ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Parenchymal cell TNF receptors contribute to inflammatory cell recruitment and respiratory failure in Pneumocystis carinii-induced pneumonia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Trends in the Epidemiology ofJournal of fungi (Basel, Switzerland) · 2023Review
- Combination Immunotherapy with Passive Antibody and Sulfasalazine Accelerates Fungal Clearance and Promotes the Resolution ofInfection and immunity · 2020Article
- NOTCH inhibits osteoblast formation in inflammatory arthritis via noncanonical NF-κB.The Journal of clinical investigation · 2014Article
- MyD88 signaling regulates both host defense and immunopathogenesis during pneumocystis infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Group V phospholipase A2 in bone marrow-derived myeloid cells and bronchial epithelial cells promotes bacterial clearance after Escherichia coli pneumonia.The Journal of biological chemistry · 2011Article
- Ablation of TNF-RI/RII expression in Alzheimer's disease mice leads to an unexpected enhancement of pathology: implications for chronic pan-TNF-α suppressive therapeutic strategies in the brain.The American journal of pathology · 2011Article
- TNF is required for the induction but not the maintenance of compression-induced BME signals in murine tail vertebrae: limitations of anti-TNF therapy for degenerative disc disease.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2011Article
- FOXO3 deficiency leads to increased susceptibility to cigarette smoke-induced inflammation, airspace enlargement, and chronic obstructive pulmonary disease.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
- Immune Modulation as Adjunctive Therapy for Pneumocystis pneumonia.Interdisciplinary perspectives on infectious diseases · 2011Article
- Current understanding of Pneumocystis immunology.Future microbiology · 2010Review
- Serum markers in interstitial pneumonia with and without Pneumocystis jirovecii colonization: a prospective study.BMC infectious diseases · 2009Article
- The effects of interleukin-1beta in tumor necrosis factor-alpha-induced acute pulmonary inflammation in mice.Mediators of inflammation · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The opportunistic organism Pneumocystis carinii (Pc) produces a life-threatening pneumonia (PcP) in patients with low CD4(+) T cell counts. Animal models of HIV-AIDS-related PcP indicate that development of severe disease is dependent on the presence of CD8(+) T cells and the TNF receptors (TNFR) TNFRsf1a and TNFRsf1b. To distinguish roles of parenchymal and hematopoietic cell TNF signaling in PcP-related lung injury, murine bone marrow transplant chimeras of wild-type, C57BL6/J, and TNFRsf1a/1b double-null origin were generated, CD4(+) T cell depleted, and inoculated with Pc. As expected, C57 --> C57 chimeras (donor marrow --> recipient) developed significant disease as assessed by weight loss, impaired pulmonary function (lung resistance and dynamic lung compliance), and inflammatory cell infiltration. In contrast, TNFRsf1a/1b(-/-) --> TNFRsf1a/1b(-/-) mice were relatively mildly affected despite carrying the greatest organism burden. Mice solely lacking parenchymal TNFRs (C57 --> TNFRsf1a/1b(-/-)) had milder disease than did C57 --> C57 mice. Both groups of mice with TNFR-deficient parenchymal cells had low bronchoalveolar lavage fluid total cell counts and fewer lavageable CD8(+) T cells than did C57 --> C57 mice, suggesting that parenchymal TNFR signaling contributes to PcP-related immunopathology through the recruitment of damaging immune cells. Interestingly, mice with wild-type parenchymal cells but TNFRsf1a/1b(-/-) hematopoietic cells (TNFRsf1a/1b(-/-) --> C57) displayed exacerbated disease characterized by increased MCP-1 and KC production in the lung and increased macrophage and lymphocyte numbers in the lavage, indicating a dysregulated immune response. This study supports a key role of parenchymal cell TNFRs in lung injury induced by Pc and a potential protective effect of receptors on radiosensitive, bone marrow-derived cells.
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