Inhibition of Ehrlichia risticii infection in murine peritoneal macrophages by gamma interferon, a calcium ionophore, and concanavalin A

Park, J; Rikihisa, Yasuko

doi:10.1128/iai.59.10.3418-3423.1991

Cited by 49 publications

(38 citation statements)

References 28 publications

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“…33, 1995 DIFFERENTIAL CHARACTERS OF E. RISTICII STRAINS 2991 rMuIFN-␥ has been shown to inhibit the growth of many facultative and obligate intracellular bacteria in macrophages (2,5,14,17,27). Inhibition of E. risticii infection in mouse peritoneal macrophages by rMuIFN-␥ has been shown previously (20,21). The presence of IFN-␥-resistant strains has been documented in Rickettsia prowazekii (28,29).…”

Section: Discussionmentioning

confidence: 99%

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Pathogenic, immunologic, and molecular differences between two Ehrlichia risticii strains

1995

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Ehrlichia risticii is the causative agent of Potomac horse fever (PHF), an acute infectious disease of horses. In the last few years, there have been several reports of PHF cases occurring even in vaccinated horses. We isolated a new strain of E. risticii (90-12 strain) from a vaccinated horse suffering from clinical PHF. The major pathogenic, immunologic, and molecular differences between the 90-12 strain and the 25-D strain, which was originally isolated during the outbreaks in 1984, were studied. The 90-12 strain was more pathogenic for mice and horses compared with the 25-D strain. In enzyme-linked immunosorbent assay and immunofluorescence assay with mouse and horse antisera of both the strains, two-to fourfold differences were observed between homologous and heterologous antigens. The differences in antigen profiles were demonstrated by Western blot (immunoblot) with mouse and horse antisera and also with the recombinant clone-specific antibodies. Though several antigens were similar in both the strains, there were significant differences between them in the 110-, 85-, 70-, 51-, and 33-kDa antigens. The 85-kDa antigen was present only in the 90-12 strain but cross-reacted with a 50-kDa antigen of the 25-D strain. The 51-kDa antigens of both strains had different migration patterns. Southern blot hybridization of the genome from both the strains with DNA probes made from the 51-, 55-, and 85-kDa recombinant clones of the 90-12 strain showed a similar pattern with probes of the 51-and 55-kDa clones for both the strains, whereas the probe of the 85-kDa clone showed a completely different pattern. The 16S rRNA gene sequences from the two strains were identical. Neither strain replicated in gamma interferontreated mouse peritoneal macrophages. In in vitro neutralization assay, sera from the 25-D strain-infected horse neutralized the homologous strain but did not neutralize the 90-12 strain, whereas sera from the 90-12 strain-infected horse neutralized both the strains. In mouse protection experiments, there was complete homologous protection. But in cross-protection, mice immunized with the 25-D strain were only partially protected against challenge with the 90-12 strain, whereas mice immunized with the 90-12 strain were completely protected against the 25-D strain challenge. These results clearly indicate that there are major differences between the 90-12 and 25-D strains which may have implications regarding the vaccine failure for PHF and the development of an efficient vaccine.

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Section: Discussionmentioning

confidence: 99%

“…Gamma interferon (IFN-␥) sensitivity. The sensitivity of the E. risticii strains in interferon-treated mouse peritoneal macrophages was tested according to published procedures (20). To obtain peritoneal macrophages, 8-to 10-week-old male CF1 mice were injected intraperitoneally with 1 ml of 5% thioglycolate broth (Difco Laboratories, Detroit, Mich.).…”

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confidence: 99%

Pathogenic, immunologic, and molecular differences between two Ehrlichia risticii strains

1995

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“…Pre-treatment with IFN-y can increase the hosts susceptibility to endotoxin with increased serum level of TNF-a and IL-6 [3,23]. On the other hand, exogenous recombinant IFN-y contributes to the resistance in the acute infections caused by Toxoplasma gondi, Leishmania, Ehrlichia, Legionella, Salmonella, Listeria, and Klebsiella [7,[19][20][21][24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Interferon-γ, interleukin-1 and tumour necrosis factor-α synthesis during experimental murine staphylococcal infection

