This report examines the effect of recombinant murine (rm)IL-10 on antigen-induced cellular recruitment into the airways of sensitized Balb/c mice. The intranasal instillation of 10 pug ovalbumin induced an early (6-24 h) increase in the number of neutrophils, and a late rise (24-96 h) in that of eosinophils in the bronchoalveolar lavage (BAL) fluid and bronchial tissue. A single intranasal instillation of 0.01-0
Infection with a virulent strain of Mycobacterium avium, but not with virulent Mycobacterium tuberculosis or avirulent Mycobacterium smegmatis, induced the formation of nitric oxide by human monocyte-derived macrophages. This process was not affected by lipopolysaccharide or cytokines such as interferon-gamma or tumor necrosis factor alpha. M. avium-induced nitric oxide production was significantly decreased by NG-monomethyl-L-arginine, a potent inhibitor of nitric oxide synthase activity, without any significant enhancement of intramacrophagic mycobacterial growth. Infection with all the three mycobacterial species induced a significant activation of phospholipase A2 activity of macrophages as evidenced by the increased release of thromboxane A2. Finally, nitric oxide production by human monocyte-derived macrophages required infection with live M. avium, as neither gamma-irradiated M. avium nor the subcellular fractions of this microorganism (cell wall, cytosol) were able to trigger nitric oxide synthesis.
Our results show that alveolar macrophages from wheezy infants are activated to release increased amounts of tumour necrosis factor-α, as in asthma, and suggest that infants with recurrent wheezing may eventually benefit from treatment with glucocorticoids.
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