Submitted to: Journal of Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 24, 1997
Publication Date: N/A
Interpretive Summary: Cryptosporidium parvum is an intestinal parasite of many vertebrates, including cattle and man. Disease caused by the parasite can be life-threatening in immunocompromised individuals. In order to elucidate which are the mechanisms involved in protection against the parasite, studies were done to characterize the cytokine immune responses generated after a primary infection of neonatal calves with C. parvum. The information acquired will allow us to design cytokine-based vaccination approaches to this pathogen. These studies showed significant changes in the cytokines interferon-gamma (IFN-g) and interleukin-12 (IL-12) in intestinal epithelial populations. These results will allow further investigations into the possibility of protecting against C. parvum using cytokins and, thus, decreasing contamination of water supplied with this parasite.
In the present study, localized changes in cytokine transcription profiles were examined in neonatal calves following a primary infection with Cryptosporidium parvus, using competitive reverse transcriptase polymerase chain reaction (RT-PCR). Total RNA was prepared from ileo-cecal lymph nodes (LN), lamina propria (LPL) and intra-epithelial (IEL) lymphocytes isolated from neonatal calves 7 days after C. parvum infection Competitive RT-PCR performed on cDNA samples containing internal cytokine gene competitor molecules showed increases in the levels of interferon- gamma (IFN-g) and interleukin-12 (IL-12) (P40) mRNA in both LPL and IEL populations but not in the draining LN. In addition, the levels of mRNA in both LPL and IEL populations but not in the draining LN. In addition, the levels of mRNA of the newly identified growth factor IL15 decreased in the IEL of the infected animals. No consistent differences were seen in any of the cell populations when the samples were analyzed for IL10; and levels of mRNA for IL2 and IL4 were low and highly variable in both infected and control groups in all three lymphocyte populations.