Tags

Type your tag names separated by a space and hit enter

Tumour necrosis factor, but not interferon-gamma, is essential for acquired resistance to Listeria monocytogenes during a secondary infection in mice.
Immunology. 1995 Oct; 86(2):256-62.I

Abstract

Mice with a secondary Listeria monocytogenes infection eliminate the bacteria much faster and more efficiently from their organs than mice with a primary infection. During the course of a secondary infection, serum concentrations of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF) are higher than during a primary infection. The aim of the present study was to determine whether these cytokines are involved in the acquired resistance to L. monocytogenes during a secondary infection in mice. In order to neutralize cytokines, alginate-encapsulated cells, which form anti-cytokine monoclonal antibodies, were injected into the nuchal region of mice during a Listeria infection. Mice recovered from a sublethal primary Listeria infection, which acquired cell-mediated immunity, received a subcutaneous injection of anti-IFN-gamma-forming cells, or anti-TNF-forming cells, and 4 days later received an intravenous injection with 10 50% lethal dose (LD50) L. monocytogenes. The number of bacteria recovered from the liver and spleen of immune mice treated with anti-IFN-gamma-forming cells was slightly larger (approximately 1 log10) than that found for immune mice treated with anti-beta-galactosidase-forming cells, called immune control mice. The organs of immune mice treated with anti-TNF-forming cells yielded significantly more (approximately 4 log10) bacteria than those of immune control mice, more than those of immune mice treated with anti-IFN-gamma-forming cells, and comparable numbers to those of non-immune mice. Taken together, these results demonstrate that TNF is essential in acquired resistance to L. monocytogenes during a secondary infection in mice, while IFN-gamma plays a minor role.

Authors+Show Affiliations

Department of Infectious Diseases, University Hospital Leiden, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7490127

Citation

Samsom, J N., et al. "Tumour Necrosis Factor, but Not Interferon-gamma, Is Essential for Acquired Resistance to Listeria Monocytogenes During a Secondary Infection in Mice." Immunology, vol. 86, no. 2, 1995, pp. 256-62.
Samsom JN, Langermans JA, Savelkoul HF, et al. Tumour necrosis factor, but not interferon-gamma, is essential for acquired resistance to Listeria monocytogenes during a secondary infection in mice. Immunology. 1995;86(2):256-62.
Samsom, J. N., Langermans, J. A., Savelkoul, H. F., & van Furth, R. (1995). Tumour necrosis factor, but not interferon-gamma, is essential for acquired resistance to Listeria monocytogenes during a secondary infection in mice. Immunology, 86(2), 256-62.
Samsom JN, et al. Tumour Necrosis Factor, but Not Interferon-gamma, Is Essential for Acquired Resistance to Listeria Monocytogenes During a Secondary Infection in Mice. Immunology. 1995;86(2):256-62. PubMed PMID: 7490127.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tumour necrosis factor, but not interferon-gamma, is essential for acquired resistance to Listeria monocytogenes during a secondary infection in mice. AU - Samsom,J N, AU - Langermans,J A, AU - Savelkoul,H F, AU - van Furth,R, PY - 1995/10/1/pubmed PY - 1995/10/1/medline PY - 1995/10/1/entrez SP - 256 EP - 62 JF - Immunology JO - Immunology VL - 86 IS - 2 N2 - Mice with a secondary Listeria monocytogenes infection eliminate the bacteria much faster and more efficiently from their organs than mice with a primary infection. During the course of a secondary infection, serum concentrations of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF) are higher than during a primary infection. The aim of the present study was to determine whether these cytokines are involved in the acquired resistance to L. monocytogenes during a secondary infection in mice. In order to neutralize cytokines, alginate-encapsulated cells, which form anti-cytokine monoclonal antibodies, were injected into the nuchal region of mice during a Listeria infection. Mice recovered from a sublethal primary Listeria infection, which acquired cell-mediated immunity, received a subcutaneous injection of anti-IFN-gamma-forming cells, or anti-TNF-forming cells, and 4 days later received an intravenous injection with 10 50% lethal dose (LD50) L. monocytogenes. The number of bacteria recovered from the liver and spleen of immune mice treated with anti-IFN-gamma-forming cells was slightly larger (approximately 1 log10) than that found for immune mice treated with anti-beta-galactosidase-forming cells, called immune control mice. The organs of immune mice treated with anti-TNF-forming cells yielded significantly more (approximately 4 log10) bacteria than those of immune control mice, more than those of immune mice treated with anti-IFN-gamma-forming cells, and comparable numbers to those of non-immune mice. Taken together, these results demonstrate that TNF is essential in acquired resistance to L. monocytogenes during a secondary infection in mice, while IFN-gamma plays a minor role. SN - 0019-2805 UR - https://www.unboundmedicine.com/medline/citation/7490127/Tumour_necrosis_factor_but_not_interferon_gamma_is_essential_for_acquired_resistance_to_Listeria_monocytogenes_during_a_secondary_infection_in_mice_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/7490127/ DB - PRIME DP - Unbound Medicine ER -