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Prolonged perturbations of tumour necrosis factor- and interferon- in mice inoculated with Clostridium piliforme

Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri, E. Rollins Road, Columbia, MO 65211, USA

Received 30 Aug. 1999; revised version received 1 Nov. 1999; accepted 7 Nov. 1999. Corresponding author: Dr R. A. Van Andel (e-mail: rvanande@lhs.org). Present address: Legacy Research, PO Box 3950, Portland, OR 97208, USA.

Abstract

Clostridium piliforme is an obligate intracellular bacterium that causes enterohepatic disease in many animal species. C. piliforme infections are commonly subclinical in laboratory rats and mice, and little is known about host regulation of disease or of the effects of C. piliforme infections on investigations that use subclinically infected animals. To assess host regulation of subclinical C. piliforme infections and the effects of those infections on laboratory mice, the expression of the pro-inflammatory cytokines tumour necrosis factor- (TNF-) and interferon- (IFN-) was evaluated at 0, 1, 3, 7, 14 and 28 days after inoculation with C. piliforme. Subclinical infection was induced in weanling C. piliforme-susceptible DBA/2 or -resistant C57BL/6 mice with either a toxic or a non-toxic C. piliforme strain. Hepatic lesions and bacteria were demonstrated histologically in both mouse strains for 14 days after inoculation with the toxigenic bacterial strain, but were never demonstrated histologically following inoculation with the non-toxigenic strain. Hepatic TNF- and IFN- mRNA and serum protein levels were similarly elevated in both mouse strains 1 day after inoculation with both C. piliforme strains, as evaluated by reverse transcription PCR and enzyme-linked immunosorbent assays, respectively. Elevation of IFN- persisted for 14 days after inoculation; TNF- remained elevated at 28 days after inoculation.

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