Loading...
Please wait, while we are loading the content...
Similar Documents
Modulation of in vitro monocyte cytokine responses to Leishmania donovani. Interferon-gamma prevents parasite-induced inhibition of interleukin 1 production and primes monocytes to respond to Leishmania by producing both tumor necrosis factor-alpha and interleukin 1.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Reiner, Neil E. Ng, Wai-Leung Wilson, Christopher B. McMaster, W. Robert Burchett, Sandra K. |
| Copyright Year | 1990 |
| Abstract | Cytokines produced by mononuclear cells are important regulatory and effector molecules and evidence has been presented to support a role at least for tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in host defense against Leishmania. In the present study, we examined the production of TNF-alpha and interleukin 1 (IL-1) by resting and IFN-gamma-primed peripheral blood monocytes infected in vitro with Leishmania donovani. Monocytes produced neither IL-1 nor TNF-alpha during challenge with Leishmania. Cells preinfected with Leishmania synthesized normal amounts of TNF-alpha, but had diminished production of IL-1 in response to stimulation with either S. aureus or lipopolysaccharide (LPS). The induction by S. aureus or LPS of IL-1 beta mRNA accumulation in infected cells was normal despite diminished intracellular or supernatant IL-1 protein and bioactivity. Thus, inhibition of IL-1 production by Leishmania most probably reflected diminished translation of IL-1 beta mRNA. Pretreatment of cells with IFN-gamma abrogated infection-induced inhibition of IL-1 production and primed cells for the production of both IL-1 and TNF-alpha upon subsequent exposure to Leishmania. These results indicate that L. donovani has evolved the capacity to infect mononuclear phagocytes, without stimulating the production of two potentially host-protective monokines. The ability of IFN-gamma to prime monocytes to produce TNF-alpha and IL-1 in response to infection with Leishmania and to prevent inhibition of IL-1 production may have implications for immunotherapy with this lymphokine. |
| File Format | PDF HTM / HTML |
| DOI | 10.1172/JCI114654 |
| PubMed reference number | 2112157 |
| Journal | Medline |
| Volume Number | 85 |
| Issue Number | 6 |
| Alternate Webpage(s) | https://dm5migu4zj3pb.cloudfront.net/manuscripts/114000/114654/cache/114654.1-20150302165505-covered-253bed37ca4c1ab43d105aefdf7b5536.pdf |
| Alternate Webpage(s) | http://dm5migu4zj3pb.cloudfront.net/manuscripts/114000/114654/JCI90114654.pdf |
| Alternate Webpage(s) | https://doi.org/10.1172/JCI114654 |
| Journal | The Journal of clinical investigation |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
