PMID- 12028810
OWN - NLM
STAT- MEDLINE
DCOM- 20020611
LR  - 20191025
IS  - 0895-8378 (Print)
IS  - 0895-8378 (Linking)
VI  - 14
IP  - 4
DP  - 2002 Apr
TI  - Ambient PM(10) extracts inhibit phagocytosis of defined inert model particles by 
      alveolar macrophages.
PG  - 369-85
AB  - We used inert melamin particles that are very well defined in size (diameters: 
      0.5, 1.9, 6.8 microm) to study the effects of ambient particles of <10 microm 
      (PM(10)) on phagocytosis. Dose-response functions were found between the amount 
      of added melamin particle mass and the toxicity. Fine particles (0.5 microm) were 
      more toxic at low and medium amounts of mass per cell added than the larger 
      particles (1.9, 6.8 microm). However, with regard to particle numbers applied per 
      cell, toxicity is reversed, with the largest particles being the most toxic. In 
      the whole dose range tested, the melamin particles used did not stimulate cells 
      to produce oxidative radicals or tumor necrosis factor-alpha (TNF alpha). Flow 
      cytometric analyses visualized the time-dependent melamin particle uptake, which 
      was inhibited by polyinosinic acid (Poly-I), suggesting that phagocytosis is 
      mediated by scavenger-type receptors. Cells exposed to an aqueous PM(10) extract, 
      which also had a dose-dependent toxic potential, were stimulated to produce 
      oxidative radicals, measured as NO(2)(-), and TNF alpha. Combined exposures with 
      the PM(10) extract followed by the inert melamin particles show that the PM(10) 
      extract inhibits inert particle uptake by alveolar macrophages. It is proposed 
      that ambient PM(10), besides being toxic for alveolar macrophages, stimulates 
      them to produce oxidative radicals and the proinflammotry cytokine TNF alpha. 
      Moreover, it inhibits their particle uptake potential. Thus PM(10) appears to 
      promote inflammation and reduce defense.
FAU - Monn, Christian
AU  - Monn C
AD  - Institute for Hygiene and Applied Physiology, Group of Environmental Hygiene, 
      Federal Institute of Technology, Zurich, Switzerland. monn@iha.bepr.ethz.ch
FAU - Fendt, Roman
AU  - Fendt R
FAU - Koller, Theo
AU  - Koller T
LA  - eng
PT  - Journal Article
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 0 (Air Pollutants)
RN  - 0 (Cytokines)
RN  - 0 (Free Radicals)
SB  - IM
MH  - Air Pollutants/*adverse effects
MH  - Animals
MH  - Cell Culture Techniques
MH  - Cytokines/biosynthesis
MH  - Dose-Response Relationship, Drug
MH  - Free Radicals
MH  - Inflammation/physiopathology
MH  - Macrophages, Alveolar/drug effects/*physiology
MH  - Oxidative Stress
MH  - Particle Size
MH  - Phagocytosis/*drug effects
MH  - Rats
EDAT- 2002/05/25 10:00
MHDA- 2002/06/12 10:01
CRDT- 2002/05/25 10:00
PHST- 2002/05/25 10:00 [pubmed]
PHST- 2002/06/12 10:01 [medline]
PHST- 2002/05/25 10:00 [entrez]
AID - 10.1080/08958370252871005 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2002 Apr;14(4):369-85. doi: 10.1080/08958370252871005.