Proinflammatory and Anti-Inflammatory Cytokine Balance in Gasoline Exhaust Induced Pulmonary Injury in Mice

Abstract

Proinflammatory and anti-inflammatory cytokine balance and associated changes in pulmonary bronchoalveolar lavage fluid (BALF) of unleaded gasoline exhaust (GE) exposed mice were investigated. Animals were exposed to GE (1 L/min of GE mixed with 14 L/min of compressed air) using a flow-past, nose-only, dynamic inhalation exposure chamber for different durations (7, 14, and 21 days). The particulate content of the GE was found to be 0.635, +/-0.10 mg PM/m3. Elevated levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were observed in BALF of GE-exposed mice, but interleukin 1beta(IL-1beta) and the anti-inflammatory cytokine interleukin-10 (IL-10) remained unaffected. GE induced higher activities of alkaline phosphatase (ALP), gamma-glutamyl transferase (gammaGT), and lactate dehydrogenase (LDH) in the BALF, indicating Type II alveolar epithelial cell injury, Clara-cell injury, and general toxicity, respectively. Total protein in the BALF increased after 14 and 21 days of exposure, indicating enhanced alveolar-capillary permeability. However, the difference in the mean was found statistically insignificant in comparison to the compressed air control. Total cell count in the BALF of GE-exposed mice ranged between 0.898 and 0.813x10(6) cells/ml, whereas the compressed air control showed 0.65x10(6) cells/mL. The histopathological changes in GE-exposed lung includes perivascular, and peribronchiolar cuffing of mononuclear cells, migration of polymorphonuclear cells in the alveolar septa, alveolar thickening, and mild alveolar edematous changes indicating inflammation. The shift in pro- and anti-inflammatory cytokine balance and elevation of the pulmonary marker enzymes indicate toxic insult of GE. This study will help in our understanding of the mechanism of pulmonary injury by GE in the light of cytokine profiles, pulmonary marker enzymes, and lung architecture.

Development of haemostatic decontaminants for the treatment of wounds contaminated with chemical warfare agents. 1: Evaluation of in vitro clotting efficacy in the presence of certain contaminants

“…Nerve agents have been shown to increase platelet numbers (Collombet et al ., ) and increase expression and modulate release of proinflammatory cytokines (interleukin‐1β, tumour necrosis factor‐α and interleukin‐6). Petrol exhaust has also been shown to increase the expression of proinflammatory cytokines, including tumour necrosis factor‐α (Sureshkumar et al ., ). These cytokines can increase platelet numbers and may be procoagulant in their own right.…”

Status of Stat3 in an Ovalbumin-Induced Mouse Model of Asthma: Analysis of the Role of Socs3 and IL-6

“…5 mg/0.1 ml/mouse at 2 h after the last OVA challenge for collection of BALF and blood. For collection of BALF, the trachea was exposed by midline incision in the neck region and 1 ml of PBS, pH 7.4 was injected into the lungs through the trachea and withdrawn after 10 s. The fluid recovered from each mouse was centrifuged at 2,000 rpm, for 5 min at 4°C and the supernatants were subjected to antibody and cytokine analysis [30]. The pellets were resuspended, cytocentrifuged and stained with hematoxylin and eosin (HE) and viewed under the microscope for eosinophil counts.…”

Oxido‐inflammatory responses and histological alterations in rat lungs exposed to petroleum product fumes

“…Under normal conditions, abnormal tissue levels of GGT, ALP, and LDH are indicators of pathological conditions,[58][59][60][61] mostly, they are present in a significant organ, but serum levels are nonspecific. Increased (P < .05) LDH activities in the lung, is indicative of endothelial injury and inflammation,62 in this instance, as a response to PPF exposures in the experimental rat.These findings are consistent with the previous report of elevated lung ALP, GGT, and LDH46,60 in mice exposed to gasoline and diesel, with parallel consequences for exposed humans.Reports show that GGT is also a potential biomarker of oxidative stress in chronic obstructive pulmonary disease, under healthy physiological conditions, tissues of the lung are a potent source of GGT 63 enzyme activity. Moreover, PPF promotes an oxidative state in the lungs of exposed rats, evidenced by an apparent decrease in GSH level, antioxidant enzyme activities, and lung histopathological changes.…”