CONTEXT: Our previous study showed that the interleukin-17 (IL-17) concentration in lung tissue and in bronchoalveolar lavage fluid (BALF) of rats with tobacco-smoke-induced chronic obstructive pulmonary disease (COPD) was higher than that of control group. However, whether IL-17 inhibitor could decrease the effect of tobacco smoking is not known yet. OBJECTIVES: To investigate the significance of IL-17 antibodies (Ab) in tobacco-smoke-exposed (TSE) mice. MATERIALS AND METHODS: Male C57/BL6 mice were randomly divided into three groups: TSE group, TSE + anti-IL-17 Ab group, and control group. The number of cells in BALF and the concentrations of IL-17, IL-6, IL-8 and MUC5AC in BALF and lung tissue homogenate were measured. Pulmonary function was measured by pressure sensors, and histologic analysis of the lungs was done in each group. RESULTS: Lung function tests in TSE + anti-IL-17 Ab group were the same compared with TSE group (P > 0.05). The total cell count and the number of neutrophil cells in BALF were significantly higher in TSE group than the normal control group (P < 0.01). Compared with the TSE group, the total cell count in TSE + anti-IL-17 Ab group was decreased, and the percentage of neutrophils in BALF was highly decreased (P < 0.01). Airway inflammation was alleviated in TSE + anti-IL-17 Ab group by histologic analysis. The concentrations of IL-17 in lung tissue were significantly lower in TSE + anti-IL-17 Ab group than in TSE group (P < 0.01). IL-17 was mainly expressed in the epithelial cells in the airways of TSE mice. The concentration of IL-6, IL-8 and MUC5AC in BALF was decreased in TSE + anti-IL-17 Ab group compared with TSE group. DISCUSSION AND CONCLUSIONS: These data support a potential role for IL-17 in airway neutrophilic inflammation in TSE mice. Anti-IL-17 decreased the number of neutrophils as well as the concentration of MUC5AC in the BALF and attenuated neutrophilic airway inflammation.
CONTEXT: Our previous study showed that the interleukin-17 (IL-17) concentration in lung tissue and in bronchoalveolar lavage fluid (BALF) of rats with tobacco-smoke-induced chronic obstructive pulmonary disease (COPD) was higher than that of control group. However, whether IL-17 inhibitor could decrease the effect of tobacco smoking is not known yet. OBJECTIVES: To investigate the significance of IL-17 antibodies (Ab) in tobacco-smoke-exposed (TSE) mice. MATERIALS AND METHODS: Male C57/BL6 mice were randomly divided into three groups: TSE group, TSE + anti-IL-17 Ab group, and control group. The number of cells in BALF and the concentrations of IL-17, IL-6, IL-8 and MUC5AC in BALF and lung tissue homogenate were measured. Pulmonary function was measured by pressure sensors, and histologic analysis of the lungs was done in each group. RESULTS: Lung function tests in TSE + anti-IL-17 Ab group were the same compared with TSE group (P > 0.05). The total cell count and the number of neutrophil cells in BALF were significantly higher in TSE group than the normal control group (P < 0.01). Compared with the TSE group, the total cell count in TSE + anti-IL-17 Ab group was decreased, and the percentage of neutrophils in BALF was highly decreased (P < 0.01). Airway inflammation was alleviated in TSE + anti-IL-17 Ab group by histologic analysis. The concentrations of IL-17 in lung tissue were significantly lower in TSE + anti-IL-17 Ab group than in TSE group (P < 0.01). IL-17 was mainly expressed in the epithelial cells in the airways of TSE mice. The concentration of IL-6, IL-8 and MUC5AC in BALF was decreased in TSE + anti-IL-17 Ab group compared with TSE group. DISCUSSION AND CONCLUSIONS: These data support a potential role for IL-17 in airway neutrophilic inflammation in TSE mice. Anti-IL-17 decreased the number of neutrophils as well as the concentration of MUC5AC in the BALF and attenuated neutrophilic airway inflammation.
Authors: Joel A Mathews; Nandini Krishnamoorthy; David I Kasahara; John Hutchinson; Youngji Cho; Jeffrey D Brand; Alison S Williams; Allison P Wurmbrand; Luiza Ribeiro; Frank Cuttitta; Mary E Sunday; Bruce D Levy; Stephanie A Shore Journal: Am J Respir Cell Mol Biol Date: 2018-03 Impact factor: 6.914
Authors: Nicholas M Mark; Julia Kargl; Stephanie E Busch; Grace H Y Yang; Heather E Metz; Huajia Zhang; Jesse J Hubbard; Sudhakar N J Pipavath; David K Madtes; A McGarry Houghton Journal: Am J Respir Crit Care Med Date: 2018-02-01 Impact factor: 21.405
Authors: Steven Bozinovski; Ross Vlahos; Desiree Anthony; Jonathan McQualter; Gary Anderson; Louis Irving; Daniel Steinfort Journal: Br J Pharmacol Date: 2015-07-08 Impact factor: 8.739