Highlights The disruption of the host immune system is the characteristic of the outbreak of COVID-19. Identifying the regulating mechanism of virus behavior will help design antiviral vaccine candidates. SARS-CoV-2 vaccines is critical to reduce morbidity and mortality.

A global pandemic has erupted as a result of the new brand coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This pandemic has been consociated with widespread mortality worldwide. The antiviral immune response is an imperative factor in confronting the recent coronavirus disease 2019 (COVID-19) infections. Meantime, cytokines recognize as crucial components in guiding the appropriate immune pathways in the restraining and eradication of the virus. Moreover, SARS-CoV-2 can induce uncontrolled inflammatory responses characterized by hyper-inflammatory cytokine production, which causes cytokine storm and acute respiratory distress syndrome (ARDS). As excessive inflammatory responses are contributed to the severe stage of the COVID-19 disease, therefore, the pro-inflammatory cytokines are regarded as the Achilles heel during COVID-19 infection. Among these cytokines, interleukin (IL-) 1 family cytokines (IL-1, IL-18, IL-33, IL-36, IL-37, and IL-38) appear to have a strong inflammatory role in severe COVID-19. Hence, understanding the underlying inflammatory mechanism of these cytokines during infection is critical for reducing the symptoms and severity of the disease. Here, the possible mechanisms and pathways involved in inflammatory immune responses are discussed.

Sepsis is a complex disease that begins with an infectious disorder and causes excessive immune responses. Curcumin is considered as an active component of turmeric that can improve the condition in sepsis due to its anti‐inflammatory and antioxidant properties. PubMed, Embase, Google Scholar, Web of Science, and Scopus databases were searched. Searching was not limited to a specific publication period. Only English‐language original articles, which had examined the effect of curcumin on sepsis, were included. At first, 1,098 articles were totally found, and 209 articles were selected after excluding duplicated data; 46 articles were remained due to the curcumin effects on sepsis. These included 23 in vitro studies and 23 animal studies. Our results showed that curcumin and various analogs of curcumin can have an inhibitory effect on sepsis‐induced complications. Curcumin has the ability to inhibit the inflammatory, oxidative coagulation factors, and regulation of immune responses in sepsis. Despite the promising evidence of the therapeutic effects of curcumin on the sepsis complication, further studies seem necessary to investigate its effect and possible mechanisms of action in human studies.

Lung cancer (LC) is the second common cancer for both women and men all over the world. Unfortunately, the number of LC deaths is increasing rapidly each year so early diagnosis of LC can be lifesaving. MicroRNAs are involved in multiple processes, such as cell differentiation, transcription, inflammation, proliferation, cell signaling, and apoptosis. In LC, microRNAs function as tumor suppressors (TS) or oncogenes depending on the targets. Changes in microRNAs expression level are related to tumor initiation, progression, and metastasis. MicroRNAs can regulate gene expression and thus affect the activity status of different signaling pathways including AKT, JAK-STAT, MAPK, TGF-β, WNT, and ERK signaling pathways. Positive or negative effects on drug resistance of LC are directly affected by microRNAs and their target genes. MicroRNAs can be beneficial in combination therapy with other drugs and chemotherapeutic agents for LC. K E Y W O R D S drug resistance, lung cancer, microRNA, signaling pathways, tumor suppressor How to cite this article: Asghariazar V, Sakhinia E, Mansoori B, Mohammadi A, Baradaran B. Tumor suppressor microRNAs in lung cancer: An insight to signaling pathways and drug resistance.

Sepsis is a severe reaction and an excessive immune response to infection, which can lead to organ dysfunction and death.

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.

The current outbreak of coronavirus disease has led to creating a public health emergency conditions since 2019. COVID-19, which is caused by SARS-CoV-2, is spread via human-to-human transmission by direct contact or droplets. Through conducting this study, we were looking for detecting SARS-CoV-2 in wastewater produced in Iran country (Ardabil, Nir, Khalkhal, and Kowsar) (wastewater collection network, wastewater treatment plant, and hospital wastewater). In this research, samples (n=76) were collected from influent and effluent of municipal and hospital wastewater treatment plants, and some samples were also collected from Ardabil municipal wastewater manholes. The sampling duration included the white (lower risk of COVID-19) and red (high risk of COVID-19) conditions. Samples were stored at −20°C for further diagnostic tests. The specific primer and probe real-time reverse transcriptasepolymerase chain reaction (real-time PCR) targeting ORF1ab and N genes (nucleoprotein gene) were applied to detect viral genomes of the SARS-CoV-2 virus in the wastewater samples. Out of 76 samples, a total of 15 samples (19.73%) collected from wastewater in Ardabil province (Ardabil, Nir, Khalkhal, and Kowsar), were positive in terms of SARS-CoV-2. Wastewater epidemiology can facilitate detection of the incidence of pathogens through metropolises, measurement of population prevalence without direct testing, and provision of information to the public health system about the efficiency of intervening efforts.

COVID-19 is a systematic disease that frequently implies neurological and non-neurological manifestations, predominantly by inducing hypoxia. Brain-derived neurotrophic factor (BDNF) is a key factor in regulating functions of nervous and respiratory systems and has been strongly related to hypoxia. Therefore, this study planned to investigate BDNF association with the COVID-19 manifestations especially neurological impairments and the infection-induced hypoxia. We enrolled sixty-four COVID-19 patients and twenty-four healthy individuals in this study. Patients were divided into two groups, with and without neurological manifestations, and their serum BDNF levels were measured by enzyme-linked immunosorbent assay (ELISA). COVID-19 patients had significantly lower BDNF levels than healthy individuals ( p = 0.023). BDNF levels were significantly lower in patients with neurological manifestations compared to healthy individuals ( p = 0.010). However, we did not observe a statistically significant difference in BDNF levels between patients with and without neurological manifestations ( p = 0.175). BDNF’s levels were significantly lower in patients with CNS manifestations ( p = 0.039) and higher in patients with fever ( p = 0.03) and dyspnea ( p = 0.006). Secondly, BDNF levels have a significant negative association with oxygen therapy requirement ( p = 0.015). These results strongly suggest the critical association between dysregulated BDNF and hypoxia in promoting COVID-19 manifestations, particularly neurological impairments. Supplementary Information The online version contains supplementary material available at 10.1007/s12031-022-02039-1.