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K A Mooney

Publications and source records attributed to K A Mooney.

5 recordsLinked to original sources
PubMed2002

Larval Taenia crassiceps secretes a protein with characteristics of murine interferon-gamma.

Previous studies have shown that excretory/secretory products of larval Taenia crassiceps have immunomodulatory activities. We report here that one of these products, termed p66, possesses activities that mimic some characteristics of murine interferon-gamma (IFN-gamma). Purified p66 cross-reacts with anti-murine IFN-gamma on immunoblots and increases concanavalin-A-induced splenic T-cell proliferative responses of normal and chronically infected mice. It has also been shown that p66 induces enhanced IFN-gamma and interleukin-10 (IL-10) production in cells from infected or normal mice. Adherent and non-adherent peritoneal exudates cells were stimulated with p66 and showed that the adherent cells were induced to produce IL-10 and that the non-adherent cells were induced to produce IFN-gamma. p66 was shown as well to upregulate nitric oxide production in macrophages and two T-cell lines, IEL and YAC-1, were shown to be stimulated to produce IFN-gamma and IL-10, respectively, by p66. Although the significance of p66 in immunoregulation is not known, we show here that this molecule mimics characteristics of IFN-gamma.

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PubMed2000

Immune destruction of larval taenia crassiceps in mice.

Immune destruction of larval Taenia crassiceps was examined by first injecting BALB/cJ mice subcutaneously with larval buds and 30 to 60 days later challenging the mice with larvae injected into the peritoneal cavity. The larvae injected intraperitoneally (i.p.) secondarily are killed by host cells that completely encase the larvae in a thick sheath. The peritoneal exudate cells and the cytokines they produced were characterized by flow cytometry, enzyme-linked immunosorbent assays (ELISAs), and reverse transcription PCR (RT-PCR). No changes in percentage of CD4(+) T cells, CD8(+) T cells, B1 cells, or macrophages were detected in the peritoneal cavities of mice that were killing larvae compared to mice with a primary 7-day infection i.p. Both RT-PCR and ELISA demonstrated a decrease in cytokines including gamma interferon (IFN-gamma), interleukin-4 (IL-4), and IL-10 in mice that were killing the larvae compared to control mice infected for 30 to 60 days i.p. alone, although there was little difference compared to mice infected for 7 days i.p. alone. Serum cytokine levels in mice that were killing the larvae showed a decrease in IFN-gamma and IL-4, an increase in IL-10 when compared to mice infected for 30 to 60 days i.p. alone, and increases in all cytokines compared to mice infected for 7 days i.p. alone. Inhibition of nitric oxide production did not significantly affect the number or the viability of larvae in the peritoneal cavity of mice that were killing larvae during secondary infection.

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PubMed1999

The systemic immune response of BALB/c mice infected with larval Taenia crassiceps is a mixed Th1/Th2-type response.

The subsets of lymphocytes and cytokines regulating the site-specific immune response in experimental cysticercosis (Taenia crassiceps) are not known. This study investigated the cells present at the site of infection (PECs) using flow cytometry and measured the cytokines produced by these cells through 50 days of infection. The results showed an expansion of B220+CD5+, B220+CD5-, alpha beta TCR+CD4+ and CD8+ cells coincident with a transient increase in IL-10 production. After the initial increase, the percentage of B220+CD5- and helper T cells decreased with a concomitant decrease in IL-10 production. CD8+ T cells continued to increase throughout infection and gamma delta TCR+ cells increased after 10 days of infection. PECs demonstrated an increased IFN-gamma and IL-4 production throughout infection when stimulated with larval antigens. Because a Th2-type polarization has been shown for spleen cells from infected BALB/c mice, cytokine profiles of spleen cells and PECs in response to ConA and larval antigens were compared. ConA and antigen-specific stimulation of spleen cells from 50-day-infected mice produced increased amounts of IL-10 while PECs showed a decreased IL-10 production suggesting that anatomically distinct lymphoid populations produce different cytokines and promote different types of responses. Surprisingly, late in infection the levels of IL-4 and IFN-gamma in serum increased substantially (460-fold and 100-fold, respectively). The systemic immune response of BALB/c mice during experimental cysticercosis, therefore, is a mixed Th1/Th2-type response.

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PubMed1999

gamma delta T cells do not play a major role in controlling infection in experimental cysticercosis.

Protective immunity against larval Taenia crassiceps has been shown to rely on T cells; however, the roles of the specific subsets of T cells during infection are not known. To investigate a possible role for gamma delta T cells, this study investigated larval infection in delta-chain knock-out C57BL/6 (deltaKO) and wild-type C57BL/6 mice. It was found that deltaKO mice and C57BL/6 mice were equally susceptible to infection suggesting gamma delta T cells do not play a major role in protective immunity. Cytokine production by concanavalin A (ConA)-stimulated spleen cells from infected deltaKO mice and C57BL/6 mice were determined. All infected mice demonstrated an increased IL-10 production suggesting a Th1-inhibitory function. Cells from infected deltaKO mice and C57BL/6 mice did not show increases in IL-4 production. Heavily-infected C57BL/6 mice showed a decrease in IFN-gamma production compared to deltaKO mice. These observations suggest that an increase in IL-10 production best correlates with a non-protective immune response. To make comparisons between in vitro cytokine production and systemic immune responses, cytokine levels in serum were determined. C57BL/6 mice and deltaKO mice showed increases in serum levels of IL-4 and IFN-gamma at 52 days post-infection. The systemic immune response of these mice, therefore, is a mixed Th1/Th2-type response and gamma delta T cells are apparently not responsible for the systemic increases in these cytokines.

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