Overview of pulmonary alveolar macrophage renewal in normal rats and during different pathological processes.

Fritsch, P.; Massé, R.

doi:10.1289/ehp.929759

Cited by 18 publications

(5 citation statements)

References 14 publications

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“…In addition, dendritic cells become refractory to subsequent stimulation (40). Furthermore, alveolar macrophages are essentially nondividing cells (41) and display a relatively long turnover time (42,43) and thus become refractory relatively easily. This results in a diminished cellular recruitment, prevents diseaseinduced weight loss and lung pathology, but still allows pathogen clearance.…”

Section: Refractory Microenvironmentmentioning

confidence: 99%

Innate Imprinting by the Modified Heat-Labile Toxin of Escherichia coli (LTK63) Provides Generic Protection against Lung Infectious Disease

Williams

Edwards

Humphreys

et al. 2004

The Journal of Immunology

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In a healthy individual, the lung contains few lymphoid cells. However, amplified immune responses, as exemplified during lung infection, can cause extensive tissue damage. We have previously demonstrated that one lung infection modulates the immunopathological outcome to a subsequent unrelated pathogen. Mimicking heterologous immunity may provide a means of enhancing both innate and acquired immunity. We now show that prior lung administration of a modified heat-labile toxin from Escherichia coli (LTK63) enhances immunity to respiratory syncytial virus, influenza virus, and the fungus Cryptococcus neoformans. Treatment with LTK63 decreased lung inflammation and tissue damage and improved the ability to resolve the infection. APCs expressing the activation markers MHC class II, CD80, and CD40 increased in number in the lung. LTK63 treatment increased the pathogen-specific IgA response in the nasal mucosa and simultaneously decreased inflammatory cytokine production (IFN-γ and TNF-α) after infection. The number of activated CD8+CD44+ T cells and the respiratory syncytial virus- or influenza-specific CD8-proliferative responses increased, although the total inflammatory infiltrate was reduced. LTK63 treatment matured lung APCs (LTK63 prevented efficient presentation of whole OVA to DO11.10 cells, whereas OVA peptide presentation was unaffected), enhanced immunity in both a Th1 and Th2 environment, was long lasting, and was not pathogen or host strain specific; the protective effects were partially independent of T and B cells. Innate imprinting by toxin-based immunotherapeutics may provide generic protection against infectious disease in the lung, without the need for coadministered pathogen-specific Ag.

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Section: Refractory Microenvironmentmentioning

confidence: 99%

Innate Imprinting by the Modified Heat-Labile Toxin of Escherichia coli (LTK63) Provides Generic Protection against Lung Infectious Disease

Williams

Edwards

Humphreys

et al. 2004

The Journal of Immunology

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“…Alveolar macrophages are capable of proliferating in vitro in the presence of the appropriate molecular growth factors (Akagawa et al, 1988;Lin et al, 1989), in contrast to expectations for terminally differentiated cells. Also, in vivo labelling studies have shown that roughly 3% of alveolar macrophages are synthesizing DNA in preparation for cell division at any given time (Blusse van Oud Alblas et al, 1983;Coggle and Tarling, 1984;Fritsch and Masse, 1992), but the authors disagree about which cells are dividing. Several theories for the origin of alveolar macrophages have been proposed and investigated:…”

Section: Alveolar Macrophage Dynamicsmentioning

confidence: 99%

“…(1) alveolar macrophages derive from migrating blood monocytes, and are normally incapable of dividing (Blusse van Oud Alblas and van Furth, 1979); (2) monocytes mature in lung capillaries and undergo a final maturation division in the alveoli (Fritsch and Masse, 1992); (3) alveolar macrophages derive from interstitial macrophages through local division and maturation (Bowden, 1984); (4) alveolar macrophages divide in situ (Coggle and Tarling, 1984;Shellito et al, 1987).…”

Section: Alveolar Macrophage Dynamicsmentioning

confidence: 99%

“…Cell death is also a significant factor. It is often difficult to determine whether cell loss is due to migration or death; quantitative studies often measure a simple loss rate that does not distinguish between the various migration routes and cell death (Fritsch and Masse, 1992). The studies referenced above attempted to quantify the rates of local proliferation, influx, death, and/or efflux, but did not address the mechanisms involved.…”

