Pretreatment with recombinant murine tumor necrosis factor alpha/cachectin and murine interleukin 1 alpha protects mice from lethal bacterial infection

doi:10.1084/jem.169.6.2021

This Article

	Full Text (PDF, 488K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Cross, A. S.
	Articles by Gemski, P.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Cross, A. S.
	Articles by Gemski, P.


Social Bookmarking

	What's this?

ARTICLES

Pretreatment with recombinant murine tumor necrosis factor alpha/cachectin and murine interleukin 1 alpha protects mice from lethal bacterial infection

AS Cross, JC Sadoff, N Kelly, E Bernton and P Gemski
Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307.

Tumor necrosis factor/cachectin (TNF/C) is the principal mediator of bacterial endotoxin-induced shock and death. We found that the C3H/HeJ mouse, which is less able to produce TNF/C in response to endotoxin, has a 1,000-fold greater susceptibility to lethal infection with Escherichia coli than the TNF-responsive congenic mouse, C3H/HeN. This surprising finding suggested that this lethal peptide may also be involved in host protection. To test this hypothesis we pretreated the C3H/HeJ mouse with a combination of recombinant murine TNF/C-alpha and IL-1 alpha. This combination protected these mice against an intraperitoneal bacterial challenge of greater than 20 LD50S (nearly 2 x 10(2) CFU) that grew to a level of greater than 10(7) CFU/ml of blood and per gram of liver in untreated mice. This suggests a significant role for these cytokines in host defenses against invasive infections that require bacterial replication within the host. These protective mechanisms may not be important for less virulent organisms. These findings may have important implications for the proposed use of anti- TNF/C agents in the treatment of septic shock.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Patel, P. C., Fisher, K. H., Yang, E. C. C., Deane, C. M., Harrison, R. E. (2009). Proteomic Analysis of Microtubule-associated Proteins during Macrophage Activation. Mol. Cell. Proteomics 8: 2500-2514 [Abstract] [Full Text]
Hu, C. K., Venet, F., Heffernan, D. S., Wang, Y. L., Horner, B., Huang, X., Chung, C.-S., Gregory, S. H., Ayala, A. (2009). The Role of Hepatic Invariant NKT Cells in Systemic/Local Inflammation and Mortality during Polymicrobial Septic Shock. J. Immunol. 182: 2467-2475 [Abstract] [Full Text]
Li, X.-L., Ezelle, H. J., Kang, T.-J., Zhang, L., Shirey, K. A., Harro, J., Hasday, J. D., Mohapatra, S. K., Crasta, O. R., Vogel, S. N., Cross, A. S., Hassel, B. A. (2008). An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity. Proc. Natl. Acad. Sci. USA 105: 20816-20821 [Abstract] [Full Text]
Ramphal, R., Balloy, V., Jyot, J., Verma, A., Si-Tahar, M., Chignard, M. (2008). Control of Pseudomonas aeruginosa in the Lung Requires the Recognition of Either Lipopolysaccharide or Flagellin. J. Immunol. 181: 586-592 [Abstract] [Full Text]
Munford, R. S. (2008). Sensing Gram-Negative Bacterial Lipopolysaccharides: a Human Disease Determinant?. Infect. Immun. 76: 454-465 [Full Text]
Metkar, S., Awasthi, S., Denamur, E., Kim, K. S., Gangloff, S. C., Teichberg, S., Haziot, A., Silver, J., Goyert, S. M. (2007). Role of CD14 in Responses to Clinical Isolates of Escherichia coli: Effects of K1 Capsule Expression. Infect. Immun. 75: 5415-5424 [Abstract] [Full Text]
Tang, A. H., Brunn, G. J., Cascalho, M., Platt, J. L. (2007). Pivotal Advance: Endogenous pathway to SIRS, sepsis, and related conditions. J. Leukoc. Biol. 82: 282-285 [Abstract] [Full Text]
Lee, J. S., Frevert, C. W., Matute-Bello, G., Wurfel, M. M., Wong, V. A., Lin, S.-M., Ruzinski, J., Mongovin, S., Goodman, R. B., Martin, T. R. (2005). TLR-4 pathway mediates the inflammatory response but not bacterial elimination in E. coli pneumonia. Am. J. Physiol. Lung Cell. Mol. Physiol. 289: L731-L738 [Abstract] [Full Text]
