Among all patients with allergic diseases, 300 million people suffers from bronchial asthma. The pathoimmune mechanisms of asthma has to be studied, particularly at the gene-molecular level [1].A large epidemiological study -The World Health Organisation, conducted on behalf of the WHO in 70 countries (out of 192), showed that the prevalence of diagnosed asthma in adults is 4.3%, ranging from 0.2% in China to 21% in Australia. Atopic pathology has acquired the status of a significant socioeconomic, medical problem for mankind. Complex mechanisms of anaphylaxis attract the attention of the scientific community [2,3].The literature describes the association between low-grade inflammation and obesity-associated bronchial asthma [4].Low-grade chronic inflammation present in advanced age and chronic diseases-but not in bronchial asthma-produces a pro-inflammatory state that triggers a dysregulated immune response, favoring development of severe forms of COVID-19 and increasing lethality. In asthma, chronic eosinophilic inflammation protects against infection by producing a reduced interferonmediated response and a reduced number of ACE2 receptors [5].The presence of low-grade inflammation correlates with the severity of respiratory disorders in bronchial asthma. According to a study by Vanessa