BACKGROUND: Infection with Mycoplasma pneumoniae (Mp) in asthma can occur both acutely and chronically with an associated Th2 inflammatory response and/or increased numbers of bronchial mast cells. Mast cells have previously been shown to promote mycoplasma clearance in mice; however, it is unknown whether mast cells would aid Mp clearance under allergic conditions. OBJECTIVE: Our aim was to determine the impact of allergic inflammation on mast cell-mediated lung Mp clearance. Furthermore, as we have previously demonstrated an essential role for IL-6 in lung Mp clearance we also investigated the role of mast cell-derived IL-6. METHODS: Mast cell-deficient (WBB6F1/J-Kit(W)/Kit(W-v)) mice were challenged with ovalbumin to induce airway inflammation before Mp infection. The role of mast cell-derived IL-6 in bacterial clearance was further investigated by reconstitution of mast cell-deficient mice with IL-6(-/-) mast cells. RESULTS: Allergic mast cell-deficient mice exhibited increased lung Mp burden compared with control littermates. Intravenous adoptive transfer of wild-type and IL-6(-/-) mast cells significantly improved Mp clearance in mast cell-deficient mice. Acutely after Mp infection, allergen-challenged mast cell-deficient mice had increased levels of the pro-inflammatory cytokines IL-6 and TNF-alpha in the bronchoalveolar lavage (BAL) fluid. The total number of neutrophils was also increased in mast cell-deficient mice. CONCLUSIONS: Our results establish that mast cells aid host defense against Mp in an allergic setting and that while IL-6 is necessary for lung Mp clearance, mast cell-derived IL-6 is not required.
BACKGROUND: Infection with Mycoplasma pneumoniae (Mp) in asthma can occur both acutely and chronically with an associated Th2 inflammatory response and/or increased numbers of bronchial mast cells. Mast cells have previously been shown to promote mycoplasma clearance in mice; however, it is unknown whether mast cells would aid Mp clearance under allergic conditions. OBJECTIVE: Our aim was to determine the impact of allergic inflammation on mast cell-mediated lung Mp clearance. Furthermore, as we have previously demonstrated an essential role for IL-6 in lung Mp clearance we also investigated the role of mast cell-derived IL-6. METHODS: Mast cell-deficient (WBB6F1/J-Kit(W)/Kit(W-v)) mice were challenged with ovalbumin to induce airway inflammation before Mp infection. The role of mast cell-derived IL-6 in bacterial clearance was further investigated by reconstitution of mast cell-deficient mice with IL-6(-/-) mast cells. RESULTS: Allergic mast cell-deficient mice exhibited increased lung Mp burden compared with control littermates. Intravenous adoptive transfer of wild-type and IL-6(-/-) mast cells significantly improved Mp clearance in mast cell-deficient mice. Acutely after Mp infection, allergen-challenged mast cell-deficient mice had increased levels of the pro-inflammatory cytokines IL-6 and TNF-alpha in the bronchoalveolar lavage (BAL) fluid. The total number of neutrophils was also increased in mast cell-deficient mice. CONCLUSIONS: Our results establish that mast cells aid host defense against Mp in an allergic setting and that while IL-6 is necessary for lung Mp clearance, mast cell-derived IL-6 is not required.
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