The eicosanoid family includes prostanoids, leukotrienes, and other oxygenated derivatives. Prostanoids are a major class of the eicosanoid family derived from metabolism of arachidonic acid by the action of cyclooxygenase enzymes (COX). They are further subdivided into three main groups: prostaglandins (PGs), thromboxanes (TXs), and prostacyclins. PGs were first discovered as uterotonic substances in human seminal fluid in 1930. In the late 1950s to mid-1960s, their structures were studied and identified as being derived from unsaturated fatty acids. Prostanoids are produced by many cell types such as vascular endothelium, leukocytes, and the pathogens themselves. Prostanoid production is controlled by expression of different enzymes engaged in prostanoid biosynthesis, and by the distribution of different specific prostanoid synthases within those cells that determine their effect on the immune system. The production of prostanoids differs from one cell type to another; for example, dendritic cells predominately produce PG E 2 (PGE 2 ) and TXA 2 , whereas mastocytes produce PGD 2 . All inflammatory cells, including monocytes/macrophages, and neutrophils, are the main source of COX metabolites. Produced in response to various physiological and pathological stimuli, PGs are noted as key participants in autoimmune immunopathology, infectious diseases, and cancer. Other reports have shown that PGIs are formed by endothelial and smooth muscle cells, and TXAs are formed by platelets and lungs; PGI 2 and some other PGs are produced by interactions between cells using enzymes in adjacent cells; for example, platelet-produced PGH 2 is converted to PGI 2 in the vascular epithelium. PGs secreted in the saliva of blood-sucking arthropods increase local blood flow and maintain the supply for feeding; they were also reported to increase immune suppression, allowing prolongation of attachment by ticks. Progressive studies demonstrated that, besides insects, pathogenic fungi, protozoa, and parasitic worms produce PGs. This review focuses on induced efforts to study prostanoids and their relation to different parasitic diseases. Abbreviations AA: Arachidonic acid; COXs: Cyclooxygenase enzymes; CyPG: Cyclopentanone; DC: Dendritic cell; GST: Glutathione-S-transferase; GA: Glycyrrhizic acid; MAP: Mitogen-activated protein; MIF: Macrophage migration inhibitory factor; NO: Nitric oxide; PBMC: Peripheral blood mononuclear cells; PG: Prostaglandin; PG12: Prostacyclin; PGE2: Prostaglandin E2; PL: Phospholipase; PPAR: Peroxisome proliferator-activated receptors; TGF: Transforming growth factor; TNF: Tumor necrosis factor; TP: Thromboxan receptor; TX: Thromboxane.

Trichomoniasis is most common sexually transmitted disease caused by T. vaginalis. The clinical manifestation varies from severe manifestation to asymptomatic condition. However, the exact virulence markers led to varied symptomatology was not well clarified. The role of leukotriene B4 (LTB4) in the pathogenesis of many parasitic diseases has been reported. The present study reports the leukotriene B4 levels on different days post infection (3rd, 7th, 14th, 21st and 28th d.p.i.) in serum and vaginal washes (VWs) and vaginal tissues of mice infected intravaginally with T. vaginalis isolates from 10 symptomatic and 10 asymptomatic women. A significant increase in LTB4 was observed on the 3rd to 28th d.p.i. in serum and VWs of mice infected with T. vaginalis isolates from asymptomatic as compared to symptomatic women. The present study also reports the histopathological changes of the posterior vaginal fornix’s and upper portion of the vagina of mice infected intravaginally with T. vaginalis isolates from 10 symptomatic and 10 asymptomatic women. The results show that there are no significant differences between symptomatic and asymptomatic isolates regarding histopathological changes.

BackgroundDientamoeba fragilis was considered as a commensal amoeba that inhabits the large intestine. Later, its association with irritable bowel syndrome drew attention to its pathogenicity. Metronidazole (MTZ) is the most recommended drug for treatment of D. fragilis and other pathogenic intestinal protozoa. Many studies reported that it is not suitable for children because of its mutagenicity and carcinogenic potential. However, still more work is needed to establish new, effective, and safe therapeutic agents against D. fragilis.Aim of the workThe present study aimed at evaluating the effect of different doses of the aqueous extract of Nigella sativa on D. fragilis in experimentally infected mice in comparison with MTZ as a standard drug.Materials and methodsIsolates of D. fragilis were obtained from patients complaining of acute/chronic intermittent diarrhea or diarrhea alternating with constipation with/without abdominal pain. Histopathological examination of cecal tissue of experimentally infected and treated mice with three different doses of N. sativa (125, 250, and 500 mg/kg/day) was compared with that of mice infected and treated by two doses of MTZ (62.5 and 125 mg/kg/day) as the standard treatment. Infected untreated mice were used as the control group.ResultsHistopathological examination of cecal tissue of the infected untreated group showed different degrees of pathological changes, which completely disappeared with the highest N. sativa dose (500 mg/kg). Concentrations below 500 mg/kg produced less severe pathological changes than in untreated animals. N. sativa in high dose significantly prevented cytopathic effect in mice 1 day after infection and for five consecutive days.ConclusionN. sativa has a potential therapeutic effect against D. fragilis infection in an experimental in vivo study. We recommend double-blind controlled clinical trials in humans to assess the use of N. sativa in management of human D. fragilis infection.

