title: Effect of diesel exhaust particulate (DEP) on immune responses: contributions of particulate versus organic soluble components.
abstract: The effect of diesel exhaust particulate (DEP) exposure on innate, cellular and humoral pulmonary immunity was studied using high-dose, acute-exposure rat, mouse, and cell culture models. DEP consists of a complex mixture of petrochemical-derived organics adsorbed onto elemental carbon particles. DEP is a major component of particulate urban air pollution and a health concern in both urban and occupational environments. The alveolar macrophage is considered a key cellular component in pulmonary innate immunity. DEP and DEP organic extracts have been found to suppress alveolar macrophage function as demonstrated by reduced production of cytokines (interleukin-1 [IL-1], tumor necrosis factor- alpha [TNF- alpha]) and reactive oxygen species (ROS) in response to a variety of agents, including lipopolysaccharide (LPS), interferon- gamma (IFN- gamma), and bacteria. Fractionation of DEP organic extract suggests that this activity was predominately in polyaromatic-containing and more polar (resin) fractions. Organic-stripped DEP did not alter these innate pulmonary immune responses. DEP also depressed pulmonary clearance of Listeria monocytogenes and Bacillus Calmette-Guerin (BCG). The contribution of the organic component of DEP is less well defined with respect to acquired and humoral immunity. Indeed, both DEP and carbon black enhanced humoral immune responses (specific immunoglobulin [Ig] E and IgG) in an ovalbumin-sensitized rat model. It is concluded that both the particulate and adsorbed organics may contribute to DEP-mediated immune alterations.
authors.affiliation: HELD, NIOSH, Morgantown, West Virginia 26505, USA. psiegel@cdc.gov
authors.forename: Paul D
authors.initials: PD
authors.lastname: Siegel
authors.forename: Rajiv K
authors.initials: RK
authors.lastname: Saxena
authors.forename: Q B
authors.initials: QB
authors.lastname: Saxena
authors.forename: Joseph K H
authors.initials: JK
authors.lastname: Ma
authors.forename: Jane Y C
authors.initials: JY
authors.lastname: Ma
authors.forename: Xue-Jun
authors.initials: XJ
authors.lastname: Yin
authors.forename: Vincent
authors.initials: V
authors.lastname: Castranova
authors.forename: Nabil
authors.initials: N
authors.lastname: Al-Humadi
authors.forename: Daniel M
authors.initials: DM
authors.lastname: Lewis
mesh_terms: D000208:Acute Disease; D000393:Air Pollutants / Q000737:chemistry / Q000633:toxicity*; D000818:Animals; D000917:Antibody Formation / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D004195:Disease Models, Animal; D004784:Environmental Monitoring; D062665:Epidemiological Monitoring; D007111:Immunity, Cellular / Q000276:immunology*; D019570:Inhalation Exposure / Q000009:adverse effects* / Q000032:analysis; D007371:Interferon-gamma / Q000276:immunology; D007375:Interleukin-1 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D016676:Macrophages, Alveolar / Q000276:immunology; D051379:Mice; D011014:Pneumonia / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D051381:Rats; D017382:Reactive Oxygen Species / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D007375:Interleukin-1; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D001335:Vehicle Emissions; D007371:Interferon-gamma