Lipopolysaccharide levels adherent to PM2.5 play an important role in particulate matter induced‐immunosuppressive effects in mouse splenocytes

Abstract

Epidemiological studies show that exposure to ambient particulate matter (PM) is associated with serious adverse health effects, including, but not limited to, those on the respiratory system. In the present study, we investigated the splenic response in mice administered PM of ≤ 2.5 μ m diameter (PM2.5). Male BALB/c mice (7 or 8 weeks old) were intratracheally administered PM2.5 (0.1 mg) four times, at 2 week intervals, and dissected 24 h after the final administration. The effect of six types of PM2.5, collected in Shenyang or Beijing (China) and Kitakyushu (Japan), on splenocytes was examined. Our results revealed a strong correlation between the levels of lipopolysaccharide (LPS), but not that of β-glucan and polycyclic aromatic hydrocarbons, attached to PM2.5 and the effect of PM2.5 on cell activity. PM2.5 with a low amount of LPS (PM2.5LL) reduced splenocyte mitogen-induced proliferation and cytokine production compared with that in control mice. The suppressive effects of PM2.5LL on proliferation and interleukin-2 production in splenocytes were rescued by the antioxidant N-acetylcysteine. Expression of heme oxygenase-1 was elevated after PM2.5LL administration, particularly in CD11b cells, while no elevation was observed in CD4 , CD8 or B220 cells. Further, dissociation of the nuclear factor erythroid 2-related factor 2 from Kelch-like ECH-associating protein 1 was observed in splenocytes of PM2.5LL-administered mice. These data suggest that LPS attached to PM2.5 modulates the splenocyte immune responses to PM2.5.

Platelet Priming and Activation in Naturally Occurring Thermal Burn Injuries and Wildfire Smoke Exposure Is Associated With Intracardiac Thrombosis and Spontaneous Echocardiographic Contrast in Feline Survivors

“…Dioxins have previously been shown to prime human platelets (37). PM 2.5bound LPS can also modulate splenocyte immune response and exacerbate airway inflammation by TLR4 and−2 pathways (38)(39)(40). We previously showed that ex vivo exposure of canine platelets to LPS primes platelets to respond to ADP via platelet TLR4 to potentiate the cyclooxygenase pathway leading to excessive release of thromboxane A 2 (TxA2) (23).…”

Platelet Priming Following Naturally Occurring Thermal Burn Injuries And Wildfire Smoke Exposure is Associated with Intracardiac Thrombosis in Feline Survivors

“…Dioxins has previously been shown to prime human platelets via the aryl hydrocarbon receptor by activating the phospholipase C and p38 MAPK pathway 33 . PM 2.5 -bound LPS can also modulate splenocyte immune response and exacerbate airway in ammation by TLR-4 and − 2 pathways [34][35][36] . We previously showed that ex vivo exposure of canine platelets to LPS primes platelets to respond to ADP via platelet TLR-4 to potentiate the cyclooxygenase pathway leading to excessive release of thromboxane A 2 (TxA2) 37 .…”

Expression Profiles of Long Noncoding RNAs in Intranasal LPS-Mediated Alzheimer’s Disease Model in Mice

“…Neither model could replicate the chronic and local inflammatory and progressive degeneration in AD. In addition, LPS was a component of the air pollutants PM2.5 [34], which can be absorbed via the nose and bypass the blood brain barrier. Research has shown that patients with AD and PD have smell loss and olfactory bulb pathology after being exposed in LPS in long terms [35, 36].…”