Cytostatic Activity of Pulmonary Alveolar Macrophages in Lung Cancer Patients

Kuda, Tomoharu

doi:10.1378/chest.100.5.1475a

Cited by 7 publications

(10 citation statements)

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“…In contrast, others have reported normal or increased cytotoxic potential of AM compared with PBM. [15][16][17][18] In one such study, Thomassen et al demonstrated low spontaneous cytotoxicity in AM, but substantial augmentation in response to y-IFN, GM-CSF, and LPS.19*51 The discrepancy between these results and those of the current study may be based in differences in the cytotoxicity assays used because our results are based on an 18-hour 51Cr release assay, whereas Thomassen ef al. used a thymidine based assay in which macrophages and target cells are cocultured for 72 to 96 hours.…”

Section: Cancer September I 199mentioning

confidence: 72%

Impaired tumoricidal function of alveolar macrophages from patients with non-small cell lung cancer

Siziopikou

Harris

Casey

et al. 1991

Cancer

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The capacity of alveolar macrophages and peripheral blood monocytes from patients with non‐small cell lung cancer to develop tumoricidal function after in vitro stimulation with different macrophage activators was investigated. Alveolar macrophages were found to be impaired in their ability to develop cytotoxic activity compared with either the peripheral blood monocytes from the same patients or alveolar macrophages from patients with nonmalignant lung disorders. This result was observed consistently under diverse culture conditions and with different macrophage activators including gamma‐interferon (γ‐IFN), granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), phorbol myristate acetate, or endotoxin. The impairment in tumoricidal function observed in alveolar macrophages was not associated with reduced target cell binding compared to peripheral blood monocytes. Alveolar macrophages from patients with lung cancer were found to secrete significantly greater amounts of tumor necrosis factor (TNF) and interleukin‐1 (IL‐1) than either peripheral blood monocytes from the same patients or alveolar macrophages from the patients with nonmalignant disorders. These results are consistent with either different regulatory pathways for cytotoxicity and cytokine secretion in the alveolar macrophages of patients with lung cancer or diversity in the subpopulations of cells responsible for these functions.

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Section: Cancer September I 199mentioning

confidence: 72%

Impaired tumoricidal function of alveolar macrophages from patients with non-small cell lung cancer

Siziopikou

Harris

Casey

et al. 1991

Cancer

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“…IL‐6 has been shown to regulate the ability of AM in lung cancer patients to be stimulated by IFN‐γ and LPS and to subsequently stimulate anti‐tumour immunity. Anti‐inflammatory cytokines such as IL‐10 and TGF‐β induce Th2/Tr1 cells which suppress anti‐tumour immunity and promote tumour progression [9,18]. Tumor‐associated macrophages from patients with non small cell lung carcinoma have been demonstrated to have reduced production of cytokines, IL‐1, IL‐6, TNF‐α, TGF‐β as well as reduced chemotactic activity, antibody‐dependent cell‐mediated cytotoxicity and cytostatic activity, similar to results reported in this study [17].…”

Section: Discussionmentioning

confidence: 99%

Alveolar macrophage function is altered in patients with lung cancer

Pouniotis¹,

Plebanski²,

Apostolopoulos³

et al. 2005

Clinical and Experimental Immunology

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SummaryThe alveolar macrophage (AM) is believed to be of central importance in the immune response against infection and tumour. We examined patients with lung cancer in order to evaluate the immuno-stimulatory potential of AM in lung cancer. Bronchoalveolar lavage fluid samples were obtained from patients with adenocarcinoma, squamous cell carcinoma, large cell undifferentiated lung carcinoma, small cell carcinoma and control subjects. AM were isolated and phagocytic function, flow cytometry and cytokine analysis were assessed. AM from patients with small and squamous cell carcinoma had impaired uptake in vitro of 40 nm fluorescent polystyrene beads. AM from patients with small, squamous and large cell undifferentiated carcinoma showed impaired uptake of 1000 nm fluorescent polystyrene beads. Secreted levels of TNF-α α α α and IL-1 from AM of patients with small, squamous, and large cell undifferentiated carcinoma were decreased compared to controls. Secreted AM IL-6 levels were decreased in small and large cell undifferentiated carcinoma. AM from adenocarcinoma patients showed similar levels of IL-10, IL-6, IL-1 and TNF-α α α α compared to controls. Phenotypic analysis demonstrated that patients with small cell carcinoma were the only group that showed a decrease in MHC class II surface expression. Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma. Mannose receptor levels were only decreased on AM from patients with squamous and small cell carcinoma but not adenocarcinoma and large cell undifferentiated carcinoma. We conclude that there are type-specific alterations in uptake ability, cytokine secretion and phenotype of AM from lung cancer patients, which may result in an inability to stimulate anti-tumour immunity. The observed differences between lung cancer subgroups may explain previously reported inconsistencies in descriptions of AM characteristics in lung cancer.

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“…In vitro, alveolar macrophages (AMs) recovered by bronchoalveolar lavage (BAL) from healthy subjects or noncancer patients, are spontaneously cytotoxic for tumour target cells, suggesting that human AMs are constitutively primed in vivo for this cytotoxic activity [148][149][150]. Thus, several agents, including lymphocyte and macrophage secretory products, were shown to "prime" the macrophage and to increase its cytotoxic activity [150][151][152].…”

Section: Macrophages and Polymorphonuclear Neutrophilsmentioning

confidence: 99%