and disassembly of intercellular junctions is a subject of intensive research. The IgG autoantibodies produced in patients with the immunoblistering skin disease pemphigus vulgaris (PV) can induce keratinocyte (KC) dyshesion (acantholysis) via mechanisms that involve signaling kinases targeting intercellular adhesion molecules, thus providing a useful model to study the physiologic regulation of KC cohesion. Previous studies showed that activation of Src and protein kinase C are the earliest events in the PV IgG-induced intracellular phosphorylation cascades and that cholinergic agonists are effective for treating patients with pemphigus. In this study, we sought to elucidate the molecular mechanisms allowing cholinergic agonists to inhibit PV IgG-induced acantholysis and phosphorylation of KC adhesion molecules. The extent of acantholysis in KC monolayers correlated closely with the degree of PV IgG-induced phosphorylation of p120-and ␤-catenins, with classic isoforms of protein kinase C mediating serine phosphorylation of ␤-catenin and Src-tyrosine phosphorylation of p120-catenin. The M 1 muscarinic agonist pilocarpine blocked phosphorylation of both catenins, which could be abolised by the M 1 antagonist MT7. The ␣7 nicotinic agonist AR-R17779 inhibited phosphorylation of P120-cateinin. The ␣7 antagonist methyllycaconitine abolished the effect of AR-R17779. Okadaic acid abrogated protective effects of agonists on phosphorylation of ␤-catenin, and pervanadate, on that of p120-catenin. Stimulation of KCs with pilocarpine significantly (p < 0.05) elevated both serine/threonine and tyrosine phosphatase activities in KCs. AR-R17779 both stimulated tyrosine phosphatase and decreased PV IgGinduced Src activity. Methyllycaconitine released Src activity in intact KCs and caused acantholysis. Thus, downstream signaling from M 1 abolished PV IgG-dependent catenin phosphorylation due to activation of both serine/threonine and tyrosine phosphatases, whereas ␣7 action involved both activation of tyrosine phosphatase and inhibition of Src. These findings identified novel paradigm of regulation of signaling kinases associated with cholinergic receptors and provided mechanistic explanation of therapeutic activity of cholinomimetics in PV patients.

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A Case of Pemphigus Vulgaris Improved by Cigarette Smoking

Cited by 49 publications

References 7 publications

Cutaneous Effects of Smoking

Cutaneous Effects of Smoking

Pemphigus Vulgaris Acantholysis Ameliorated by Cholinergic Agonists

Differential Coupling of M1 Muscarinic and α7 Nicotinic Receptors to Inhibition of Pemphigus Acantholysis

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