Khan I, Collins S M
Intestinal Disease Research Programme, Health Science Centre, McMaster University, Hamilton, Ontario, Canada.
Gastroenterology. 1994 Sep;107(3):691-700. doi: 10.1016/0016-5085(94)90116-3.
BACKGROUND/AIMS: Trichinella spiralis infection in the rat produces mucosal injury and inflammation and causes changes in muscle function and neurotransmitter release in the longitudinal muscle myenteric plexus (LMMP). Whether these changes in LMMP reflect the production of inflammatory mediators in the LMMP remains unknown. The objective of this study was to investigate the profile of interleukins (IL) 1-alpha, 1-beta, and 6 and tumor necrosis factor (TNF) alpha in the LMMP of infected rats. Because muscle changes are T-cell dependent, we also studied the cytokine profile in infected athymic rats.
Cytokine messenger RNA (mRNA) was examined using semiquantitative polymerase chain reaction, and protein was measured by enzyme-linked immunosorbent assay, radioimmunoassay, or bioassay.
There was increased expression of IL1-alpha and -beta, IL-6, and TNF-alpha mRNA and protein in the LMMP of both euthymic and athymic infected rats. Increased expression of each cytokine was observed by 24 hours postinfection and, in the case of IL1-beta and TNF-alpha, remained elevated by day 6 postinfection.
Mucosal injury following T. spiralis infection is accompanied by enhanced expression of proinflammatory cytokines in the LMMP. The expression of IL1-, IL-6, and TNF-alpha in infected athymic rats suggests that these cytokines do not contribute to the changes in muscle growth or contraction but may mediate the previously described changes in neurotransmitter release in this model.
