COVID-19 in Northeast Bosnia and Herzegovina and patient's length of hospitalization.

BACKGROUND: Since the outbreak of COVID-19 pandemic, clinical data from various parts of the world have been reported. Up till now, there has been no clinical data with regards to COVID-19 from Bosnia and Herzegovina (B&H). The aim was to report on the first cohort of patients from B&H and to analyze factors that influence COVID-19 patient's length of hospitalization (LOH). METHODS: This retrospective cohort study was conducted at Tuzla University Clinical Center (UKC), B&H. It involved 25 COVID-19 positive patients that needed hospitalisation between March 28th and April 27th 2020. The LOH was measured from the time of admission to discharge. Factors analyzed induced age, BMI, presence of known comorbidities, serum creatinine and O2 saturation upon admission. RESULTS: The mean age was 52.92 ± 19.15 years and BMI 28.80 ± 4.22. LOH for patients with BMI < 25 was 9 ± SE2.646 days (CI 95% 3.814-14.816) vs 14.182 ± SE .937 (CI 95% 12.346-16.018 p < 0.05; HR 5.148 CI95% 1.217 to 21.772 p = 0.026) for ≥25 BMI. The mean LOH of patients with normal levels of O2 ≥ 95% was 11.667 ± SE1.202 (CI95% 8.261 to 13.739; p = 0.046), while LOH for patients with < 95% was 14.625 ± SE 1.231 CI95% 12.184 to 16.757 p = 0.042; HR 3.732 CI95%1.137-12.251 p = 0.03). Patients without known comorbidities had a mean LOH of 11.700 ± SE1.075 (CI 95% 9.592-13.808), while those with comorbidities had a mean of 14.8 ± 1.303 (CI 95% 12.247-17.353; p = 0.029) with HR2.552. CONCLUSION: LOH varied among COVID-19 patients and was prolonged when analyzed for BMI ≥25, comorbidities, elevated creatinine, and O2 saturation < 95%. Furthermore, risk factors for COVID-19 patients in B&H do not deviate from those reported in other countries.

A Novel CD206 Targeting Peptide Inhibits Bleomycin Induced Pulmonary Fibrosis in Mice.

Activated M2 polarized macrophages are drivers of pulmonary fibrosis in several clinical scenarios such as Acute Respiratory Disease Syndrome (ARDS) and Idiopathic Pulmonary Fibrosis (IPF), through the production of inflammatory and fibrosis-inducing cytokines. In this study, we investigated the effect of targeting the CD206 receptor with a novel fragment of a Host Defense Peptide (HDP), RP-832c to decrease cytokines that cause fibrosis. RP-832c selectively binds to CD206 on M2 polarized bone marrow derived macrophages (BMDM) in vitro , resulting in a time-dependent decrease in CD206 expression, and a transient increase in M1 marker TNFα, which resolves over a 24hr period. To elucidate the antifibrotic effect of RP-832c, we used a murine model of bleomycin (BLM) -induced early-stage pulmonary fibrosis. RP-832c significantly reduced bleomycin-induced fibrosis in a dosage dependent manner, as well as decreased CD206, TGF-ß1 and α-SMA expression in mouse lungs. Interestingly we did not observe any changes in the resident alveolar macrophage marker CD170 expression. Similarly, in an established model of lung fibrosis, RP-832c significantly decreased fibrosis in the lung, as well as significantly decreased inflammatory cytokines TNFα, IL-6, IL-10, INF-γ, CXCL1/2, and fibrosis markers TGF-ß1 and MMP-13. In comparison with FDA approved drugs, Nintedanib and Pirfenidone, RP-832c exhibited a similar reduction in fibrosis compared to Pirfenidone, and to a greater extent than Nintedanib, with no apparent toxicities observed on body weight or blood chemistry. In summary, RP-832c is a potential agent to mitigate the overactivity of M2 macrophages in pathogenesis several pulmonary fibrotic diseases, including SARS-CoV-2 induced lung fibrosis.