The Role of Macrophage-derived Chemoattractant Activities in the Early Inflammatory Events of Bleomycin-induced Pulmonary Injury<sup>1–</sup><sup>4</sup>

Kaelin, Rainer M.; Center, David M.; Bernardo, John; Grant, Margaret M.; Snider, Gordon L.

doi:10.1164/arrd.1983.128.1.132

Cited by 34 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lymphocytes might have contributed to the migration but in that case the experimental setup would more closely resemble the situation in vivo than a model using a purified AM suspension. KAELIN et al [9] also reported similar results measuring the chemotactic activity of isolated AM or with cells from airways without previous separation.…”

Section: Discussionmentioning

confidence: 57%

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Snella

Rylander

1985

Agents and Actions

View full text Add to dashboard Cite

Guinea-pigs were exposed to an aerosol of bacterial endotoxin (lipopolysaccharide, LPS). The free lung cell response and alveolar macrophage (AM) chemotaxis were studied. Neutrophils from guinea-pig blood gave larger migration responses than those obtained by intraperitoneal glycogen stimulation or human neutrophils. An increase in the number of neutrophils in the airways was found with a peak at 12-24 hours after exposure. In animals pre-treated with LPS inhalation for 4 months, the reaction was of shorter duration and smaller magnitude. AM showed in vitro chemotactic activity up to 4 hours after exposure; no difference was found in pre-treated animals. The results suggest that the neutrophil invasion in the airways after LPS is dependent on two mechanisms, the initial being AM chemotaxis, which is not modified by pre-exposure to LPS, and another unknown factor, which is modified by pre-exposure to LPS.

show abstract

Section: Discussionmentioning

confidence: 57%

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Snella

Rylander

1985

Agents and Actions

View full text Add to dashboard Cite

show abstract

“…It is, however, improbable that lymphocytes play any major role in the control of PMN migration since it has been demonstrated that stimulated lymphocytes, in contrast with stimulated monocytes, do not release PMN chemotactic factors [14,26]. On the other hand, the diminution of peritoneal lymphocytes by rAMS could be secondary to the diminution of macrophages since these cells are known to release chemotactic factors for lymphocytes [6,12,27].…”

Section: Discussionmentioning

confidence: 99%

Blockade by antimacrophage serum of the migration of PMN neutrophils into the inflamed peritoneal cavity

1985

View full text Add to dashboard Cite

The effect of rat antimacrophage serum (rAMS) was tested on the influence of normal or thioglycollate-stimulated macrophage populations of the rat peritoneal cavity on the migration of polymorphonuclear neutrophils (PMN) induced by carrageenin, heterologous serum (rabbit) and sheep red blood cells. The rAMS used did not cross-react with PMN or lymphocytes nor did it affect circulating white cells, complement levels or lysed PMN present in the inflammatory exudate. It did, however, give a positive immunofluorescence reaction with resident and stimulated macrophages. The rAMS inhibited macrophage function as tested by sheep red blood cell phagocytosis in vivo and release of a PMN chemotactic factor(s) in vitro. Thioglycollate-stimulated peritoneal cavities showed an increased macrophage population and responded with increased PMN migration when challenged with heterologous serum or carrageenin, as compared with control rats. The presence of rat antimacrophage antibodies inhibited PMN migration induced by heterologous serum, sheep red blood cells and carrageenin. It is concluded that resident macrophages participate in the control of PMN migration to the site of an acute inflammation by acting as 'alarm cells' and triggering several defence mechanisms which ultimately protect the host from injurious stimuli.

show abstract

“…In human, an early and transient neutrophil alveolitis, soon followed by a lymphocytes accumulation, was shown after antigen inhalation in EAA (11). In a bleomycin-induced lung injury model, AM sequentially secreted chemoattractant specific for neutrophils followed by a factor specific for lymphocytes (16). Our model does not lead to the accumulation of large quantities of lymphocytes as seen in human EAA, although guinea pig AM are able to secrete a chemotactic factor for lymphocytes (8).…”

Section: Discussionmentioning

confidence: 56%

Production of H₂O₂ by Alveolar Macrophages in Experimental Allergic Alveolitis

Tremblay¹,

Thibault²,

Cormier³

1991

Microbiology and Immunology

View full text Add to dashboard Cite

Experimental extrinsic allergic alveolitis (EAA) was induced in guinea pigs with Saccharopolyspora rectivirgula. Bronchoalveolar lavages were performed before inducing EAA (day 1, BAL 1), on day 23 (BAL 2), and on day 48 (BAL 3). The number of cells/ml in lavage fluid was increased at BAL 2 (4.79 × 106) and BAL 3 (4.29 × 106) compared with BAL 1 (0.56 × 106). The number of major cell types increased simultaneously, neutrophil becoming the predominant cell type over alveolar macrophages (AM). The production of H2O2 by AM was measured at the different phases of EAA. Adherent AM were either non‐stimulated or triggered with phorbol myristate acetate (PMA), zymosan, S. rectivirgula opsonized with normal guinea pig serum (SRNS), or S. rectivirgula opsonized with guinea pig anti‐S. rectivirgula serum (SRAS). Stimulated AM produced larger quantities of H2O2 than unstimulated cells, PMA being the most potent stimulus. At day 1, AM stimulated with S. rectivirgula and zymosan produced similar quantities of H2O2. After the induction of the disease, AM stimulated with S. rectivirgula produced larger quantities of H2O2 than with zymosan. Production of H2O2 by AM stimulated with S. rectivirgula or PMA, respectively, stayed the same at day 1 and 23, but increased sharply for both stimuli at day 48. There was no difference between H2O2 production by AM triggered with SRNS or with SRAS. This study shows that: 1) H2O2 production is enhanced, especially by the offending agent, in the course of the disease; 2) the enhanced production of H2O2 by AM is preceded by the development of alveolitis; and, 3) the opsonization with specific antibodies does not enhance the avidity of AM for the antigen.

show abstract

The Role of Macrophage-derived Chemoattractant Activities in the Early Inflammatory Events of Bleomycin-induced Pulmonary Injury^1–⁴

Cited by 34 publications

References 0 publications

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Blockade by antimacrophage serum of the migration of PMN neutrophils into the inflamed peritoneal cavity

Production of H₂O₂ by Alveolar Macrophages in Experimental Allergic Alveolitis

Contact Info

Product

Resources

About

The Role of Macrophage-derived Chemoattractant Activities in the Early Inflammatory Events of Bleomycin-induced Pulmonary Injury1–4

Cited by 34 publications

References 0 publications

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Endotoxin inhalation induces neutrophil chemotaxis by alveolar macrophages

Blockade by antimacrophage serum of the migration of PMN neutrophils into the inflamed peritoneal cavity

Production of H2O2 by Alveolar Macrophages in Experimental Allergic Alveolitis

Contact Info

Product

Resources

About

The Role of Macrophage-derived Chemoattractant Activities in the Early Inflammatory Events of Bleomycin-induced Pulmonary Injury^1–⁴

Production of H₂O₂ by Alveolar Macrophages in Experimental Allergic Alveolitis