Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography

Mailhot-Larouche, Samuel; Deschênes, Louis; Lortie, Katherine; Gazzola, Morgan; Marsolais, David; Brunet, David; Robichaud, Annette; Bossé, Ynuk

doi:10.3791/57778-v

Cited by 2 publications

(1 citation statement)

References 7 publications

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“…Following CEES administration, all groups exhibited a spectrum of respiratory dysfunction, notably featuring tachypnea, heightened ventilation volumes, conspicuous wheezing, and cyanotic episodes. A cited study utilized plethysmography for a more meticulous quantitative evaluation of murine respiratory functional changes [ 28 ]. However, its application is constrained by the requirement for the animals to be anesthetized or in a quiescent state [ 29 ], limiting broader applicability.…”

Section: Discussionmentioning

confidence: 99%

Establishment of a Mouse Model of Mycoplasma pneumoniae-Induced Plastic Bronchitis

Jin,

Zhao,

Zhang

et al. 2024

Microorganisms

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Plastic bronchitis (PB) constitutes a life-threatening pulmonary disorder, predominantly attributed to Mycoplasma pneumoniae (MP) infection. The pathogenic mechanisms involved remain largely unexplored, leading to the absence of reliable approaches for early diagnosis and clear treatment. Thus, the present investigation aimed to develop an MP-induced mouse model of PB, thereby enhancing our understanding of this complex condition. In the first stage, healthy BALB/c mice were utilized to investigate the optimal methods for establishing PB. This involved the application of nebulization (15–20 min) and intratracheal administration (6–50 μL) with 2-chloroethyl ethyl sulfide (CEES) concentrations ranging from 4.5% to 7.5%. Subsequently, the MP model was induced by administering an MP solution (2 mL/kg/day, 108 CFU/50 μL) via the intranasal route for a duration of five consecutive days. Ultimately, suitable techniques were employed to induce plastic bronchitis in the MP model. Pathological changes in lung tissue were analyzed, and immunohistochemistry was employed to ascertain the expression levels of vascular endothelial growth factor receptor 3 (VEGFR-3) and the PI3K/AKT/mTOR signaling pathway. The administration of 4.5% CEES via a 6 µL trachea was the optimal approach to establishing a PB model. This method primarily induced neutrophilic inflammation and fibrinous exudate. The MP-infected group manifested symptoms indicative of respiratory infection, including erect hair, oral and nasal secretions, and a decrease in body weight. Furthermore, the pathological score of the MP+CEES group surpassed that of the groups treated with MP or CEES independently. Notably, the MP+CEES group demonstrated significant activation of the VEGFR-3 and PI3K/AKT/mTOR signaling pathways, implying a substantial involvement of lymphatic vessel impairment in this pathology. This study successfully established a mouse model of PB induced by MP using a two-step method. Lymphatic vessel impairment is a pivotal element in the pathogenetic mechanisms underlying this disease entity. This accomplishment will aid in further research into treatment methods for patients with PB caused by MP.

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Section: Discussionmentioning

confidence: 99%

Establishment of a Mouse Model of Mycoplasma pneumoniae-Induced Plastic Bronchitis

Jin,

Zhao,

Zhang

et al. 2024

Microorganisms

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Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity

Su,

Xu,

Zhu

et al. 2024

Nature

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Exaggerated airway constriction triggered by repeated exposure to allergen, also called hyperreactivity, is a hallmark of asthma. Whereas vagal sensory neurons are known to function in allergen-induced hyperreactivity1–3, the identity of downstream nodes remains poorly understood. Here we mapped a full allergen circuit from the lung to the brainstem and back to the lung. Repeated exposure of mice to inhaled allergen activated the nuclei of solitary tract (nTS) neurons in a mast cell-, interleukin-4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA sequencing, followed by RNAscope assay at baseline and allergen challenges, showed that a Dbh+ nTS population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted hyperreactivity whereas chemogenetic activation promoted it. Viral tracing indicated that Dbh+ nTS neurons project to the nucleus ambiguus (NA) and that NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that directly drive airway constriction. Delivery of noradrenaline antagonists to the NA blunted hyperreactivity, suggesting noradrenaline as the transmitter between Dbh+ nTS and NA. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. This knowledge informs how neural modulation could be used to control allergen-induced airway hyperreactivity.

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Assessment of Respiratory Function in Conscious Mice by Double-chamber Plethysmography

Cited by 2 publications

References 7 publications

Establishment of a Mouse Model of Mycoplasma pneumoniae-Induced Plastic Bronchitis

Establishment of a Mouse Model of Mycoplasma pneumoniae-Induced Plastic Bronchitis

Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity

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