Molecular detection and identification of type I interferon mRNAs

Lai, Mary C.; Boyer, S.J.; Beilharz, Manfred W.

doi:10.1016/1050-3862(94)90004-3

Cited by 6 publications

(3 citation statements)

References 16 publications

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“…This is consistent with the literature, which states that the majority of IFN regulation occurs at the transcriptional level (25). The ␣4 species of IFN-␣ was chosen because it has previously been reported to be produced by L929 cells in larger amounts than the other IFN species (8). Neither of the two housekeeping genes was affected by cocaine, indicating that the increase in IFN mRNA levels was not due to an overall increase in transcription.…”

Section: Fig 7 Effects Of Cocaine On the Level Of Poly(i⅐c)-inducedsupporting

confidence: 70%

Cocaine Causes Increased Type I Interferon Secretion by both L929 Cells and Murine Macrophages

Grattendick

Jansen

Lefkowitz

et al. 2000

Clin Diagn Lab Immunol

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Cocaine has been demonstrated to have a number of different effects on immune cell functions. We have reported alterations of cellular functions by macrophages (M) exposed to cocaine in vitro, including the inhibition of mouse hepatitis virus replication. Here, we present evidence that cocaine stimulates the secretion of an antiviral product that is neutralized by anti-interferon (anti-IFN). A dose-dependent increase in the secretion of IFN by both M and L929 cells incubated with cocaine, with a concomitant decrease in virus replication, is also reported. The increase in IFN secretion was most pronounced when cells were cultured in the presence of the IFN inducer poly(I⅐C). The effect of cocaine on IFN production was found to be primarily at the transcript level in both M and L929 cells. These findings further support our previous research demonstrating an antiviral activity of cocaine in vitro. The relevance of this activity to viral infections in general remains to be determined.Cocaine has been reported to exhibit a variety of immunomodulatory effects on different immune functions (30). Previous reports by us and others have demonstrated that macrophages (M) exposed to cocaine in vitro displayed increased phagocytosis of microorganisms (10), with an increased production of reactive oxygen intermediates (28, 29) as well as decreased cytokine secretion (24) and production of reactive nitrogen intermediates (27). Further studies have reported that cocaine enhanced neutrophil phagocytosis, increased natural killer (NK) cell activity and distribution (26), reduced the Tcell mitogen response (13), and reduced the cytotoxic ability of splenic immune cells (14). Taken together, these studies indicate that the effects of cocaine vary considerably depending on which parameter of the immune repertoire is investigated as well as the tools used to measure them.The chronic use of illicit drugs has been linked to an increased susceptibility to viral infections (3, 5). In a series of studies by Peterson et al., cocaine was reported to increase the production of p24 antigen in human immunodeficiency virus (HIV)-infected, activated peripheral blood mononuclear cells (PBMC) (18)(19)(20). This increase was taken to indicate an increase in HIV replication. Other researchers reported that cocaine increased p24 production in unstimulated PBMC but not in chronically infected mononuclear cell lines (1). Palamara et al. have described an increase in Sendai virus replication in epithelial cells cultured with cocaine in vitro, possibly caused by decreasing intracellular glutathione levels and increasing the redox state of the cells (15). Recently, our lab has described an antiviral activity of cocaine on murine peritoneal M infected with mouse hepatitis virus (MHV) in vitro (9). However, the mechanism(s) involved in this activity was not previously characterized.The principal nonspecific mechanism used by cells to inhibit . In this study, we have further characterized the effect of cocaine on virus replication in vitro. Using both prima...

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Section: Fig 7 Effects Of Cocaine On the Level Of Poly(i⅐c)-inducedsupporting

confidence: 70%

Cocaine Causes Increased Type I Interferon Secretion by both L929 Cells and Murine Macrophages

Grattendick

Jansen

Lefkowitz

et al. 2000

Clin Diagn Lab Immunol

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“…Total RNA was extracted from spleen and liver samples with RNAzol B (BIO TECX Lab. Inc.) in accordance with the manufacturer's recommendations and treated with DNase (16). The concentration and integrity of the resulting RNA were checked by spectrophotometry and formaldehyde-agarose gel electrophoresis.…”

Section: Reverse Transcription (Rt)-pcr-dot Blot Hybridization Detectmentioning

confidence: 99%

“…A 10-l volume of the RT-PCR products was analyzed on a 2% agarose gel. For increased sensitivity, 1 l of the RT-PCR products was also dot blotted onto a nylon membrane and hybridized at 65ЊC to a mixture of [␥-32 P]ATP-labelled oligonucleotides specific for MuIFNAs (16) and MuIFNB. The MuIFNB-specific oligonucleotide has the sequence 5Ј-CGTCTC CTGGATGAACTCCACC-3Ј, which corresponds to the region coding for amino acids 82 to 89 of the MuIFN-␤ sequence.…”

Section: Reverse Transcription (Rt)-pcr-dot Blot Hybridization Detectmentioning

confidence: 99%

Alpha/beta interferons increase host resistance to murine AIDS

Heng

Price

Lai

et al. 1996

J Virol

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Murine AIDS (MAIDS) is caused by a defective retrovirus present in the LP-BM5 murine leukemia virus mixture. Strains of inbred mice differ in resistance to MAIDS development; some are susceptible (e.g., C57BL/6), while others are resistant (e.g., CBA and B10.BR). As an early block to viral replication in resistant mice has been demonstrated previously by PCR studies, we postulated that alpha/beta interferons (IFN-␣/␤) may be involved in resistance to MAIDS. Susceptible C57BL/6 mice infected with LP-BM5 were treated with IFN-␣/␤ or Newcastle disease virus. Newcastle disease virus induces high endogenous IFN-␣/␤ production in mice. Both treatments delayed the development of MAIDS, as assessed by splenomegaly and T-and B-cell proliferation. In addition, an IFN-␣/␤ response was detected by reverse transcription-PCR and dot blotting 3, 6, and 9 h after LP-BM5 infection in resistant mice but not in susceptible mice. These results suggest that the ability to produce IFN-␣/␤ in response to LP-BM5 infection may contribute to host resistance to MAIDS.

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