Objective: To establish molecular characterization of Plasmodium falciparum field isolates in Jazan Area of Saudi Arabia measured with highly polymorphic genetic marker, i.e. the merozoite surface protein 2 (MSP 2). Methods: Blood samples were collected from 128 clinically suspected patients attending both Jazan and Sabia hospitals, Kingdom of Saudi Arabia. Both hospitals reflected urban and rural settings respectively. Analysis of central polymorphic region of MSP 2 (3D7 and FC27 allelic families) was performed using nested PCR for malaria patients. Results: For MSP 2 allelic families of Plasmodium falciparum, 16 cases (53.3%) carried FC27 type and 14 cases (46.7%) carried 3D7 type, whereas no malaria cases harbored both allelic types. The present study showed that in urban area, 80% of FC27 fragments were 500 bp while in rural area it was 45.5% (P = 0.08). The FC27 400 bp allele was more prevalent in patients from rural than those from the urban area (P = 0.08). The most prevalent infecting 3D7 allele was the 3D7 300 bp in both areas. In the present study, there were no multiple infections. Conclusions: The limited genetic diversity which was observed in Jazan (considered as an endemic area) may be attributed to the small sample size or sustained malaria control program.

Background: Malaria is one of the main causes of mortality in tropical zone.Specific immune responses are induced by parasite, including the release of cytokines from peripheral blood mononuclear cells.Sickle cell trait confers a high degree of resistance to severe and complicated malaria.The present study aims to assess immunological response of P. falciparum infection by measuring of total IgG level and IL-6, IL-12 & IL-18 levels for P. falciparum among Saudi Arabian patients with and without sickle-cell trait.Patients and Methods: Thirty patients who had clinical suspicion of malaria and sickle-cell trait attending Jazan general hospital in KSA were included in the study.Malaria patients with sickle-cell trait will be matched with a control (thirty patients diagnosed to have malaria but without sickle-cell trait).Diagnosis of malaria was done by Immunochromatography strip and blood film.Diagnosis of Sickle-cell trait was done by hemoglobin electrophoresis assessment of total IgG titre and Interleukin 6, 12, 18 levels using ELIZA.Results: Cytokines and IgG in uncomplicated clinical malaria (n = 22) and severe malaria (n = 7) were IL6 (83.1 pg/mL) versus (75.2 pg/mL), IL12 (19.4 pg/mL) versus (16.3 pg/mL), IL18 (22.45 pg/mL) versus (24.2 pg/mL) and IgG (13.3 SD) versus (4.5 SD).Differences in the IL6, IL12 and IgG were statistically significant (p value >0.02, >0.004 & >0.002 respectively).Among malaria patients with sickle cell trait, Cytokines and IgG in asymptomatic (n = 19) and uncomplicated clinical malaria (n = 11) were IL6 (88.9 pg/mL) versus (79.2 pg/mL), IL12 (24 pg/mL) versus (22.9 pg/mL), IL18 (24.2 pg/mL) versus (31.2 pg/mL) and IgG (27 SD) versus (7.35 SD).Differences in IgG were statistically significant (p value ≥ 0.003).Serum IL6 levels were higher in patients with uncomplicated clinical malaria without sickle cell trait (median 83.1 ± 5.1 pg/mL) than in patients with uncomplicated clinical malaria with sickle cell trait (medians 79.2 ± 4.5 pg/mL).This difference was statistically significant (p value = 0.003).Serum IgG levels were higher in patients with uncomplicated clinical malaria without sickle cell trait (median 13.3 ± 10.84) than in patients with uncomplicated clinical malaria with sickle cell trait (medians 7.35 ± 2.95) while in asymptomatic malaria and severe malaria, medians (27 ± 11.13 versus 4.5 ± 2.75).This difference was statistically highly significant (p value = 0.0009).Conclusion: Malaria protection by HbAS involves the enhancement of not only innate but also of acquired immunity to the parasite.Cytokins (IL6, IL12) and IgG play an important role in protection against severe malaria.The presence of HbAS is associated with increased acquired immunity to malaria.Further work will be done to work out how this change in immunity occurs but treatment of anyone with malaria, whatever their sickle cell status, is essential.