Ramphal, R., Balloy, V., Huerre, M., Si-Tahar, M., Chignard, M. (2005). TLRs 2 and 4 Are Not Involved in Hypersusceptibility to Acute Pseudomonas aeruginosa Lung Infections. J. Immunol. 175: 3927-3934 [Abstract] [Full Text]
Munford, R. S. (2005). Invited review: Detoxifying endotoxin: time, place and person. Innate Immunity 11: 69-84 [Abstract]
Fairchild, K. D., Singh, I. S., Patel, S., Drysdale, B. E., Viscardi, R. M., Hester, L., Lazusky, H. M., Hasday, J. D. (2004). Hypothermia prolongs activation of NF-{kappa}B and augments generation of inflammatory cytokines. Am. J. Physiol. Cell Physiol. 287: C422-C431 [Abstract] [Full Text]
Kawasaki, K., Ernst, R. K., Miller, S. I. (2004). 3-O-Deacylation of Lipid A by PagL, a PhoP/PhoQ-regulated Deacylase of Salmonella typhimurium, Modulates Signaling through Toll-like Receptor 4. J. Biol. Chem. 279: 20044-20048 [Abstract] [Full Text]
Skerrett, S. J., Liggitt, H. D., Hajjar, A. M., Wilson, C. B. (2004). Cutting Edge: Myeloid Differentiation Factor 88 Is Essential for Pulmonary Host Defense against Pseudomonas aeruginosa but Not Staphylococcus aureus. J. Immunol. 172: 3377-3381 [Abstract] [Full Text]
Knapp, S., de Vos, A. F., Florquin, S., Golenbock, D. T., van der Poll, T. (2003). Lipopolysaccharide Binding Protein Is an Essential Component of the Innate Immune Response to Escherichia coli Peritonitis in Mice. Infect. Immun. 71: 6747-6753 [Abstract] [Full Text]
Bochud, P.-Y., Calandra, T. (2003). Science, medicine, and the future: Pathogenesis of sepsis: new concepts and implications for future treatment. BMJ 326: 262-266 [Full Text]
Joshi, V. D., Kalvakolanu, D. V., Hebel, J. R., Hasday, J. D., Cross, A. S. (2002). Role of Caspase 1 in Murine Antibacterial Host Defenses and Lethal Endotoxemia. Infect. Immun. 70: 6896-6903 [Abstract] [Full Text]
Gumenscheimer, M., Mitov, I., Galanos, C., Freudenberg, M. A. (2002). Beneficial or Deleterious Effects of a Preexisting Hypersensitivity to Bacterial Components on the Course and Outcome of Infection. Infect. Immun. 70: 5596-5603 [Abstract] [Full Text]
Joshi, V. D., Kalvakolanu, D. V., Hasday, J. D., Hebel, R. J., Cross, A. S. (2002). IL-18 Levels and the Outcome of Innate Immune Response to Lipopolysaccharide: Importance of a Positive Feedback Loop with Caspase-1 in IL-18 Expression. J. Immunol. 169: 2536-2544 [Abstract] [Full Text]
Cross, A. S. (2002). Invited review: Endotoxin tolerance -- current concepts in historical perspective. Innate Immunity 8: 83-98
Singh, I. S., He, J.-R., Calderwood, S., Hasday, J. D. (2002). A High Affinity HSF-1 Binding Site in the 5'-Untranslated Region of the Murine Tumor Necrosis Factor-alpha Gene Is a Transcriptional Repressor. J. Biol. Chem. 277: 4981-4988 [Abstract] [Full Text]
Echtenacher, B., Freudenberg, M. A., Jack, R. S., Mannel, D. N. (2001). Differences in Innate Defense Mechanisms in Endotoxemia and Polymicrobial Septic Peritonitis. Infect. Immun. 69: 7271-7276 [Abstract] [Full Text]
Le Roy, D., Di Padova, F., Adachi, Y., Glauser, M. P., Calandra, T., Heumann, D. (2001). Critical Role of Lipopolysaccharide-Binding Protein and CD14 in Immune Responses against Gram-Negative Bacteria. J. Immunol. 167: 2759-2765 [Abstract] [Full Text]
Goto, M., Deriy, L. V., Chen, Y. J., Beno, D. W. A., Uhing, M. R., Jiyamapa-Serna, V. A., Kimura, R. E. (2001). TNF-{alpha} increases sensitivity to LPS in chronically catheterized rats. Am. J. Physiol. Heart Circ. Physiol. 280: H2857-H2862 [Abstract] [Full Text]
Parmely, M. J., Wang, F., Wright, D. (2001). Gamma Interferon Prevents the Inhibitory Effects of Oxidative Stress on Host Responses to Escherichia coli Infection. Infect. Immun. 69: 2621-2629 [Abstract] [Full Text]
