The results revealed that the serum levels of IL-29 were not different between patients and controls. Due to the fact that the hospitalized SARS-CoV-2 infected patients suffer from pro-inflammatory reactions, and based on the fact that IL-29, as a pro-inflammatory cytokine, did not alter in the patients, hence it may be concluded that inflammation in the hospitalized SARS-CoV-2 infected patients is independent of IL-29. However, based on the fact that a main source of IL-29 is the epithelial cells [14], and SARS-CoV-2 infected the ells, so it may be hypothesized that local production of IL-29 participates in the defense against SARS-CoV-2, which is not associated with its elevated serum levels. Thus, it seems that evaluation of the local levels of IL-29 can be useful to understand the roles played by IL-29 against SARS-CoV-2 and its pathogenesis. In parallel with our results, Fallah Vastani et al., reported that serum levels of IL-29 were not changed between the SARS-CoV-2 infected patients with mild and severe symptoms [15]. The results demonstrated that IL-29 does not participate in the induction of inflammation in the SARS-CoV-2 patients. However, they reported that IL-29 levels were significantly higher in recovered patients when compared to the dead patients [15]. The protective roles played by IL-29 against viral infection of respiratory epithelial cells have been reported by Wang and colleagues [16]. Accordingly, they demonstrated interaction of IL-29 with alveolar type II epithelial cells leads to induction of antiviral genes, such as IFN-stimulated gene 56 (ISG56), myxovirus resistance protein 1,2'-5'-oligoadenylate synthetase 1 [16]. Thus, it appears that IL-29 may be considered as an important local molecule against SARS-CoV-2. In agreement with our hypothesis, a review article by and colleagues revealed that IL-29 participates in protection of epithelial surfaces barriers against viral infections without generating systemic immune system activation [17]. Our results also demonstrated that IL-29 did not increase systematically in the hospitalized SARS-CoV-2 infected patients.
The results also demonstrated that miR185-5p was decreased in the patients when compared to healthy controls, but it was not statistically significant. A study by Martínez-Fleta et al., demonstrated that plasma levels of miR185-5p were decreased in the severe in comparison to the mild patients [18]. Nicoletti and colleagues also revealed that serum levels of miR185-5p significantly decreased in the SARS-CoV-2 infected patients with severe when compared to the mild symptoms [19]. Additionally, it has been documented that miR185-5p plays anti-inflammatory roles in the resident macrophages [12]. Our results also demonstrated that, men patients had lower levels of miR185-5p than women. Thus, gender may be considered as an important factor to expression of the miR. However, Grehl et al., reported that serum levels of miR185-5p were significantly increased in the severe COVID-9 patients when compared to the mild patients [20]. Due to the controversy, it appears that more investigations regarding the roles played by miR185-5p in the COVID-19 needs to be done to clear the main pro-inflammatory mechanisms.