PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

Abstract

PM2.5 can exacerbate asthma. Organic substances adsorbed on PM2.5-rich dust (PM2.5rd) were inactivated by heating at 360 °C. To characterize the role of organic substances, the effects of PM2.5rd and heated PM2.5-rich dust (H-PM2.5 rd) on allergic lung inflammation were investigated. BALB/c mice were intratracheally administered PM2.5rd or H-PM2.5rd with or without ovalbumin (OVA) four times at 2-week intervals. PM2.5rd, but not H-PM2.5rd, caused neutrophilic alveolitis and bronchitis. In the presence of OVA, PM2.5rd caused severe eosinophil infiltration and goblet cells proliferation in airways, along with a marked induction of the Th2 cytokines interleukin (IL)-4 and IL-13, and the eosinophil-related cytokine IL-5 in bronchoalveolar lavage fluid (BALF). OVA + H-PM2.5rd caused a weaker response. PM2.5rd showed adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production, but H-PM2.5rd showed minimal effects. These findings suggested that PM2.5rd-bound substances might aggravate lung eosinophilia. To clarify the roles of TLR2, TLR4, and MyD88 on cytokine production in PM2.5rd, murine bone marrow-derived macrophages (BMDMs) from wild-type (WT), TLR2(-/-), TLR4(-/-), and MyD88(-/-) BALB/c mice were stimulated with dust. Cytokine production was low or undetectable in TLR4(-/-) cells, but occurred from TLR2(-/-) cells, and production by MyD88(-/-) cells was higher than by TLR4(-/-) cells. These results suggest that TLR4 and TLR2 ligands (LPS and β-glucan, respectively) mainly contributed to cytokines production induced by PM2.5rd. In addition to chemical substances, PM2.5-bound microbial substances might act in inflammatory and allergic lung diseases.

The acute airway inflammation induced by PM2.5 exposure and the treatment of essential oils in Balb/c mice

“…TLRs in host cells could sense the stimulus and induce the synthesis of pro-IL-1β41. Some in vitro studies also revealed that TLR4 mainly contributed to cytokines production induced by PM 2.5 42. Activated NLRP3 inflammasome activates caspase-1 which subsequently cleaves pro-IL-1β into the mature form, IL-1β4344.…”

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

“…PAHs were analyzed according to a previously reported method (He et al ., , , ,b). Briefly, samples collected in the Teflon filter were extracted twice with a 20 ml portion of dichloromethane at 15°C by ultrasonic extraction.…”

“…Six mice from each group were used to examine the free cell contents from BALF. BALF and cell counts were determined in the same manner as detailed in previous studies (He et al ., , , , ,b,c). In brief, tracheas were cannulated after the collection of blood.…”

“…After separation of the lobes, 2 mm thick blocks were taken for paraffin embedding. Embedded blocks were sectioned at a thickness of 3 μm, and stained with hematoxylin and eosin to evaluate inflammation in the lung (He et al ., , , , ,b).…”

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

“…Then, PM2.5 was collected. PM2.5 “Kitakyushu Apr 2011” (PM2.5‐rich dust, with 83% PM2.5) was collected using a high‐volume air sampler (Sibata Scientific Technology, Taito‐ku, Japan) with a Teflon filter (He et al, ). The remaining four samples of PM2.5 from Shenyang were collected using a four‐stage multi‐nozzle cascade impactor (Tokyo Dyle, Tokyo, Japan) (He et al, ).…”