Theileria orientalis, long considered a benign haemoprotozoan, is now recognised as an emerging pathogen causing clinical theileriosis in cattle across the globe. This study investigated the clinical presentation and immunopathological responses associated with natural T. orientalis infections in northern Kerala, India. Blood samples were collected from clinically suspected (n = 52) and healthy cattle (n = 148). Infection was confirmed via Giemsa-stained blood smear examination, species-specific PCR targeting the major piroplasm surface protein (MPSP) gene, and subsequent sequencing. Among clinically suspected cases, 63.5% were smear-positive and PCR-confirmed, while subclinical infection was identified in 46.6% of healthy cattle. Morphological analysis revealed marked polymorphism of intraerythrocytic piroplasms. Clinical signs included anaemia, pyrexia, lymphadenopathy, and systemic debilitation. To elucidate host immune responses, expression levels of key pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) were quantified in peripheral blood mononuclear cells using SYBR Green-based quantitative real-time PCR. Clinically affected animals exhibited significantly elevated expression of IL-6 and IL-1β (p < 0.05), indicative of a heightened inflammatory response, whereas TNF-α expression showed a non-significant downward trend. Correlation analysis revealed that parasite burden was positively associated with IL-6 and IL-1β expression but not with TNF-α, linking parasite load to the inflammatory response. The suppressed TNF-α response suggests a possible immune evasion strategy unique to T. orientalis, contrasting with the elevated TNF-α typically seen in T. annulata and T. parva infections. These findings indicate that IL-6 and IL-1β may serve as potential biomarkers of severe oriental theileriosis. These findings provide new insights into the immunopathogenesis of oriental theileriosis and suggest that cytokine dysregulation contributes to clinical disease severity. Furthermore, the high prevalence of subclinical infections underscores the role of carrier animals in sustaining transmission cycles, complicating disease control efforts in endemic regions. This study highlights the need for improved diagnostic strategies and targeted immunomodulatory interventions in managing T. orientalis infections.

Lymphatic filariasis results in chronic edema, pain, elephantiasis and disfigurement in humans. It was previously reported that platelet aggregation is inhibited in lymphatic filariasis patients, compared to healthy controls. However, it was not clear whether the inhibition was due to filarial parasite infection or due to the presence of edema. This study was planned to compare platelet functions, plasma proteins and lipids in filarial and non-filarial edema patients. Edema patients were tested for the presence of filarial antigens and antibodies in their blood and were grouped as filarial and non-filarial edema patients accordingly. Platelet aggregation, size distribution, platelet activation markers, plasma proteins and lipids were measured in collected blood samples. Results showed that platelet aggregation was significantly inhibited in filarial edema patients, compared to non-filarial edema patients. Soluble P-selectin and beta thromboglobulin showed significant positive correlation with each other only in non-filarial edema patients. Plasma total cholesterol was lower in filarial edema patients, and HDL was lower in only female filarial edema patients. Observations confirm that inhibition of platelet functions is due to filarial parasite infection, not merely due to the presence of edema. Results also indicate uncoupling and disturbances of platelet activation processes.

Ocular toxoplasmosis (OT) is a common cause of posterior uveitis worldwide, primarily caused by Toxoplasma gondii. The immune response plays a crucial role in OT pathogenesis. However, a study using aqueous humour samples has limited applicability due to the invasive procedure. This study used peripheral blood samples to compare the concentrations and ratios of cytokines involved in Th1, Th17 and Treg immune responses between OT patients and seropositive individuals without ocular lesions (SP) who met the inclusion criteria. The ELISA method was used to measure cytokine concentrations, and the cytokine ratio was determined by comparing the concentration of two cytokines. This study revealed the differences in the concentrations of IL-17 (p = 0.015), IFN-α (p = 0.015) and IL-6 (p = < 0.001) between OT and SP groups, as well as the ratio of IFN-α/TGF-β (p = 0.012), IFN-β/TGF-β (p = 0.020), IL-17/TGF-β (p = 0.018), TNF-α/TGF-β (p = 0.015), IL-17/IL-6 (p = 0.003), IL-6/IFN-γ (p = < 0.001) and IL-6/TNF-α (p = < 0.001). Among the variables, the IFN-α concentrations and IL-6/TNF-α ratio were the most significant factors influencing the risk of OT. The novel findings of this study regarding the involvement of IFN-α in the pathogenesis of OT are considered important and have the potential to reveal a predictive factor for the occurrence of OT in humans.

