**1. Introduction**

The human coronavirus SARS-CoV-2 or COVID-19 that emerged in late 2019 causes a respiratory tract infection of the COVID-19 disease and, according to the official website of the Ministry of Health, which reports World Health Organization data, has currently resulted in more than 627 million confirmed cases and over 6.58 million deaths worldwide up to October 2022.

The characteristic symptoms presented by patients affected by SARS-CoV-2 led to the belief that it was a pneumonia with an interstitial component, very often bilateral, associated with respiratory symptoms which in the early phase are generally limited, but which can subsequently lead to progressive clinical instability with respiratory failure. The phenomenon of the so-called "silent hypoxemia", characterized by low blood oxygenation values in the absence of subjective feeling of dyspnea, is characteristic of this phase of the disease. This scenario, in a number of people, can evolve towards a worsening clinical picture dominated by a cytokine storm, the excessive immune response from the uncontrolled release of a series of interleukins, chemokines, interferons, and tumour necrosis factors and the consequent hyperinflammatory state, which determines local and systemic consequences. Such a response represents a negative prognostic factor producing, at the pulmonary level, pictures of arterial and venous thrombi of small vessels and evolution towards severe and sometimes permanent pulmonary lesions (pulmonary fibrosis) [1]. In particular, vascular permeability is increased, resulting in a large amount of fluid and blood cells entering the alveoli, causing dyspnoea and even respiratory failure, desquamation

**Citation:** Traina, G. The Connection between Gut and Lung Microbiota, Mast Cells, Platelets and SARS-CoV-2 in the Elderly Patient. *Int. J. Mol. Sci.* **2022**, *23*, 14898. https://doi.org/ 10.3390/ijms232314898

Academic Editor: Maria Teresa Mascellino

Received: 24 October 2022 Accepted: 25 November 2022 Published: 28 November 2022

**Copyright:** © 2022 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

of alveolar cells and hyaline membrane formation. A mass of fluid similar to mucus accumulates in the lungs, and this accumulation is caused by an excessive immune response due to signalling molecules, in particular interleukin-(IL)-6, IL-8, and tumour necrosis factor (TNFα) [1–4]. Cytokine overproduction and cytokine storm induce clinically relevant extrapulmonary effects on various key organs such as heart, kidney, liver and intestine and dysbiosis [3]. The final stages of this very severe clinical picture can lead to multi-organ failure, with cardiovascular, gastrointestinal, haematological, respiratory, neurological and renal complications [5].
