Leishmaniasis is a zoonotic and vector-borne infectious disease that is caused by the genus Leishmania belonging to the trypanosomatid family. The protozoan parasite has a digenetic life cycle involving a mammalian host and an insect vector. Leishmaniasisis is a worldwide public health problem falling under the neglected tropical disease category, with over 90 endemic countries, and approximately 1 million new cases and 20,000 deaths annually. Leishmania infection can progress toward the development of species–specific pathologic disorders, ranging in severity from self-healing cutaneous lesions to disseminating muco-cutaneous and fatal visceral manifestations. The severity and the outcome of leishmaniasis is determined by the parasite’s antigenic epitope characteristics, the vector physiology, and most importantly, the immune response and immune status of the host. This review examines the nature of host–pathogen interaction in leishmaniasis, innate and adaptive immune responses, and various strategies that have been employed for vaccine development.

Although only 0.8–1% of SARS-CoV-2 infections are in the 0–9 age-group, pneumonia is still the leading cause of infant mortality globally. Antibodies specifically directed against SARS-CoV-2 spike protein (S) are produced during severe COVID-19 manifestations. Following vaccination, specific antibodies are also detected in the milk of breastfeeding mothers. Since antibody binding to viral antigens can trigger activation of the complement classical - pathway, we investigated antibody-dependent complement activation by anti-S immunoglobulins (Igs) present in breast milk following SARS-CoV-2 vaccination. This was in view of the fact that complement could play a fundamentally protective role against SARS-CoV-2 infection in newborns. Thus, 22 vaccinated, lactating healthcare and school workers were enrolled, and a sample of serum and milk was collected from each woman. We first tested for the presence of anti-S IgG and IgA in serum and milk of breastfeeding women by ELISA. We then measured the concentration of the first subcomponents of the three complement pathways (i.e., C1q, MBL, and C3) and the ability of anti-S Igs detected in milk to activate the complement in vitro. The current study demonstrated that vaccinated mothers have anti-S IgG in serum as well as in breast milk, which is capable of activating complement and may confer a protective benefit to breastfed newborns.

Background: Properdin and factor H (FH), the two regulatory proteins of the alternative complement pathway, oppose each other to maintain the complement system’s activation. While properdin upregulates, FH downregulates the complement alternative pathway. The current study evaluated the expression of properdin and FH transcripts and proteins in the placental tissues and umbilical cords (UC) of preeclampsia (PE), gestational diabetes mellitus (GDM), and recurrent pregnancy loss (RPL) compared to normal healthy pregnancy (N). Methods: The tissue histology of PE, GDM and RPL were observed using haematoxylin-eosin and Masson’s trichrome staining. To understand the expression and distribution of properdin and FH, RT-qPCR, western blot, and immunohistochemistry were carried out. The expressions of two additional complement components, C3 and C5, were also detected by western blot. Results: The placentae from PE and GDM showed substantial collagen and fibrinoid deposition, thicker foetal blood capillaries, and a considerable number of syncytial knots. There was a significant rise in the level of properdin and significant decline in the level of FH at both mRNA and protein levels in the placentae and umbilical cord of PE compared to N; in GDM placentae, both properdin and FH were significantly elevated compared to N. In the case of RPL placentae, similar to PE, properdin expression was high while FH expression level was low. In both PE and RPL placentae, C3 and C5 levels were high, suggesting possibility of overactivation of complement proteins in the placenta. Discussion: The observed elevated properdin level can contribute to the heightened inflammatory response in PE, GDM and RPL placentae. Low FH and high C3 and C5 in the placenta possibly suggests dysregulated complement activation in PE and RPL.

Cleome genus is commonly known as spider flower plant or cat’s whiskers, and is the largest genus of the family Cleomaceae, with around 200 species containing a range of remedial applications. Several species of Cleome genus show anti-cancer properties, however, nothing has been reported with genus spinosa, an anti-inflammatory and immunomodulatory plant. Thus, the present study examined the likely anti-cancer property of ethanolic leaf extract of Cleome spinosa (CSE) in Ehrlich ascites carcinoma (EAC) cells in vitro and in vivo. CSE treatment in vitro significantly caused higher percentage of death in EAC in a dose dependent manner compared to control groups (untreated and ethanol treated). Bright field, fluorescence and electron microscopies revealed apoptotic changes such as surface blebbings, nuclear fragmentation, chromatin condensation and apoptotic body formation, which probably could be the cause of death in EAC cells with CSE treatment. Apoptosis of CSE-treated EAC cells appeared to be mediated through upregulation of pro-apoptotic protein p53 and downregulation of anti-apoptotic protein, Bcl-xL expression, as ascertained through western blot both in vitro and in vivo. CSE was protective toward murine splenocytes by scavenging free radicals; it also reduced the ascitic tumor burden and increased the survival of the tumor-bearing mice compared to the control. Gas Chromatography-Mass Spectrometry (GCMS) analysis identified 43 phytocompounds in CSE. In silico molecular docking analysis indicated that a number of bioactive compounds, such as cycloartenol, stigmasterol, clionasterol, beta-sitosterol, lupenone, and sitostenone that were abundant in the CSE extract, exhibited strong binding affinities for the key apoptosis-regulating proteins, p53 and Bcl-xL. Thus, CSE derived-compounds appear to act as natural antioxidants, and have anti-cancer properties via induction of apoptosis in EAC possibly through upregulation of p53 and downregulation of Bcl-xL proteins in murine model. Hence, CSE could be considered as a promising natural compound for future cancer therapies.