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Abstract

Morbidity and mortality rates during the COVID-19 pandemic have been particularly high among elderly people (>65 years). This review summarises some of the important physiological and clinical aspects in the background of augmented risk. Airway clearance provides defence against inhaled particles, including viruses. Some relevant studies have indicated that clearance from the small and large airways is slower in elderly people. Cough peak flow (the speed of expiratory airflow during coughing, or cough power) is another important parameter that reflects the defence capacity of the respiratory system. Age has likewise been shown to induce inspiratory and expiratory muscle weakness and, as a consequence, a low cough peak flow. In addition to the weakening of these non-specific defences in elderly people, the specific immune response against the SARS-CoV-2 virus has been found to be nearly blocked in aged mice, and the augmented synthesis of prostaglandin D2 (PGD2) was found to play a role in this phenomenon. Aged animals were protected from death by a specific antagonist of PGD2. Among aged people suffering from COVID-19, there were disproportionally more patients with low CD8 T lymphocyte counts and high plasma concentrations of interleukin 6 (IL-6). This combination of deficient cellular immunity and overt inflammatory response in COVID-19 has been identified as a significant risk factor of mortality.

Open access

The effect of potassium channel blockers tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by immunohistochemistry with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.

Restricted access
Acta Physiologica Hungarica
Authors:
N. Eszes
,
A. Bohács
,
Á. Cseh
,
G. Toldi
,
A. Bikov
,
I. Ivancsó
,
V. Müller
,
I. Horváth
,
J. Rigó
,
B. Vásárhelyi
,
Gy Losonczy
, and
Lilla Tamási

Asthmatic inflammation during pregnancy poses a risk for maternal and fetal morbidities. Circulating T cell immune phenotype is known to correlate with airway inflammation (detectable by fractional concentration of nitric oxide present in exhaled breath (FENO)) in non-pregnant allergic asthmatics. The aim of this study was to assess the relationship of peripheral T cell phenotype to FENO and clinical variables of asthma during pregnancy.We examined 22 pregnant women with allergic asthma in the 2nd/3rd trimester. The prevalence of Th1, Th2, regulatory T (Treg) and natural killer (NK) cell subsets was identified with flow cytometry using cell-specific markers. FENO, Asthma Control Test (ACT) total score and lung function were evaluated.Peripheral blood Th1, Th2, Treg, and NK cell prevalence were not significantly correlated to airway inflammation assessed by FENO in asthmatic pregnant women (all cells p > 0.05; study power > 75%). However, an inverse correlation was detected between Th2 cell prevalence and ACT total scores (p = 0.03) in asthmatic pregnancy.Blunted relationship between T cell profile and airway inflammation may be the result of pregnancy induced immune tolerance in asthmatic pregnancy. On the other hand, increased Th2 response impairs disease control that supports direct relationship between symptoms and cellular mechanisms of asthma during pregnancy.

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