Extremely low-level microwaves attenuate immune imbalance induced by inhalation exposure to low-level toluene in mice

Abstract

Purpose: To clarify whether extremely low-level microwaves (MW) alone or in combination with p38 inhibitor affect immune cell responses to inhalation exposure of mice to low-level toluene.

Materials and methods: The cytokine profile, heat shock proteins expression, and the activity of several signal cascades, namely, NF-κB, SAPK/JNK, IRF-3, p38 MAPK, and TLR4 were measured in spleen lymphocytes of mice treated to air-delivered toluene (0.6 mg/m³) or extremely low-level microwaves (8.15–18 GHz, 1μW/cm², 1 Hz swinging frequency) or combined action of these two factors.

Results: A single exposure to air-delivered low-level toluene induced activation of NF-κB, SAPK/JNK, IFR-3, p38 MAPK and TLR4 pathways. Furthermore, air toluene induced the expression of Hsp72 and enhanced IL-1, IL-6, and TNF-α in blood plasma, which is indicative of a pro-inflammatory response. Exposure to MW alone also resulted in the enhancement of the plasma cytokine values (e.g. IL-6, TNF-α, and IFN-γ) and activation of the NF-κB, MAPK p38, and especially the TLR4 pathways in splenic lymphocytes. Paradoxically, pre-exposure to MW partially recovered or normalized the lymphocyte parameters in the toluene-exposed mice, while the p38 inhibitor XI additionally increased protective activity of microwaves by down regulating MAPKs (JNK and p38), IKK, as well as expression of TLR4 and Hsp90-α.

Conclusions: The results suggest that exposure to low-intensity MW at specific conditions may recover immune parameters in mice undergoing inhalation exposure to low-level toluene via mechanisms involving cellular signaling.

Keywords:

• Low-level microwaves
• low-level air toluene
• signaling pathways
• cytokines
• mice

Acknowledgements

The work was supported by Program of Russian Academy of Sciences “Molecular and Cellular Biology” and by Russian Foundation for Basic Research, grant Nos 14-44-03558 and 16-34-00231. The authors thank Elsevier WebShop Language Service for help with language editing and Dr S. Alekseev for the useful discussion of the data.

Disclosure statement

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.

Additional information

Funding

The work was supported by Program of Russian Academy of Sciences ?Molecular and Cellular Biology? and by Russian Foundation for Basic Research, grant Nos 14-44-03558 and 16-34-00231. The authors thank Elsevier WebShop Language Service for help with language editing and Dr S. Alekseev for the useful discussion of the data.