Alterations in Macrophage Functions by Environmental Chemicals

Gardner, Donald E.

doi:10.2307/3429713

Cited by 19 publications

(16 citation statements)

References 105 publications

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“…Cytotoxicity to fibroblasts (Osornio-Vargas et al, 1996) and suppression of phagocytosis-related production of reactive oxygen species essential for bactericidal activity of macrophages (Geertz et al, 1994) were also associated to metal contents of ambient air particulate materials. Negative effects of inhaled toxic metals on host resistance to infections is a classical paradigm of pulmonary toxicology (Gardner, 1984), a notion which appears to be forgotten in the current debate on the biological plausibility of health impacts of low-level particulate air pollution. Direct evidence of increased bacterial infectivity in the lungs of mice treated with urban particulate matter has been presented a decade ago (Hatch et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…This effect can be attributed tentatively to metals (Geertz et al, 1994;Leduc et al, 1994). The consequence of lower production of reactive oxygen species could be ineffective bactericidal activity of macrophages (Gardner, 1984). This appears consistent with the fact that urban particles increase bacterial infectivity in vivo when instilled in the lungs of mice (Hatch et al, 1985).…”

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confidence: 99%

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Regulation of Promoter-CAT Stress Genes in HepG2 Cells by Suspensions of Particles from Ambient Air

et al. 1997

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A panel of HepG2-derived cell lines (CAT-Tox [L] assay, Xenometrix), harboring stress genes consisting of a sequence for chloramphenicol acetyltransferase (CAT) under the transcriptional regulation from mammalian promoters and response elements, was exposed for 18-24 hr to aqueous suspensions of urban dusts (SRM-1648, SRM-1649, EHC-93) or PM2.5 particles (particulate matter < 2.5 fim). Expression of CAT protein was measured by enzymelinked immunosorbent assay. Induction of the CAT genes was verified with benzo[a]pyrene (CYPlAl, cytochrome P450 1A1 promoter; GSTYa, glutathione transferase subunit Ya promoter; XRE, xenobiotic response element), cadmium sulfate, and copper sulfate (HMTIIa, metallothionein ria promoter; HSP70, heat shock protein 70 promoter). The urban dust suspensions were active on CYPlAl, GSTYa, and XRE cell lines. SRM-1648 and SRM-1649 were twice as potent as EHC-93 per unit mass in inducing the xenobiotic-dependent responses, which correlated with contents in polycyclic aromatic hydrocarbons. These three reference particles, as well as six PM2.5 preparations collected on hivol filters in the Great Lakes basin, were also found to induce HMTIIa and HSP70, the magnitude of the responses correlating closely with the amount of soluble copper in the particulate preparations. The results indicate that bioavailable chemical species in the unfractionated particles can directly and quantitatively induce xenobiotic, metal, and stress-dependent responses in a target cell model, resulting in patterns of gene induction consistent with the chemical compositions of the environmental materials. We propose that cell culture models could be helpful for toxicodynamic inferences in adjunct to environmental monitoring and exposure assessments.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Regulation of Promoter-CAT Stress Genes in HepG2 Cells by Suspensions of Particles from Ambient Air

et al. 1997

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“…Cigarette smoke is known to elicit a variety of effects on PAM, including a considerable increase in the number of cells, an enlargement in their mean diameter, formation of cytoplasmic inclusions containing pigmented residues of the smoke, as well as a wide range of biochemical alterations (19,36). In PAM preparations of smokers, especially if smoking shortly before bronchoalveolar lavage, we found an increased ability to reduce Cr(VI) and a stimulation of enzyme activities, such as G6PD and 6PGD, and NADPH-and NADH-dependent diaphorases.…”

Section: Discussionmentioning

confidence: 99%

“…These cells are well known to play an important role as defense mechanisms ofthe respiratory tract against inhaled foreign material ( 19) and have been demonstrated to interact with chromium also. In fact, this and other metals could be detected by x-ray analysis in cells of welders (20).…”

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confidence: 99%

Metabolic reduction of chromium by alveolar macrophages and its relationships to cigarette smoke.

et al. 1986

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“…[2][3][4] Alveolar macrophages exist on the alveolar surface and play an important role in the host defense against inhaled microorganisms. [5][6][7] The macrophage functions of bactericidal activity, [8][9][10] phagocytosis, [8][9][10][11][12][13][14] and lysosomal hydrolysis 8,15,16) are impaired by high levels of ozone (e.g., 2.5 ppm). However, few studies 9,10) have focused on the impairment of alveolar macrophages by low levels of ozone (e.g., 0.2 ppm).…”

Section: Introductionmentioning

confidence: 99%

Impairment of Microbial Killing and Superoxide-Producing Activities of Alveolar Macrophages by a Low Level of Ozone.

Mochitate

Katagiri

Miura

2001

JOURNAL OF HEALTH SCIENCE

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Male Wistar rats were exposed to 0.2 ppm ozone for up to 14 days, during which alveolar macrophages were collected by pulmonary lavage to assess the effect of ozone on their microbial killing and superoxide-producing activities. For rapid assessment of microbial killing activity, we measured the release of 3 H-radioactivity into the supernatant by deoxycholate-lysis of the macrophages that had phagosytosed and killed 3 H-uridine-labeled microbes. The killing activity against Escherichia coli and Candida albicans was reduced to 70-80% of control levels on day 3. However, phagocytosis by and the activity of lysosomal enzymes of the macrophages were not impaired. On day 14 the killing activity against E. coli had returned to control levels, whereas that against C. albicans was still reduced. Because active oxygen species plays an important role in microbial killing activity of macrophages, the effects of ozone on respiratory burst and superoxide production were examined. Aliquots of alveolar macrophages were stimulated with phorbol myristate acetate (PMA), opsonized zymosan, or lipopolysaccharide (LPS) plus cytochalasin E (Cyt.E). The respiratory burst, oxygen consumption for rapid superoxide production, was decreased to 60-80% of control levels on day 3. On day 14, the respiratory burst by opsonized zymosan was still 80% reduced, whereas that by PMA or LPS plus Cyt.E had returned to control levels. In addition, the superoxide-producing activity of ozone-exposed macrophages was 10-60% decreased on day 3. On day 14, the superoxide production by stimulation with opsonized zymosan was still 60% reduced, whereas that by PMA or LPS plus Cyt.E had returned to control levels. In conclusion, because of their decreased production of superoxide, the host defense activity of alveolar macrophages was impaired by in vivo exposure to 0.2 ppm ozone. In particular, the C. albicans-associated defect lasted throughout the exposure period.

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Alterations in Macrophage Functions by Environmental Chemicals

Cited by 19 publications

References 105 publications

Regulation of Promoter-CAT Stress Genes in HepG2 Cells by Suspensions of Particles from Ambient Air

Regulation of Promoter-CAT Stress Genes in HepG2 Cells by Suspensions of Particles from Ambient Air

Metabolic reduction of chromium by alveolar macrophages and its relationships to cigarette smoke.

Impairment of Microbial Killing and Superoxide-Producing Activities of Alveolar Macrophages by a Low Level of Ozone.

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