فهرست مطالب h .mojiri forushani

Opportunistic fungal infections following COVID-19 is problematic. Antifungal medications are as well used to treat people who have fungal infections. The aim of the present study was to evaluate the prevalence of fungal infections and the usage of antifungal medications before and after the COVID-19 pandemic.

The present descriptive, analytical, and retrospective study was conducted in 2021.The records of patients who were hospitalized in Abadan hospitals in the year before or the first two years of the COVID-19 pandemic and received at least one of the antifungal medication’s fluconazole, caspofungin, or amphotericin B were extracted and assessed for the present study. Demographic information of patients, type of ward, and type of fungal infection, history of previous infection with covid-19 and severity of disease were extracted from patient files. Descriptive analysis, chi-square, and ANOVA statistics were used to analysis the data.

The results indicated that the mucormycosis and aspergillus fungal infections had dramatically increased in the two years since the COVID-19 pandemic initiated. Although it was not statistically significant, the usage of antifungal medications rose in the two years following the beginning of COVID-19 compared to the prior two years. The mucormycosis fungus was the most prevalent fungal infection. The lung was the most commonly infected organ. All patients with fungal infection had a history of severe COVID-19 following the COVID-19 pandemic. The most often used medication was amphotericin B. This difference was substantial (P< 0.001) when aspergillosis patients received capsofungin, mucormycosis patients received amphotericin B, and candida patients received fluconazole.

The present indicated that aspergillosis and mucormycosis fungal infections were more common during the COVID-19 pandemic, and as a result, antifungal medication use has increased as well. Additionally, all three medications (fluconazole, caspofungin, and amphotericin B) were administrated according guidelines.

Inflammation is a protective physiologic response against pathogens, trauma and injury (1, 2). Inflammation pathway are different in human body and some main pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α have key role in pathogenesis of inflammation (3). Current anti-inflammatory drugs including corticosteroids and non-steroid anti-inflammatory drugs have serious side effects (6), so, research on new compounds with anti-inflammatory property is necessary. Astaxanthin is a natural carotenoid with various pharmacological effects. Haematococcus Algae is one of the marine sources of astaxanthin. Anti-inflammatory and antioxidant effects of astaxanthin were reported in previous studies (8-10), but the molecular mechanism of the anti-inflammatory effect of astaxanthin on the peripheral cells of the immune system is not clear. The aim of this study was to evaluate anti-inflammatory effects of astaxanthin on TLR4 gene expression and secretion of key inflammatory cytokines including IL-1, IL-6, and TNFα in RAW264.7 macrophage cells.

Methods and Material: 

The RAW264.7 macrophage cells was used in this study. Astaxanthin was extracted from Haematococcus Algae, then different doses of 25, 50, 100 μM of astaxanthin were used to treat the cells. Cells divided to three groups: one group received LPS (1µg/ml), Treatment group received LPS (1µg/ml) in combination to different dose of astaxanthin (25, 50, 100 μM) and control group without LPS astaxanthin. After 24 hour incubation, cell viability was assay with MMT test.TLR4 gene expression was measured by RT-PCR at 24 and 48 hours after induction with LPS. β-actin was considered as housekeeping gene. The levels of IL-1β, IL-6, and TNFα cytokines were measured with a commercial sandwich ELISA kit. The optic absorbance was read at 45 nm. Descriptive statistics and one-way ANOVA test were used to analyze the data. To analysis the fold change of gene expression, formula 2 -ΔΔCT   was used.

None of different doses of astaxanthin (25, 50, 100 μM) and LPS (1µg/ml) had no toxicity effect on macrophages cell. (P>0.05). LPS increased TLR 4 gene expression at both 24 and 48 hours after induction, (P <0.001) in compare to control group.