Page Banner

United States Department of Agriculture

Agricultural Research Service


item Sonea, Ioana
item Schwarz, Melinda
item Harp, James

Submitted to: Conference Research Workers Disease Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 11/12/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: One of the major factors contributing to the defense against C. parvum infection is increased production of interferon-gamma (IFN-gamma) by the host. Substance P, the most abundant neurotransmitter in the gut, upregulates IFN-gamma production in some inflammatory conditions. We sought to determine whether production of IFN-gamma during C. parvum infection was regulated by substance P. C57BL/6J mice were infected at 1 wk of age with 10**4 C. parvum oocysts. Spleens, mesenteric lymph nodes and cecal tonsil explants were collected at 3 and 4 wk of age, and cultured in the presence or absence of substance P for 24 h. IFN-gamma content in supernatants was measured by ELISA; the relative amounts of mRNA for IFN-gamma in cecal tonsil explants were determined using semi- quantitative reverse transcription polymerase chain reaction (RT-PCR). Age-matched uninfected C57BL/6J mice were used as controls. The amount of IFN-gamma produced depended on age, infection status and source of lymphocytes, as well as on presence or absence of substance P. In all groups, splenocytes produced IFN-gamma, and IFN-gamma levels increased in the presence of substance P. In contrast, mesenteric node lymphocytes from uninfected mice did not produce detectable IFN-gamma, whereas those from infected mice did. Substance P had no significant effect on IFN- gamma production by mesenteric lymphocytes in either group. Cecal tonsil explants did not produce detectable levels of IFN-gamma, although mRNA for IFN-gamma could be detected. These results suggest that substance P is unlikely to contribute to the upregulation of IFN-gamma in response to C. parvum at 3 wk of age, but may do so at later ages.

Last Modified: 05/23/2017
Footer Content Back to Top of Page