Rozalska¹

1993

FEMS Immunology and Medical Microbiology

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Several exotoxins of Staphylococcus aureus were shown to modulate the host immune system by stimulation of monokine release. BALB/c mice infected intravenously (i.v.) with live cells if S. aureus, strain Cowan 1, had a detectable serum level of TNF-alpha at 3, 4 and 5 h after injection. When S. epidermidis (strain E3380, clinical isolate) was used to infect mice, the level of TNF-alpha was lower (the detection limit of the cytotoxicity assay with WEHI cells was 40 pg ml-1). Kinetics of TNF synthesis was different from that observed in experimental infections caused by Gram-negative bacteria. Similarly to TNF-alpha, IL-1 alpha appears in a measurable level at 3 h after i.v. injection of bacteria. The highest serum level of IFN-gamma was observed 12 h after infection with both S. aureus and S. epidermidis. A quantity ten times more of S. epidermidis than of S. aureus cells was required to induce similar levels of TNF-alpha and IFN-gamma. Recombinant IFN-gamma administered in vivo in four daily doses followed by infection of S. aureus resulted in increased elimination of bacteria from the spleen, liver and peritoneal cavity of mice.

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“…All mice were fed antibiotic-free commercial laboratory chow and water ad libitum. Mice were injected intraperitoneally with 2 ml of sterile 5% thioglycolate broth (Difco Laboratories, Detroit, Mich.), to collect peritoneal macrophages as previously described (17).…”

Section: Methodsmentioning

confidence: 99%

Tumor necrosis factor alpha, interleukin-1 alpha, interleukin-6, and prostaglandin E2 production in murine peritoneal macrophages infected with Ehrlichia risticii

et al. 1993

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Ehrlichia risticii is a gram-negative obligate intracellular bacterium which primarily infects macrophages and crypt epithelial cells in the intestinal wall and is the etiologic agent of Potomac horse fever. To understand the pathogenesis of the disease, we tested whether E. risticii induces inflammation-associated products in thioglycolate-induced mouse peritoneal macrophages. Mouse peritoneal macrophages produced larger amounts of interleukin-la (IL-la) but lower levels of tumor necrosis factor alpha (TNF-a), IL-6, and prostaglandin E2 (PGE2) when exposed to live or killed E. risticii than when exposed to Escherichia coli lipopolysaccharide (LPS). Preincubation of macrophages with live or killed E. risticii suppressed TNF-a, IL-6, and PGE2 generation but not IL-la production in response to LPS. Murine gamma interferon treatment of macrophages did not influence TNF-a, IL-la, IL-6, or PGE2 production regardless of exposure to E. risticii. Intracellular cyclic AMP was significantly greater in E. risticii-infected macrophages than in uninfected macrophages. These results suggest that increased levels of IL-la but not TNF-a or PGE2 production by macrophages may be primarily involved in the pathogenesis of the disease caused by E. risticii. Increased intracellular concentration of cyclic AMP in infected macrophages may be chiefly responsible for the high level of IL-la and inhibition of TNF-a production in response to LPS. concentration of 106 cells/ml in RPMI 1640 (GIBCO)-10% FBS-2 mM L-glu-1% antibiotics (10,000 U of penicillin G sodium, 10,000 ,ug of streptomycin sulfate, and 25 ,ug of amphotericin B [GIBCO] per ml) and incubated at 37°C for 24 h in 5% C02-air. The medium and floating cells were removed, and the macrophages were washed twice with sterile phosphate-buffered saline (2 mM KH2PO4, 6 mM Na2HPO4, 2 mM KCl, 136 mM NaCl). Then, DH82 lysate, 4333 on July 16, 2020 by guest . 1989. Tumor necrosis factor alpha is a cytotoxin induced by murine Chlamydia trachomatis infection.

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Inhibition of Ehrlichia risticii infection in murine peritoneal macrophages by gamma interferon, a calcium ionophore, and concanavalin A

Cited by 49 publications

References 28 publications

Pathogenic, immunologic, and molecular differences between two Ehrlichia risticii strains

Pathogenic, immunologic, and molecular differences between two Ehrlichia risticii strains

Interferon-γ, interleukin-1 and tumour necrosis factor-α synthesis during experimental murine staphylococcal infection

Tumor necrosis factor alpha, interleukin-1 alpha, interleukin-6, and prostaglandin E2 production in murine peritoneal macrophages infected with Ehrlichia risticii

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