Reaction of eosinophilic granulocytes of guinea pigs airways to the experimental allergic inflammation according to the morphometric study

Background. After creating an animal model of experimental airways allergic inflammation using ovalbumin, scientists mainly studied the reaction of the cellular and humoral links of the acquired specific immunity. At the same time, it is known that the development of allergic inflammation of the airways to the effect of the environmental chemoattractants is primarily the result of the local innate immune system response. Pulmonary neuroendocrine cells of the airway epithelium with the help of neuropeptides activate the secretion of IL-5 and IL-13 by type 2 innate lymphoid cells IL-5 determines the eosinophilic inflammation. The question of the reaction of the components of innate immunity of the respiratory tract to the allergic inflammation in most aspects remains open. open. Objective. The purpose of the current study was to define the reaction of eosinophilic granulocytes in guinea pigs lungs as an important component of the innate immunity of the respiratory tract to experimental ovalbumin-induced allergic inflammation according to the data of a morphometric study. Methods. Histological, morphometric, statistical methods were used to study the topographic features and the number of eosinophils in the lungs of male 48 guinea pigs on the 23rd, 30th, 36th and 44th days after initiation of the experimental ovalbumin-induced allergic airway inflammation. Results. Our study demonstrates a significant reaction occurs on the part of the cellular link of innate immunity, which consists in the activation of eosinophils, in the experimental model of ovalbumin-induced airways allergic inflammation. The most significant changes were observed in the distal parts of the intrapulmonary airways and in the structures of the pulmonary acinus in the early period of the development of the inflammatory process (23rd and 30th days after the start of the experiment). The late (36th and 44th days after the start of the experiment) period of the development of an allergic inflammatory process in the lungs is accompanied by a gradual decrease in the activity of eosinophilic inflammation. At the same time, the quantitative indicators remain statistically significantly higher in the intact and control groups, which indicates the continuation of allergic inflammation in the absence of the action of the allergen and is a manifestation of the violation of the recovery and adaptation processes in the local immune system of the lung. Conclusion. After ovalbumin-sensitization and aeroallergization eosinophilic inflammation develops in the lungs of a guinea pig, as a result of the reaction of the innate immunity to the action of an allergen. Actively and first of all, allergic eosinophilic inflammation develops in the distal airways (terminal bronchioles) and in the connective tissue stroma of the pulmonary acinus.

Deposition of Submicron Particles by Chaotic Mixing in the Pulmonary Acinus

In this review, the authors outline the evidence that emerged some 30 years ago that the mechanisms thought responsible for the deposition of submicron particles in the respiratory region of the lung were inadequate to explain the measured rate of deposition. They then discuss the background and theory of what is believed to be the missing mechanism, namely chaotic mixing. Specifically, they outline how that the recirculating flow in the alveoli has a range of frequencies of oscillation and some of these resonate with the breathing frequency. If the system is perturbed, the resonating frequencies break into chaos, and they discuss a number of practical ways in which the system can be disturbed. The perturbation of fluid particle trajectories results in Hamiltonian chaos, which produces qualitative changes in those trajectories. They end the review with a discussion of the effects of chaotic mixing on the deposition of inhaled particles in the respiratory region of the lung.

Internal pressure driven finite element model of a single pulmonary acinus

A computer simulated, poroelastic, hyperelastic model was developed to replicate the pressure-volume response of a single pulmonary acinus (15th branch of the respiratory tree and daughter branches) with air flow at its core. An internal pressure driven approach was taken upon a small spherical geometry (99.2 mm3 in volume) representing this small segment of lung parenchyma. A reference porcine tracheal pressure at tidal breathing was adjusted from 1471 Pa to 998 Pa to accommodate for pressure drop, and the pressure of 998 Pa was applied to the model for parametric analysis of its pressure-volume characteristics. In targeting a proportional tidal volume change of approximately 15% while also inducing a pressure-volume hysteresis, material parameters of Young’s modulus of 4 kPa, Poisson’s ratio of 0.4, and a permeability of 5×10-5 cm3s-1cm-2 were identified as suitable. The energy loss over a single pressure-volume cycle for a pulmonary acinus was found to be 6.3×10-6 J. This model was qualitatively compared to the pressure-volume relationship of the original porcine data source, and then with experimental findings of the material parameters for lung parenchyma in medical literature, demonstrating same-order agreement.