Toxoplasma gondii is a protozoan parasite causing Toxoplasmosis in humans. Interleukin-6 (IL-6) is a multifunctional cytokine that controls infection and helps maintain pregnancy. The study investigated the impact of IL-6 promoter polymorphism on blood IL-6 levels and pregnancy outcomes in T. gondii-infected women. A cross-sectional study was conducted on 244 women, including 83 infected in Group 1 (Group 1a = 43, Group 1b = 40), 81 uninfected with RPL (Group 2), and 80 controls (Group 3). Blood and placental tissue samples were collected, and screened for IL-6 levels using ELISA. The DNA was isolated, amplified for T. gondii DNA and the IL-6 gene by PCR, and the IL-6 gene was sequenced using the Sanger method. The genotypic (p < 0.001) and allelic (p < 0.001) frequencies were significantly variable. Highly prevalent genotypes were A10T11/A10T11 in Group 1a (28%), A9T11/A9T11 in Group 1b (27.5%) and Group 2 (33.3%), while A8T12/A10T10 and A10T10/A10T10 were in Group 3 (20% each). The mean blood IL-6 levels were significantly variable in all the study groups (p < 0.0001). The A9T11/A9T11 genotype was significantly linked with high IL-6 levels, while the A10T10/A10T11, A10T11/A10T11 and A10T10/A10T10 genotypes were associated with low IL-6 levels. In conclusion IL-6 AnTn polymorphism is associated with changed IL-6 levels and RPL in women infected by T. gondii.

This study aimed to elucidate how osteopontin (OPN) affects the growth, invasion, and extrahepatic metastasis of Echinococcus multilocularis (Em) through the p38MAPK signalling pathway of host hepatocytes. C57BL/6J mice were randomly divided into the control group (n = 10), the LV-OPN-0423 group (n = 10), the anti-p38MAPK group (n = 10), and the anti-p38MAPK + LV-OPN-0423 group (n = 10). Em infection models in mice were set up. The mice were fed for 6 weeks under suitable conditions. The mice in the anti-p38MAPK group and the anti-p38MAPK + LV-OPN-0423 group were then given SB202190 (this is an inhibitor of p38MAPK) for 4 weeks, and the mice in each group were injected with corresponding lentivirus diluent once a week for 8 weeks. After the intervention was completed, the liver volume and weight were measured, and the liver was embedded in paraffin and sectioned. Sections were subjected to haematoxylin and eosin (HE), periodic acid-Schiff (PAS), and immunohistochemical staining to observe the growth and invasion of Em, as well as the expression levels of OPN, p38MAPK, and p-p38MAPK of the host. SB202190 hindered Em's growth, invasion, and migration. The level of OPN facilitated Em's growth, invasion, and migration, which can be reversed by SB202190. The OPN level promoted the expression of p38MAPK and p-p38MAPK. These results suggested that OPN could regulate Em's growth and metastasis through the p38MAPK signalling pathway in host hepatocytes, providing evidence that OPN and p38MAPK may be novel molecular targets for treating alveolar echinococcosis.

Patients undergoing haemodialysis are known to have compromised immune function, which can increase their susceptibility to infections, including intestinal parasitic diseases. These infections can manifest more severely in this population. Typically, the immune response to parasitic infections involves a shift from a Th1-dominant response-more effective against intracellular pathogens-to a Th2-dominant response, which promotes eosinophilia and IgE production. Participants were categorised into eosinophilic and non-eosinophilic groups based on eosinophil counts (< 10 cells/mL). T-bet and GATA-3 gene expressions were quantified using SYBR Green real-time PCR. The overall prevalence of intestinal parasitic infections was 11.9%, including Blastocystis hominis (5.9%), Endolimax nana (3.7%), Entamoeba coli (1.5%), and Giardia lamblia (0.7%). A significant association was found between parasitic infections and eosinophilia (p = 0.01). No significant difference in IgE levels was observed between the two groups. GATA-3 expression was significantly higher in eosinophilic patients compared to non-eosinophilic ones within the 90% confidence interval. A negative correlation was identified between eosinophil count and GATA-3 expression (r = -0.37, p = 0.05). Haemodialysis patients exhibit disruptions in both humoral and cellular immune responses. Further research is necessary to elucidate the role of eosinophilia and Th1/Th2 balance biomarkers in the diagnosis and prognosis of mortality risk among this population.