Section: Alveolar Macrophage Dynamicsmentioning

confidence: 99%

“…Fritsch and Masse (1992) reported death rates of 5-6%/day and efflux rates of 2-3%/day in rats. Table 1. Other researchers do not distinguish between death and efflux, but report loss rates ranging from 1 to 18%/day (Blusse van Oud Alblas et al, 1983;Coggle and Tarling, 1984;Shellito et al, 1987).…”

Section: Simulationsmentioning

confidence: 99%

See 2 more Smart Citations

Homeostasis of peripheral immune effectors

Warrender

Forrest

Segel

2004

Bulletin of Mathematical Biology

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In this paper, we use both mathematical modeling and simulation to explore homeostasis of peripheral immune system effector cells, particularly alveolar macrophages. Our interest is in the distributed control mechanisms that allow such a population to maintain itself. We introduce a multi-purpose simulator designed to study individual cell responses to local molecular signals and their effects on population dynamics. We use the simulator to develop a model of growth factor regulation of macrophage proliferation and survival. We examine the effects of this form of regulation in the context of two competing hypotheses regarding the source of new alveolar macrophages. In one model, local cells divide to replenish the population; in the other, only cells migrating from circulation divide. We find that either scenario is plausible, although the influx-driven system is inherently more stable. The proliferation-driven system requires lower cell death and efflux rates than the influx-driven system.

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Genotoxic changes in the pulmonary alveolar macrophages of mice, rats and hamsters treated with tobacco smoke

Blagoeva¹,

Mircheva²,

Atanassova

et al. 1997

J Cancer Res Clin Oncol

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To determine whether tobacco smoke (TS) is genotoxic for lung tissue macrophages (pulmonary alveolar macrophages, PAM) as a general result of its inhalatory action BD6 rats, Syrian golden hamsters and BDF1 (C57BlxDBA2) mice were subjected to wholebody exposure for 90 or 60 min daily (600 cm3 mainstream smoke in 16-1 glass chamber, 9 or 6 exposures of 15 min each, respectively), for different periods ranging up to 30 days. A significant enhancement of the frequency of polynucleated macrophages (BiN PAM) was observed in all animal species after more than 10-days of repeated exposure to TS. The increased level of BiN PAM (the number of bi- (+) poly-nucleated PAM) correlates with the duration of exposure to TS: on day 20 after the start of inhalation, more than 25/1000 of mice PAM were polynucleated, while on day 30 this applied to approximately 50/1000. Furthermore, a highly significant increase in the level of micronucleated PAM (MN PAM) was also established after 10 days TS treatment of mice and persisted to the end of these examinations. TS was effective in enhancing the micronucleated and polynucleated PAM levels in hamsters irrespective of their sex, as it was in male BD6 rats aged 2 or 11 months. It appears that TS induces a more pronounced elevation of polynucleated PAM frequency in rats than in hamsters and mice. These data suggest that inhaled TS is genotoxic in alveolar macrophages in all exposed species of laboratory animals. An attempt was made to trace the possible clastogenic effect of a single i.p. administration of cyclophosphamide (CP, 15 mg/kg) in mice simultaneously in bone marrow and in PAM. A definite clastogenic effect in bone marrow 24 h and 48 h after CP injection and a total absence of changes in PAM from the lungs during the 15-day period after clastogen exposure were established. These data may support the hypothesis of local production of PAM in the lung from their proliferative precursor. The results provide evidence that PAM in laboratory animals are a sensitive and useful target for assessing harmful effects associated with environmental chemical factors that can be inhaled, including TS.

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Overview of pulmonary alveolar macrophage renewal in normal rats and during different pathological processes.

Cited by 18 publications

References 14 publications

Innate Imprinting by the Modified Heat-Labile Toxin of Escherichia coli (LTK63) Provides Generic Protection against Lung Infectious Disease

Innate Imprinting by the Modified Heat-Labile Toxin of Escherichia coli (LTK63) Provides Generic Protection against Lung Infectious Disease

Homeostasis of peripheral immune effectors

Genotoxic changes in the pulmonary alveolar macrophages of mice, rats and hamsters treated with tobacco smoke

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