An Interaction Between Genetic Factors and Gender Determines the Magnitude of the Inflammatory Response in the Mouse Air Pouch Model of Acute Inflammation

The increased life expectancy of the population has led to increasing incidences of cancer, chronic inflammatory and autoimmune diseases. Thus the continuous search for new drugs is necessary because ineffectiveness and adverse effects have been described for standard drugs. Essential oils are important sources of bioactive metabolites and several clinical trials have been developed using them. The Pterodon genus has been used in traditional medicine to treat rheumatic disorders, thus this work investigated the properties of essential oil from Pterodon polygalaeflorus fruits (EsOPpg) on acute inflammation and lymphocyte activation. The essential oil was obtained by hydrodistillation and its components were identified by GC/MS. The anti-inflammatory response was assessed using the air pouch model. Antinociceptive potential was evaluated using the writhing model. Lymphocyte phenotyping, cell cycle and apoptosis were analyzed by flow cytometry. EsOPpg promoted a reduction in leukocyte counts and protein concentration in the exudate, and reduced vasodilatation and inflammatory cell infiltrate in air pouch tissue. No antinociceptive effect was demonstrated for the doses tested. EsOPpg inhibited lymphocyte proliferation, arresting the cell cycle in G1phase, and induced apoptosis in these cells. EsOPpg downregulated both the total number of CD8+T cells and the activated subpopulation (CD8+CD69+), while promoting upregulation of the total number of CD19+and CD19+CD69+B cells. In conclusion, Pterodon polygalaeflorus essential oil diminished the acute inflammatory response and inhibited lymphocyte proliferation, reducing neutrophil recruitment into the cavity and air pouch tissue and promoting distinct modulations of the activation level of each lymphocyte subpopulation.

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Acute inflammatory response to cobalt chromium orthopaedic wear debris in a rodent air-pouch model

Journal of The Royal Society Interface ◽

10.1098/rsif.2012.0006 ◽

2012 ◽

Vol 9 (74) ◽

pp. 2109-2119 ◽

Cited By ~ 23

Author(s):

Moeed Akbar ◽

Alasdair R. Fraser ◽

Gerard J. Graham ◽

James M. Brewer ◽

M. Helen Grant

Keyword(s):

Inflammatory Response ◽

Wear Debris ◽

Inflammatory Responses ◽

Flow Cytometric Analysis ◽

Hip Resurfacing ◽

Acute Inflammatory Response ◽

Cobalt Chromium ◽

Air Pouch ◽

Gene Transcripts ◽

Air Pouch Model

This study used a rodent air-pouch model to assess the acute inflammatory response to cobalt–chromium (CoCr) alloy wear debris from a metal-on-metal hip resurfacing implant that may contribute to joint failure. Air-pouches were injected with either sterile phosphate-buffered saline, 1 μg lipopolysaccharide (LPS) or 2.5 mg CoCr wear debris. The in situ inflammatory response was monitored 4, 24, 48 and 72 h and 7 days later. A flow cytometric analysis of the inflammatory exudates showed that CoCr wear debris induced a different inflammatory pattern compared with LPS. LPS induced a strong early (4 h) neutrophil influx, with monocyte/macrophage influx peaking at 24 h, whereas CoCr wear debris initiated almost equal numbers of early monocyte/macrophage and neutrophil recruitment. Histological analyses also showed CoCr debris accumulated in the pouch wall and this was accompanied by vast cellular infiltration and fibrosis around the debris throughout the duration of the experiment. Assessment of inflammatory gene transcripts from air-pouch tissue showed that CoCr wear debris increased the expression of cytokines involved in promoting inflammation and fibrosis (IL-1β, TGF-β) and chemokines that promote the recruitment of neutrophils and monocytes/macrophages (CXCL2 and CCL2). The data suggest that inflammatory responses to CoCr debris induce a specific acute process in which the recruitment of monocytes/macrophages is key.

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