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Vanadium Pentoxide Inhalation Provokes Germinal Center Hyperplasia and Suppressed Humoral Immune Responses
Identifier
029503
Type of Spiritual Experience
None
Background
Preamble
Vanadium (V) has recently become recognized as an important air pollutant (Fortoul et al., 1996, 2002) in the atmosphere of Mexican cities. There, as elsewhere, it is a component of residual oil fly ash (ROFA; Samet et al., 1999) that enters the organism, mainly by inhalation (Brook et al., 2004; Nemmar et al., 2004). Another important source of vanadium is as an atmospheric contaminant generated from combusted fuel products. Occupational exposure to one major chemical form that is also found in urban air, vanadium pentoxide (V2O5), occurs during the cleaning of oil-fired boilers and furnaces, during handling of catalysts in chemical plants, and during the refining, processing, and burning of vanadium-rich fossil fuels, especially Venezuelan or Mexican oils (Nriagu, 1998; Ivancsits et al., 2000).
There is ample epidemiological evidence showing that exposure to particulate matter with diameters less than 2.5 μ m (PM2.5)-bearing air pollution aggravate respiratory diseases and impairs the cardiovascular function (Dockery et al., 1993; Ackermann-Liebrich et al., 1997; Pope et al., 1999; Gold et al., 2000; Laden et al., 2000), especially if the individuals are exposed to peaks of air pollution (Peters et al., 1999). At this particle size, metals are adsorbed by inhalation and enter the systemic circulation, thus exerting its toxic effect in other organs and tissues (Dockery and Pope, 1994).
A description of the experience
Vanadium Pentoxide Inhalation Provokes Germinal Center Hyperplasia and Suppressed Humoral Immune Responses
G. Piñon-Zarate, V. Rodriguez-Lara, M. Rojas-Lemus, M. Martinez-Pedraza, A. Gonzalez-Villalva, P. Mussali-Galante,
https://doi.org/10.1080/15476910802085749
Vanadium, an important air pollutant derived from fuel product combustion, aggravates respiratory diseases and impairs cardiovascular function.
In contrast, its effects on immune response are conflicting. The aim of our work was to determine if spleens of vanadium-exposed CD1 mice showed histological lesions that might result in immune response malfunction. One hundred and twelve CD-1 male mice were placed in an acrylic box and inhaled 0.02 M vanadium pentoxide (V2O5); actual concentration in chamber ≈1.4 mg V2O5/m3) for 1 hr/d, twice a week, for 12 wk. Control mice inhaled only vehicle. Eight mice were sacrificed prior to the exposures.
Eight control and eight V2O5-exposed mice were sacrificed 24 hr after the second exposure of each week until the 12-wk study was over. Another 8 mice that completed the 12-wk regimen were immunized with recombinant Hepatitis B surface antigen (HBsAg; three times over an 8-wk period) before sacrifice and analyses of their levels of anti-HBsAg antibody (HBSAb) using ELISA.
In all studies, at sacrifice, blood samples were obtained by direct heart puncture and the spleen was removed, weighed and processed for H-E staining and quantitation of CD19 cells. The results indicated that the spleen weight of V2O5-exposed animals peaked at 9 wk (546 ± 45 vs. 274 ± 27 mg, p < 0.0001) and thereafter progressively decreased (321 ± 39 mg at 12 wk, p < 0.001; control spleen = 298 ± 35 mg). Spleens of V2O5-exposed animals showed an increased number of very large and non-clearly delimited germinal centers (that contained more lymphocytes and megakaryocytes) compared to those of control mice.
In addition, their red pulp was poorly delimited and had an increase in CD19+ cells within hyperplasic germinal nodes. The mean HBsAb levels in immunized control mice were greater than that in the exposed hosts (i.e., OD = 0.39 ± 0.03 vs. 0.11 ± 0.05, p < 0.01). HBsAb avidity dropped to a value of 40 in V2O5-exposed animals vs. 86 in controls (p < 0.0001). We conclude that the chronic inhalation of V2O5, a frequent particle (PM2.5) component, induces histological changes and functional damage to the spleen, each of which appear to result in severe effects on the humoral immune response.
Keywords : Vanadium, pentoxide, humoral immune response