Changes in pulmonary calcitonin gene-related peptide and protein gene product 9.5 innervation in rats infected with Mycoplasma pulmonis.
Changes in the expression of calcitonin gene-related peptide (CGRP) and polyneural protein gene product 9.5 (PGP) in hilar peribronchial innervation was investigated by immunohistochemistry in specific pathogen-free rats chronically infected with Mycoplasma pulmonis. Image analysis of immunostained sections revealed a reduction of approximately 62% in the amount of CGRP- and PGP-immunoreactive innervation of the peribronchial area in the infected animals. The portion of the total bronchial perimeter occupied by bronchus-associated lymphoid tissue was increased six-fold. The decrease in the CGRP-immunoreactive area could be the result either of an enhanced CGRP release or of a loss of nerve fibres. The decrease in the PGP-immunoreactive fibres indicates a degenerative loss of nerves. Increased bronchus-associated lymphoid tissue and decreased bronchial innervation by neurons releasing the immunomodulatory neuropeptide CGRP might both contribute to the pathophysiology and symptoms of mycoplasmosis in the rat.[1]References
- Changes in pulmonary calcitonin gene-related peptide and protein gene product 9.5 innervation in rats infected with Mycoplasma pulmonis. Nohr, D., Buob, A., Gärtner, K., Weihe, E. Cell Tissue Res. (1996) [Pubmed]
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