Haziot, A., Hijiya, N., Gangloff, S. C., Silver, J., Goyert, S. M. (2001). Induction of a Novel Mechanism of Accelerated Bacterial Clearance by Lipopolysaccharide in CD14-Deficient and Toll-Like Receptor 4-Deficient Mice. J. Immunol. 166: 1075-1078 [Abstract] [Full Text]
Singh, I. S., Viscardi, R. M., Kalvakolanu, I., Calderwood, S., Hasday, J. D. (2000). Inhibition of Tumor Necrosis Factor-alpha Transcription in Macrophages Exposed to Febrile Range Temperature. A POSSIBLE ROLE FOR HEAT SHOCK FACTOR-1 AS A NEGATIVE TRANSCRIPTIONAL REGULATOR. J. Biol. Chem. 275: 9841-9848 [Abstract] [Full Text]
Jiang, Q., Cross, A. S., Singh, I. S., Chen, T. T., Viscardi, R. M., Hasday, J. D. (2000). Febrile Core Temperature Is Essential for Optimal Host Defense in Bacterial Peritonitis. Infect. Immun. 68: 1265-1270 [Abstract] [Full Text]
Myokai, F., Takashiba, S., Lebo, R., Amar, S. (1999). A novel lipopolysaccharide-induced transcription factor regulating tumor necrosis factor alpha �gene expression: Molecular cloning, sequencing, characterization, and chromosomal assignment. Proc. Natl. Acad. Sci. USA 96: 4518-4523 [Abstract] [Full Text]
Jiang, Q., DeTolla, L., van Rooijen, N., Singh, I. S., Fitzgerald, B., Lipsky, M. M., Kane, A. S., Cross, A. S., Hasday, J. D. (1999). Febrile-Range Temperature Modifies Early Systemic Tumor Necrosis Factor Alpha Expression in Mice Challenged with Bacterial Endotoxin. Infect. Immun. 67: 1539-1546 [Abstract] [Full Text]
Warren, G. W., Poloyac, S. M., Gary, D. S., Mattson, M. P., Blouin, R. A. (1999). Hepatic Cytochrome P-450 Expression in Tumor Necrosis Factor-alpha Receptor (p55/p75) Knockout Mice After Endotoxin Administration. J. Pharmacol. Exp. Ther. 288: 945-950 [Abstract] [Full Text]
Held, T. K., Weihua, X., Yuan, L., Kalvakolanu, D. V., Cross, A. S. (1999). Gamma Interferon Augments Macrophage Activation by Lipopolysaccharide by Two Distinct Mechanisms, at the Signal Transduction Level and via an Autocrine Mechanism Involving Tumor Necrosis Factor Alpha and Interleukin-1. Infect. Immun. 67: 206-212 [Abstract] [Full Text]
Mackowiak, P. A. (1998). Concepts of Fever. Arch Intern Med 158: 1870-1881 [Abstract] [Full Text]
Crawford, E. K., Ensor, J. E., Kalvakolanu, I., Hasday, J. D. (1997). The Role of 3' Poly(A) Tail Metabolism in Tumor Necrosis Factor-alpha Regulation. J. Biol. Chem. 272: 21120-21127 [Abstract] [Full Text]
Lindberg, F. P., Bullard, D. C., Caver, T. E., Gresham, H. D., Beaudet, A. L., Brown, E. J. (1996). Decreased Resistance to Bacterial Infection and Granulocyte Defects in IAP-Deficient Mice. Science 274: 795-798 [Abstract] [Full Text]
Fisher, C. J., Agosti, J. M., Opal, S. M., Lowry, S. F., Balk, R. A., Sadoff, J. C., Abraham, E., Schein, R. M.H., Benjamin, E., The Soluble TNF Receptor Sepsis Study Group, (1996). Treatment of Septic Shock with the Tumor Necrosis Factor Receptor:Fc Fusion Protein. NEJM 334: 1697-1702 [Abstract] [Full Text]
Windsor, A. C. J., Mullen, P. G., Walsh, C. J., Fisher, B. J., Blocher, C. R., Jesmok, G., Fowler, A. A. III, Sugerman, H. J. (1994). Delayed Tumor Necrosis Factor {alpha} Blockade Attenuates Pulmonary Dysfunction and Metabolic Acidosis Associated With Experimental Gram-negative Sepsis. Arch Surg 129: 80-89 [Abstract]
Sawyer, R. G., Adams, R. B., May, A. K., Rosenlof, L. K., Pruett, T. L. (1993). Anti--Tumor Necrosis Factor Antibody Reduces Mortality in the Presence of Antibiotic-Induced Tumor Necrosis Factor Release. Arch Surg 128: 73-78 [Abstract]
Sanchez-Cantu, L., Rode, H. N., Yun, T. J., Christou, N. V. (1991). Tumor Necrosis Factor Alone Does Not Explain the Lethal Effect of Lipopolysaccharide. Arch Surg 126: 231-235 [Abstract]
Moore, F. D. Jr, Socher, S. H., Davis, C. (1991). Tumor Necrosis Factor and Endotoxin Can Cause Neutrophil Activation Through Separate Pathways. Arch Surg 126: 70-73 [Abstract]