Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes

Byrd, T F

doi:10.1172/jci119436

Cited by 90Tuberculosis Research and EpidemiologyImmune responses and vaccinationsInfectious Diseases and Tuberculosis

Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes

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Byrd, T F·1997·Journal of Clinical Investigation

DOI 10.1172/jci119436PMC PMC508093

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Abstract

The human immune response to Mycobacterium tuberculosis is not well characterized. To better understand the cellular immune response to tuberculosis, a human mononuclear phagocyte culture system using a low-infecting inoculum of M. tuberculosis to mimic in vivo conditions was developed. Using this system, monocytes treated with IFNgamma/TNFalpha/ calcitriol (CytD) were permissive for the growth of virulent M. tuberculosis. In the presence of iron, however, these monocytes suppressed the growth of M. tuberculosis. The enhanced permissiveness of CytD-preincubated monocytes was found to be due to TNFalpha, however, the ability of iron to suppress M. tuberculosis growth also required preincubation with TNFalpha. Iron-mediated growth suppression was correlated with selective suppression of TNFalpha release from infected monocytes. In addition, removal of TNFalpha from CytD-treated monocytes 2 d after infection mimicked the suppressive effect of iron, suggesting that iron may also be decreasing monocyte sensitivity to exogenously added TNFalpha. In the absence of iron, permissive, CytD-treated monocytes formed large infected cellular aggregates. With iron treatment, aggregation was suppressed, suggesting that the iron-suppressive effect on M. tuberculosis growth may be related to suppression of monocyte aggregation and diminished cell-to-cell spread of M. tuberculosis. The results of this study indicate that TNFalpha preincubation is required for human monocytes to exert an iron-mediated suppressive effect on M. tuberculosis growth. In the absence of iron, however, the continued presence of TNFalpha has a growth-promoting effect on M. tuberculosis in human monocytes. Iron may be an important early modulator of M. tuberculosis growth via its effects on TNFalpha.

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High intracellular iron levels inhibit the transcription of TNF or other IFN-γ inducible pathways such as induction of NOS2, degradation of tryptophan or formation of neopterin in human monocytes.
“In addition, high intracellular iron levels inhibit the transcription of TNF (Byrd, 1997) or other IFN-γ inducible pathways such as induction of NOS2, degradation of tryptophan or formation of neopterin in human monocytes (Melillo et al., 1997;Weiss et al., 1992Weiss et al., , 1994)).”
From Iron in infection and immunity (2020) · cites this paper as Byrd, 1997
The Discussion reports that iron-treated, M. tuberculosis-infected human monocytes released less TNFα. It does not establish that iron inhibited TNF transcription; Byrd (1997) is not the citation attached to the sentence’s other IFN-γ-inducible pathways. (LLM, conf=0.88)
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Authors: Byrd, T. F.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Byrd, T F
ORCID: Byrd, T F
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1997-05-15
Volume: 99
Issue: 10
Pages: 2518-2529
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci119436
PMC: PMC508093
OpenAlex: W2020365793
Cited by: 90
References: 65
Citations by year: 2026: 2 · 2025: 2 · 2023: 4 · 2022: 2 · 2020: 4 · 2019: 3 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 1
FWCI: 3.51
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs
American Lung Association
Strong
National Institutes of Health
National Institute of Allergy and Infectious Diseases (AI-93-03)
Topics: Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
Health Sciences › Medicine › Surgery › Infectious Diseases and Tuberculosis
Keywords: Mycobacterium tuberculosis, TNF-α, iron, monocytes, bacterial growth inhibition, cell-to-cell transmission, interferon-gamma, 1,25-dihydroxyvitamin D3
MeSH terms: Adult, Calcitriol, Cells, Cultured, Humans, Interferon-gamma, Interleukin-1, Iron, Monocytes, Mycobacterium tuberculosis, Recombinant Proteins, Time Factors, Tumor Necrosis Factor-alpha, Virulence, Interleukin-6, Granulocyte-Macrophage Colony-Stimulating Factor, Macrophage Inflammatory Proteins, Chemokine CCL4

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Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes

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