Minocycline Treatment of Allergic Asthmatic Patients and BPO-KLH Sensitized Mice at the Peak of the Hapten Specific IgE Response Suppresses IgE, but not IgM, IgG or IgA Responses

Article Outline

• Rationale
• Methods
• Results
• Conclusion
• Copyright

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Rationale 

Successful anti-allergy therapy should suppress patient IgE responses while leaving other immune responses intact.

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Methods 

UniCap Total IgE Fluoroenzymeimmunoassay, nephelometry, specific ELISPOT assay, ELISA. Allergic asthmatic patients (serum IgE: 505 ± 535 IU/ml) received minocycline (150 mg po BID) as add-on therapy (n = 6) and controls (IgE 579 ± 505 IU/ml) received standard care (n = 7) for up to 10 months. Levels of IgM, IgG, IgE and IgA in serum were determined each month. BPO-KLH sensitized mice were fed with minocycline (10-100 mg/kg) or vehicle at the peak of the hapten specific IgE response (day 44) (5 mice/group), and the numbers of BPO-specific IgG, IgE and IgA AFC in mesenteric LN and spleen, and levels of IgM, IgG, IgE and IgA in serum were determined on days 45-70.

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Results 

Minocycline treatment suppressed serum IgE levels of allergic asthmatic patients (mean 26 IU/ml or 9%/month; in patients treated 10 months ∼90%), but had no effect on levels of serum IgM, IgG or IgA, which always were in normal ranges. Similarly, minocycline, but not vehicle, treatment of BPO-KLH sensitized mice strongly suppressed BPO specific IgE AFC responses and serum IgE levels in dose dependent fashion (>98%), with peak suppression lasting 5-7 days, but had no effect on other immunoglobulin responses.

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Conclusion 

Minocycline is a good candidate for an anti-allergy drug; ideal candidates would be minocycline derivatives lacking antibiotic activity. Mechanisms of suppression can be studied in our mouse model.