The genotyping of cryptosporidium clinical isolates obtained from 36 gastrointestinal symptomatic patients were identified by nested PCR for amplification of 18S rRNA followed by RFLP analysis using Ssp1 and Vsp1, and then pathological changes between different cryptosporidium genotypes were evaluated in experimentally infected mice. Cryptosporidium genotypes (C. parvum, C. hominis & C. melegridies) were detected (66.7%, 27.7% & 5.6%) respectively in human isolates. Different degrees of pathological changes were found among infected mice by different Cryptosporidium genotypes. Moderate and severe degrees of pathological changes with infection score ranging from 2 to 4 were found in all infected mice with C. parvum (except one isolate), while mild degree of pathological changes with infection score of 2 was found in all mice with C. melegridies. The results showed statistically significant relation between genotype and pathological degrees. There were no differences in the average number of oocysts per smear in Group II and Group III while in Group I, there was no oocysts shedding.

A total of 180 children of age group 5-12 years old in both sexes, of whom 90 were symptomatic and negative for other parasites, rotavirus or pathogenic bacteria. Another 90 children were asymptomatic, but with B. hominis in stools. Direct smear, formaline-ethyl acetate sedimentation concentration, kinyon carbol-fuchin stain, stool culture, enzyme immunoassay, culturing, morphometric study, gel electrophoresis and experimental infection of mice were done. The results showed that the central body cysts (CB), granular and multivacuolar forms isolated from symptomatic patients were larger than those from asymptomatic ones. The CB form was common compared to other forms and isolated from 104 cases. B. hominis infection was prevalent among males rather than females (60.5% versus 39.5%). The clinical data showed that diarrhea was the most common symptom (58.9%). The infection intensity had a direct relation with illness duration. The polyacrylamide gel electrophoresis showed that isolates from symptomatic and asymptomatic patients ranged between 24-130 kDa. All isolates showed similar banding patterns. Only minor differences was in low MW (30, 50 kDa) and in high MW (118 kDa) in samples from symptomatic patients. The histopathological examination of caecum, colon and small intestine of B. hominis mice infected from symptommatic patients showed infiltration with inflammatory cells and tissue invasion by the parasite.

The effect of exogenous nitric oxide (NO) on growth, viability and ultra-structural of B. hominis was assessed in vitro by sodium nitrite (NaNO2) in 0.6 mM, 0.8 mM & 1 mM concentrations. The viability of B. hominis was identified using neutral red stain. The role of NO as an endogenous oxidant was assessed by identifying its level in cecum tissue, ileum tissue, blood and stool elutes of mice infected with B. hominis symptomatic human isolates using reactive nitrogen assay compared to control. In vitro study revealed that NaNO2 inhibited the growth and decreased viability of B. hominis with minimal lethal concentra-tion dose 1 mM on the 4th day while, minimal effects were detected with 0.6 and 0.8 mM. Transmission electron microscopy study proved that apoptotic-like features were observed in growing axenic culture of B. hominis upon exposure to NaNO2. These changes were not only found on the vacuolar (central body) form but also they were detected on granular, multi-vacuolar and cyst forms. In vivo study proved that high levels of NO were found in infected mice compared to low changes in control group. The high levels were in cecum tissue particularly. The mean levels of NO among infected mice were 211.8 +/- 20.7 microM in cecum, 90.4 +/- 11.6 microM in ileum, 60.1 +/- 4.7 microM in blood and 63.6 +/- 7.3 microM in stool elutes while, the mean levels of NO in control mice were 70.2 +/- 3.1 in cecum, 67.8 +/- 4.7 microM in ileum, 30.9 +/- 4.2 microM in blood and 28.1 +/- 2.9 microM in stool elutes. The differences were statistically highly significant. NO-donor drugs proved useful in treatment and increase the host resistance to B. hominis.

The effect of exogenous administration of antioxidant (Anttox) on the course of B. hominis in experimentally infected mice was studied. B. hominis isolates were obtained from 10 gastrointestinal symptomatic adult patients. Three groups of 30 infected mice (3/isolate) were used. GI was untreated infected, GII was treated by antox for 4 weeks after infection diagnosis (treatment strategy), and GIII antox treated by for 4 weeks before infection (prophylactic strategy). Mild pathological changes were detected on 13.4%, 19.9% & 86.8% of mice in Gs I, II & III, respectively. Moderate pathological changes were found in 29.9%, 26.6% & 6.6% of mice in Gs I, II & III, respectively. While, the majority of severe pathological changes were in Gs I & II (56.7% & 53.5%) as compared to GIII (6.6%). Meanwhile, 86.8% of mice in GIII had B. hominis forms > 10/high power field compared to 3.3% in Gs I & II, respectively. Although 19.8% of mice in GII were positive for B. hominis by direct smear, no growth resulted in vitro and all the forms were non-viable by using neutral red stain. All the differences were statistically significant. So, antioxidant exacerbated B. hominis intensity but it decreased the pathological changes.