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Microcirculation contributes significantly to blood flow resistance, with upper airway microcirculation in obstructive sleep apnea (OSA) affected by endothelial activation, perturbed blood flow shear stress, and snoring-induced tissue vibration. The relevance of these mechanisms on microcirculation response and remodeling remains largely unknown but may influence management decisions in OSA. This study analyzed pharyngeal muscle tissue from non-obese, young adult patients with OSA and chronic heavy snoring. We assessed arteriole morphometry and quantified the expression of endothelial activation markers: 8-isoprostane, vascular cell adhesion molecule-1, E-selectin, vascular endothelial growth factor, endothelin-1, and endothelial cell specific molecule-1. Morphometric analysis of 319 arterioles (mean of 8 vessels per patient) revealed thicker walls in severe OSA compared to mild OSA without lumen reduction, indicating outward hypertrophy, and a positive correlation between the apnea–hypopnea index (a measure of OSA severity) and arteriole wall thickness. However, analysis of 1872 arterioles showed no increase in endothelial activation markers with disease severity, either in the arteriole walls or muscle tissue. This suggests that, in young non-obese adults, severe OSA likely leads to adaptive, mechanically driven microcirculation outward hypertrophy, potentially due to perturbed shear stress, with potential implications for OSA management.

Both systemic and organ-specific autoimmune diseases are major manifestations of IgA deficiency (IgAD), the most common primary immunodeficiency. In addition, to discuss the clinical findings of IgAD patients, we proposed a hypothesis to explain the high association with autoimmune phenomena. Based on observations, interactions of monomeric IgA with FcαRI result in a partial phosphorylation of FcRγ-associated FcαRI, notably in the immunoreceptor tyrosine-based activation motif (ITAM) inducing the recruitment of the SHP-1 tyrosine phosphatase. This leads to deactivation of several activating pathways of the immune system including immunoreceptors that bear ITAM motif and ITAM-independent receptors. Consequently, inflammatory reactions and auto-immune process would be prevented.

Immunoglobulin A deficiency (IgAD) is considered the most common form of primary immunodeficiency. The majority of IgA-deficient individuals are considered asymptomatic, even though IgAD has been associated with an increased frequency of recurrent infections, allergy, and autoimmune diseases. In this study we evaluate the Natural autoantibodies (NatAbs) reactivity to phosphorylcholine (PC) and to some pro-inflammatory molecules in IgAD with or without autoimmune disorders. We observed that in the absence of IgA there is an enhancement of IgG subclasses functioning as NatAbs against PC. Immunoglobulin G (IgG) against lipopolysaccharide, C-reactive protein, and IgA was found in IgAD, regardless of the autoimmune manifestations. Nonetheless, IgAD patients with autoimmune disease showed significantly higher IgG reactivity against pro-inflammatory molecules, such as cardiolipin, oxidized low-density lipoproteins, and phosphatidylserine, with positive correlation between them. In conclusion, the IgG NatAbs against PC may represent a compensatory defense mechanism against infections and control excess of inflammation, explaining the asymptomatic status in the IgA deficiency.