Cytokine storm syndrome is a cascade of escalated immune responses disposing the immune system to exhaustion, which might ultimately result in organ failure and fatal respiratory distress. Infection with severe acute respiratory syndrome-coronavirus-2 can result in uncontrolled production of cytokines and eventually the development of cytokine storm syndrome. Mast cells may react to viruses in collaboration with other cells and lung autopsy findings from patients that died from the coronavirus disease that emerged in 2019 (COVID-19) showed accumulation of mast cells in the lungs that was thought to be the cause of pulmonary edema, inflammation, and thrombosis. In this review, we present evidence that a cytokine response by mast cells may initiate inappropriate antiviral immune responses and cause the development of cytokine storm syndrome. We also explore the potential of mast cell activators as adjuvants for COVID-19 vaccines and discuss the medications that target the functions of mast cells and could be of value in the treatment of COVID-19. Recognition of the cytokine storm is crucial for proper treatment of patients and preventing the release of mast cell mediators, as impeding the impacts imposed by these mediators could reduce the severity of COVID-19.

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Species of Marshallagia are abomasal parasites in free-ranging and domesticated ungulates in temperate climatic zones throughout the world. Pervasiveness of these nematodes is significant in various parts of the world. There has been limited research in the area of Marshallagi amarshalli pathogenesis. The aim of this study was to investigate the effects of M. marshalli on the acid secretory capacity of the abomasal mucosa and the morphological changes due to parasitic migration to different parts of abomasal tissue in sheep. Ten lambs, approximately around 6 months old, were allotted to two groups of five (A and B). The sheep from group A were infected orally with a dose of 5000 third-stage larvae (L3) of M. marshalli whereas the sheep of group B were not infected. The results indicated that the development of M. marshalli in the abomasal glands of ruminants causes pathophysiological changes, which include a reduced acidity of the abomasal contents, increased abomasal pH and increased serum pepsinogen concentrations. The reduced acid secretion is explained by a replacement of functional parietal cells by undifferentiated cells. Histology changes include mucosal cell hyperplasia, loss of parietal cells and inflammatory cell infiltration, which includes numerous granulocytes and lymphocytes.

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Marshallagia marshalli is found in the abomasums of sheep, goats and wild ruminants in tropical and sub tropical climates. In Iran among different species of Ostertagiinae that can infect sheep, M. marshalli is currently the major cause of parasitic gastroenteritis in ruminant. Having a donor animal is essential for various studies. In the present study we compared the efficacy of two different method of M. marshalli donor sheep production. In the first method, M. marshalli donor sheep was produced by transplanting of adult forms of this worm into abomasum of a lamb (6 months of age) through a surgically established cannula. In the second method, 5,000 infective larvae (L3) from the female M. marshalli culture were given to a worm-free lamb of 6 months age through a stomach tube. After 3 days of transplanting, few eggs of M. marshalli appeared in the cannulated lamb's faeces. The number of eggs per gram of faeces (EPG) increased in the following days. The average number of EPG reached up to 23.5 ± 11.26 per day in 2 months. In larval infected lamb by day 21 post infection the eggs were appeared in faeces. The average number of EPG reached up 53.5 ± 42.5 per day in 2 months. In comparison between cannulation and larval infected, the number of eggs laid by worms transplanted in cannulated lamb was less than that of larval infected lamb. However, the abomasal cannulation method seems more preferable due to some advantages such as defined number of worms transplanted into abomasums, rapid access to the eggs and their culture.

:  Because there appeared to be no data available on serum gastrin concentrations in animals infected with Marshallagia marshalli, and considering the high prevalence of this parasite in livestock throughout many countries, we decided to perform research in the field using experimental infection. After surgical implantation of abomasal cannula into 10 male Baluchi sheep, each animal was orally infected with 5,000 M. marshalli larvae. Serum gastrin concentrations and abomasal pH were measured with a human ELISA kit and a PHM LE438 standard pH electrode, respectively. According to the results obtained from the study, serum gastrin increased after 14 and 21 days post-infection (dpi), while abomasal pH increased after 7 dpi and reached a maximal value 16 dpi. The increase in serum gastrin concentration was revealed 6 days after elevation in abomasal pH, which could be the result of reduced acid secretion. Generally, the present study pointed out that a limited number of M. marshalli could increase serum gastrin concentrations.

Objective: To determine whether captopril could prevent spinal cord damage after induction of ischemia-reperfusion injury in rats. Materials and Methods: We randomly divided 24 adult male Wistar rats, weighing 230 - 350 g, into 4 groups (n= 6 in each group): Spinal cord ischemia-reperfusion with captopril, spinal cord ischemia-reperfusion, sham operated with captopril, and SHAM. 24 and 1.5 hours before ischemia induction, captopril was administered intragastrically (100 mg/kg) to the SHAM+Cap and the SCI-R+Cap groups. Abdominal aortic clamping was performed in the SCI-R and SCI-R+Cap groups for 40 minutes. Hindlimb motor function was evaluated using the Tarlov Scale at 4, 6, 12, 24, 48, and 60 hours after SCI. Biomarkers of oxidative stress were measured to evaluate biological responses to therapeutic interventions (MDA, FRAP and PAB assays). Results: Throughout the study period, the SCI-R group had significantly lower motor function scores than the other groups (P < 0.05). The MDA and PAB levels were higher in the SCI-R group than in the SHAM group (P < 0.05). The FRAP value was lower in the SCI-R group than that in the SHAM group (P < 0.05). The SCI-R+Cap had higher motor function scores than the SCI-R group at all time points (P < 0.05). There were no notable differences in MDA concentration, FRAP and PAB values between the SCI-R+Cap and the SCI-R groups (P > 0.05). Conclusion: Captopril may act as a protective agent against spinal cord ischemia-reperfusion injury in rats based on hind limb motor function assessment.