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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The effect of leukocyte depletion on pulmonary M2 muscarinic receptor function in parainfluenza virus-infected guinea-pigs.

1. Parainfluenza infections of the airways cause dysfunction of inhibitory M2 muscarinic receptors on the pulmonary parasympathetic nerves. To distinguish the direct effects of virus from the effects of virus-induced airway inflammation on M2 muscarinic receptor function, guinea-pigs were depleted of leukocytes by pretreating with cyclophosphamide (30 mg kg-1, i.p. daily for 7 days) after which they were infected with parainfluenza virus type 1 (Sendai virus). 2. Guinea-pigs were anaesthetized, tracheotomized, and ventilated. The vagus nerves were isolated and cut, and the distal ends were electrically stimulated causing bronchoconstriction. In control animals, pilocarpine (1-100 micrograms kg-1, i.v.) inhibited and gallamine (0.1-10 mg kg-1, i.v.) potentiated vagally-induced bronchoconstriction by stimulating or blocking M2 muscarinic receptors on the vagus. These effects of pilocarpine and gallamine were almost completely lost in virus-infected animals, demonstrating loss of M2 receptor function. 3. Cyclophosphamide depleted peripheral blood leukocytes and inhibited the virus-induced influx of inflammatory cells into the lung. Depletion of leukocytes protected M2 receptor function from viral infection in some, but not all, guinea-pigs tested. 4. Among infected animals that had been depleted of leukocytes, the viral content (expressed as the log of the number of tissue culture infectious doses per g lung tissue) of those that retained normal M2 receptor function was 4.29 +/- 0.05 (mean +/- s.e. mean), while the viral content of those that lost M2 receptor function despite leukocyte depletion was 5.45 +/- 0.20 (P = 0.011).(ABSTRACT TRUNCATED AT 250 WORDS)[1]

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