The alveolar macrophage

Fels, Anna; Cohn, Z. A.

doi:10.1152/jappl.1986.60.2.353

Cited by 445 publications

(200 citation statements)

References 0 publications

Supporting

Mentioning

189

Contrasting

Unclassified

Order By: Relevance

“…Macrophages are known to play a variety of important roles in the lung, including that of serving as accessory cells. While alveolar macrophages are the best-characterized accessory cells (Fels and Cohn, 1986), in our study PIMs showed a more vigorous response to halothane than any other pulmonary macrophage .…”

contrasting

confidence: 42%

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

Atwal

McDonell

2005

Anat. Rec.

View full text Add to dashboard Cite

The pulmonary intravascular macrophages (PIMs) of equines contain a unique electron-dense surface coat that is predominantly composed of lipoproteins. A single exposure of inhalatory halothane causes mobilization of the surface coat into the endocytotic system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. Simultaneously, the cells of the lymphocytic series show hyperplasia in the form of mitotic changes inside the microvascular compartment of the lung. Halothane is known to cause acute and chronic hepatotoxicity because of its biotransformation into trifluoroacytelated polypeptides. The present study was designed to examine the comparative effects of reexposures of inhalatory doses of halothane, isoflurane, and the intravenous barbiturate thiamylal sodium in ponies to evoke a stronger response in the PIMs after four exposures at increasing intervals of 1, 2, and 6 weeks. Ultrastructural and cytochemical evidence is presented that halothane induced translocation of the surface coat into the vacuolar system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. The cell membrane was thrown into extraordinary lamellipodial extensions, which enabled the PIMs to interact with platelets within the narrow confines of the pulmonary capillaries. The relationship between PIMs and platelets developed into large platelet aggregates. Isoflurane and thiamylal sodium did not affect the circulating platelets, although the surface coat was translocated into the endolysosomes in both situations. Although isoflurane is a lipid-soluble inhalant anesthetic similar to halothane, it is subject to very little biotransformation after use and in the present model demonstrates no immune response.

show abstract

contrasting

confidence: 42%

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

Atwal

McDonell

2005

Anat. Rec.

View full text Add to dashboard Cite

show abstract

“…As the resident professional phagocyte, AMs provide a first line of host defense by internalizing and degrading microbial pathogens encountered on the respiratory surface. 1 Upon pathogen exposure, AMs express cytokines that influence recruitment and activation of inflammatory cells and modify adaptive immune responses in a pathogen-selective fashion. 2 In this way, cytokines released from pathogen-exposed AMs provide important molecular "links" between innate and adaptive immunity in the lung.…”

Section: Introductionmentioning

confidence: 99%

GM-CSF, via PU.1, regulates alveolar macrophage FcγR-mediated phagocytosis and the IL-18/IFN-γ–mediated molecular connection between innate and adaptive immunity in the lung

Berclaz

Shibata

Whitsett

et al. 2002

Blood

119

101

View full text Add to dashboard Cite

Severely impaired pulmonary microbial clearance was observed in granulocyte-macrophage colony-stimulating factor (GM-CSF)–deficient mice. To determine mechanisms by which GM-CSF mediates lung host defense, FcγR-mediated phagocytosis (opsonophagocytosis) by alveolar macrophages (AMs) was assessed in GM-CSF–sufficient (GM+/+) and –deficient (GM−/−) mice and in GM−/− mice expressing GM-CSF only in the lungs from a surfactant protein C (SPC) promoter (SPC-GM+/+/GM−/−). Opsonophagocytosis by GM−/− AMs was severely impaired and was restored by pulmonary GM-CSF expression in vivo or by PU.1 expression in vitro. Defective opsonophagocytosis by GM−/− AMs was associated with decreased FcγR expression. Because interferon-γ (IFN-γ) augments macrophage FcγR levels, the role of GM-CSF/PU.1 in the regulation of AM FcγR expression by IFN-γ was assessed during adenoviral lung infection. Adenoviral infection stimulated IFN-γ production and augmented FcγR levels on AMs in GM-CSF–expressing but not GM−/− mice. However, IFN-γ exposure ex vivo stimulated FcγR expression on GM−/− AMs. Because interleukin-18 (IL-18) and IL-12 stimulate IFN-γ production during adenoviral infection, their role in GM-CSF/PU.1 regulation of IFN-γ–augmented FcγR expression on AMs was assessed. Adenoviral infection stimulated IL-18 and IL-12 production in GM-CSF–expressing mice, but both were markedly reduced or absent in GM−/−mice. IL-18 expression by GM−/− AMs was severely impaired and was restored by pulmonary GM-CSF expression in vivo or by PU.1 expression in vitro. Pulmonary administration of IL-18 in GM−/− mice stimulated IFN-γ production and restored FcγR expression on AMs. These results show that GM-CSF, via PU.1, regulates constitutive AM FcγR expression and opsonophagocytosis and is required for the IFN-γ–dependent regulation of AM FcγR expression, enabling AMs to release IL-18/IL-12 during lung infection.

show abstract

“…CAM are far more effective than AAM in killing intracellular pathogens although they do not take in bacteria as profusely as AAM. Alveolar macrophages, which are the resident macrophage population in the lung, have been classified as alternatively activated due to the receptor types they express and their balanced, regulated immune response (9). Hence, AAM are the dominant macrophage type in healthy lung tissue.…”

mentioning

confidence: 99%

Modeling the immune rheostat of macrophages in the lung in response to infection

Day¹,

Friedman²,

Schlesinger

2009

Proc. Natl. Acad. Sci. U.S.A.

126

View full text Add to dashboard Cite

In the lung, alternatively activated macrophages (AAM) form the first line of defense against microbial infection. Due to the highly regulated nature of AAM, the lung can be considered as an immunosuppressive organ for respiratory pathogens. However, as infection progresses in the lung, another population of macrophages, known as classically activated macrophages (CAM) enters; these cells are typically activated by IFN-␥. CAM are far more effective than AAM in clearing the microbial load, producing proinflammatory cytokines and antimicrobial defense mechanisms necessary to mount an adequate immune response. Here, we are concerned with determining the first time when the population of CAM becomes more dominant than the population of AAM. This proposed ''switching time'' is explored in the context of Mycobacterium tuberculosis (MTb) infection. We have developed a mathematical model that describes the interactions among cells, bacteria, and cytokines involved in the activation of both AAM and CAM. The model, based on a system of differential equations, represents a useful tool to analyze strategies for reducing the switching time, and to generate hypotheses for experimental testing.alternatively activated macrophages ͉ lung innate immunity ͉ mycobacteria tuberculosis

show abstract

The alveolar macrophage

Cited by 445 publications

References 0 publications

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

GM-CSF, via PU.1, regulates alveolar macrophage FcγR-mediated phagocytosis and the IL-18/IFN-γ–mediated molecular connection between innate and adaptive immunity in the lung

Modeling the immune rheostat of macrophages in the lung in response to infection

Contact Info

Product

Resources

About