Inflammatory Responses and Mucus Secretion in Rats With Acute Bronchiolitis Induced by Nickel Chloride

Abstract

The effects of inhaled particulate matter in the workplace and outdoor environment on sensitive subpopulations are not sufficiently investigated in human and animal models. Thus, animal models for pulmonary diseases are necessary for appropriate risk assessment of toxic materials. We studied biochemical characteristics of an acute inflammatory process induced by inhalation of nickel chloride aerosols in rats. Acute bronchiolitis was induced by inhalation of nickel chloride aerosols for 5 days in Wistar rats according to the method described by Kyono et al. (1999). Deterioration and recovery from inflammatory responses were evaluated by analyzing markers of inflammation in bronchoalveolar lavage (BAL) fluid. Experimental animals were sacrificed during and after the nickel aerosol exposure period. The number of neutrophils markedly increased to approximately 0.5 x 10(3) cells/microl BAL fluid during nickel aerosol exposure, accompanied by increase of total protein, soluble L-selectin, cytokine-induced neutrophil chemoattractant/growth-regulated gene products (CINC/GRO), elastolytic activity, trypsin inhibitory capacity, beta-glucuronidase activity, fucose, and sialic acid in BAL fluid compared with those of the control group. There was correlation between number of leukocytes and soluble L-selectin concentration. The number of pulmonary macrophages in BAL fluid decreased to approximately 15% of those of the control group on the days of nickel aerosol exposure. The level of CINC/GRO recovered to that of the control group on day 3 after cessation of the nickel aerosol exposure. However, other inflammatory markers remained at the elevated levels. Changes in the markers of inflammation during and after the nickel aerosol exposure were consistent with previously reported morphological findings. The results indicated that this animal model is potentially useful as an acute bronchiolitis model.

Local administration of 2% trimecaine affects the content of fucosylated glycoconjugates in goblet cells in rabbit tracheal epithelium

“…It is reported that the proportion of fucosylated glycoconjugates increases in some respiratory diseases. However, as we evaluated the effects of only one dose 10 min after administration, it is impossible to trace the long-time changes to compare them directly with those found in various respiratory pathologies (Otori et al 1998;Finkbeiner 1999;Majima et al 1999;Glick et al 2001;Ishihara 2002). Nevertheless, the effects of local anaesthesia clearly altered the proportion of the goblet cells containing fucosylated glycoconjugates.…”

“…1999; Glick et al. 2001; Ishihara 2002). Nevertheless, the effects of local anaesthesia clearly altered the proportion of the goblet cells containing fucosylated glycoconjugates.…”

“…Both secretedand bound to cellular surfaces, they also serve as adhesion sites for various antigens (Adam et al 1997;Gebert & Posselt 1997;Ló pez-Ferrer et al 2000). An increased proportion of fucosylated glycoconjugates in airway secretions was described in sinusitis (Otori et al 1998), chronic bronchitis (Finkbeiner 1999;Freney et al 2001), asthma (Finkbeiner 1999), cystic fibrosis (Finkbeiner 1999;Glick et al 2001) and acute bronchiolitis in rats (Ishihara 2002). In adult humans, the a(1-2) linkage of fucose (Fuc) to galactose is the most common one (Sato et al 1986;Biol-N'Garagba et al 2002).…”

“…In adult humans, the a(1-2) linkage of fucose (Fuc) to galactose is the most common one (Sato et al 1986;Biol-N'Garagba et al 2002). Under pathological conditions like inflammation (Otori et al 1998;Blander et al 1999;Ishihara 2002) or cystic fibrosis (Glick et al 2001), fucosylation in other linkages [a(1-3), a(1-4) and a(1-6) to N-acetyl glucosamine] increases at the expense of a(1-2) position and sialylation as well.…”

“…1998; Blander et al. 1999; Ishihara 2002) or cystic fibrosis (Glick et al. 2001), fucosylation in other linkages [ α (1–3), α (1–4) and α (1–6) to N ‐acetyl glucosamine] increases at the expense of α (1–2) position and sialylation as well.…”