Dust events, pulmonary diseases and immune system

Abstract

Incidences of sand storms have increased in recent years and there is evidence that these dusts can move across long distances. Sand dusts have different adverse effects on health, but one of the most important of them is pulmonary disease. After inhalation of dust, many dust particles are moved to the airways. Dust particles can be sensed by airways epithelial cells, activate macrophages, dendritic cells and innate immune cells and then initiate responses in various populations of specific immune cells such as T helper cells subsets (Th1, Th2, Th17), T cytotoxic cells and B cells. Initiation of inflammatory immune responses, activation of immune cells and releases of many cytokines, chemokines and other inflammatory molecules, have variable pathologic affects on lung in different respiratory diseases. Unfortunately control of desert dusts is more difficult than control of air pollution. For prevention and treatment of respiratory diseases that are caused by desert dusts, researchers need well-designed epidemiological studies, combined with analysis of the precise composition of sand dusts, and the precise mechanisms of the immune responses. Recognizing the exact cellular and molecular immune mechanisms would be very useful to find new approaches for treatment of desert dust associated pulmonary diseases.

Keywords: Sand dusts; T helper cells; cytokines and chemokines; pulmonary disease.

Figure 1

Immune responses to different particles in desert dust. Various components of dust that penetrate into the airways have effects on the epithelium. In addition to the physical barrier role of airway epithelial cells, these cells also play important roles for the immune response. Interacting with airway epithelial cells, macrophages, dendritic cells and innate lymphoid cells are activated and contribute to the inflammatory immune response. Furthermore, cross-talk between epithelial cells and dendritic cells (DCs) can mature the antigen presenting capabilities. DCs can present antigen to different subsets of T helper cells. As result of the cellular interactions, other immune cells such as B cells and T cytotoxic cells can also be activated in response to dust particles in the airways. Finally activation of immune responses and release of various cytokines and chemokines contributes to different pulmonary diseases including asthma, chronic obstructive pulmonary disease (COPD), pulmonary arterial hypertension (PAH) and silicosis. Abbreviations: Dcs = Dendritic cells, MQs = Macrophages, ILCs = Innate lymphoid cells, TCs = T cytotoxic cells, Th1 = T helper cell type 1, Th2 = T helper cell type 2, Th17 = T helper cell type 17.