The progression of murine
mycoplasma pneumonia is dependent on T cells and other immune cells. The role of
cytokines in immunity are complex, and identifying the network of
cytokines produced after
infection of mice is essential in dissecting the key
cytokine cascades involved mycoplasma disease pathogenesis. In the present study,
mRNA expression of 143 different
cytokines,
chemokines, or receptors were evaluated in lung tissues from both susceptible (BALB/c and C3H/HeN) and resistant (C57BL/6) mice after Mycoplasma pulmonis
infection. To accomplish this, membrane-based
cDNA microarrays were used to monitor changes
mRNA expression in lungs. There was a clear association with
disease susceptibility and development of
cytokine mRNA expression. In addition to proinflammatory
cytokines,
mRNA expression of an anti-inflammatory
cytokine,
interleukin-10, increased with disease severity, suggesting an attempt to moderate the severity of the inflammatory response. Furthermore, it is clear that an array of
chemokines produced in susceptible mice could contribute to the recruitment and maintenance of inflammatory cells at the site of disease. In support of this, there was an increase in
macrophage inflammatory protein 1beta (
MIP-1beta; CCL4) and
monocyte chemoattractant protein 2 (MCP-2; CCL8)
mRNA levels from mycoplasma-infected mice and a corresponding accumulation of CD4+ Th cells expressing the
MIP-1beta/MCP-2
receptor, CCR5, in the lungs of mice. Furthermore, MIP-1beta- and MCP-2-producing cells and CD4+ T cells were found to be in close association in pulmonary lesions. Thus, there was a significant
cytokine response associated with disease pathogenesis, and these studies provide important leads and insights into ongoing
cytokine- and
chemokine-mediated processes in this persistent inflammatory disease.