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Published ahead of print on September 4, 2003, doi:10.1164/rccm.200302-303OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 12, December 2003, 1462-1470

A more recent version of this article appeared on December 15, 2003
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Submitted on March 9, 2003
Accepted on August 29, 2003

Modulation of bacterial growth by TNF-{alpha} in vitro and in vivo

Jin-Hwa Lee1, Lorenzo Del Sorbo1, Aye Aye Khine1, Joyce de Azavedo2, Donald E Low2, David Bell1, Stefan Uhlig3, Arthur S Slutsky1, and Haibo Zhang1*

1 Anaesthesia, Critical Care Medicine and Pathology, Division of Respiratory Medicine, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada, 2 Microbiology, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada, 3 Anaesthesia, Critical Care Medicine and Pathology, Division of Respiratory Medicine, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada; Division of Pulmonary Pharmacology, Research Center Borstel, Borstel, Germany

* To whom correspondence should be addressed. E-mail: haibo.zhang{at}utoronto.ca.

Tumor necrosis factor-alpha (TNF-alpha) plays an important role in innate immunity. Recent in vitro studies have shown that TNF-alpha may also serve as a growth factor for some bacteria. We examined the physiological relevance of this phenomenon both in vitro and in vivo. Recombinant mouse TNF-alpha increased in vitro proliferation of E. coli but not P. aeruginosa in a concentration-dependent manner, and this effect was attenuated by anti-TNF-alpha antibodies. However, in vivo, TNF-alpha gene-deficient (TNF-alpha-/-) mice showed higher mortality than wild-type (TNF-alpha+/+) mice after inoculation of intranasal bacteria. An impaired bacterial clearance in TNF-alpha-/- mice was associated with decreased systemic concentrations of chemokine macrophage inflammatory protein-2 (MIP-2), reduced pulmonary neutrophil recruitment and depressed expression of neutrophil CD11b and CD16/CD32, suggesting that the effect of TNF-alpha on E. coli growth was outweighed by the recruited neutrophils. We also demonstrated that neutropenic TNF-alpha+/+ mice had approximately 100-fold higher E. coli counts in their lungs than TNF-alpha-/- mice, although survival rates in both groups were similar. We conclude that TNF-alpha augments E. coli growth in vitro and in vivo. However, in vivo this effect becomes only apparent in neutropenic animals. The relevance of these findings for immune compromised patients remains to be investigated.
Key words: cytokines, phagocytosis, neutrophils, lung, transgenic/knockout




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