Human babesiosis is an emerging infectious disease caused by a bloodborne single-celled parasite belonging to the genus Babesia. Cases of human babesiosis are commonly reported in the United States, Western Europe and Asia. In the United States, the two major causative agents are Babesia microti and Babesia duncani. Transmitted to humans through tick bites, the parasite infects host red blood cells (RBCs). It induces flu-like symptoms and has evolved mechanisms to manipulate the immune system, enabling its persistence. One key mechanism is the secretion of extracellular vesicles (EVs) which carry bioactive molecules, including proteins, lipids and genetic material that modulate pathogen-host interactions and disease development. The inhibition of the secretion of these vesicles may lead to disease control. One potential inhibitor of extracellular vesicle secretion is linoleic acid (LA), a polyunsaturated lipid that has demonstrated inhibitory properties in other parasites. To study the effects of development stage-dependent stimuli on B. duncani, we employed a B. duncani in vitro continuous culture system and evaluated the use of sorbitol for synchronising parasite development. Microscopy techniques showed successful sorbitol-induced synchronisation. Using nanoparticle tracking analysis and scanning electron microscopy, we assessed the effects of LA on parasite morphology and EV characteristics. Our studies indicate that exposure of Babesia parasites to LA did not cause significant observable changes in RBC morphology or reduce EV concentrations under the tested conditions.

As an effort towards vaccine development against African trypanosomiasis, we studied key parasite molecules that mediate VSG functions, specifically the major surface protease-B of Trypanosoma brucei that catalyses proteolytic removal of old VSGs for expression of new ones, an important stage-specific function that allows the parasite to survive in its host, thus making it an attractive candidate for vaccine development. Herein, the Tbmsp-b gene was cloned into a pVAX-1 plasmid to produce the pVAX-1-Tbmsp-b construct for DNA vaccine trials. BALB/c mice were immunised by intradermal injection with a 100 μg dose of the construct thrice on Days 0, 21 and 42, then inoculated with 2000 parasites on Day 56. Anti-trypanosome-specific antibody (IgG) and cytokine (IFN-γ) were monitored by ELISA from sera of immunised and unimmunised mice. Immunised mice showed significantly (p < 0.05) higher IgG and IFN-γ responses, lower parasitaemia (by 75% and 51.2% of parasitaemic scores on the first and fifth week of infection) and longevity by up to 22 days compared to unimmunised mice. These results showed that the construct provided partial protection to virulent T. b. brucei (Federe strain) infection in susceptible BALB/c mice, suggesting the potential for using MSP-B as an antigen in DNA vaccine development against African trypanosomiasis.

Toxoplasma gondii is a parasitic protozoan that infects nucleated cells and poses a major threat to human and animal health. Developing effective vaccines is critical for controlling toxoplasmosis. Immune Mapped Protein 1 (IMP1) is a protective antigen located on the plasma membrane of T. gondii. This study aimed to evaluate the efficacy of IMP1 as a DNA vaccine, either alone or combined with IL-12 as an adjuvant, in BALB/c mice. The use of IL-12 as an adjuvant was based on its well-documented ability to enhance Th1 immune responses in DNA vaccines against T. gondii. Mice were divided into five groups: group I served as a control (100 μL PBS), group II received empty pcDNA3.1, group III received pcIL12, group IV received pcTgIMP1, and group V received a combination of pcTgIMP1 and pcIL12 (50 μg each). Immunisation was administered three times on days zero, 14, and 28 with the same dose. Two weeks post-final vaccination, mice from each group were either challenged with a lethal dose of T. gondii for survival monitoring or euthanised for evaluating immune responses, including antibody levels, lymphocyte proliferation, and cytokine production. Results showed that mice immunised with pcIMP1 + pcIL-12 or pcTgIMP1 alone exhibited robust immune responses against Toxoplasmosis. These responses included elevated levels of IgG1 and IgG2a antibodies, a strong lymphoproliferative response, and higher levels of IFN-γ and IL-4 production compared to the other groups. Furthermore, mice immunised with pcIMP1 + pcIL-12 demonstrated prolonged survival times compared to the empty pcDNA3.1, pcIL-12 alone, and control groups (p < 0.05). Our finding underscores the potential of IMP1 as a vaccine candidate and highlights the adjuvant effect of IL-12 in enhancing protective immunity against toxoplasmosis.

Cancer is one of the main causes of morbidity and mortality worldwide. Toxoplasma gondii (T. gondii) infection and antigens can be used to exert valuable antitumor effects. We studied the effect of Toxoplasma lysate antigen and excretory/secretory antigens (ESAs) produced by T. gondii tachyzoites on Ehrlich solid carcinoma (ESC)-bearing mice by histopathology (H&E), immunohistochemistry (iNOS, VEGF, caspase 3), immunological (IFN-γ and specific anti-T. gondii IgG) and biochemical studies (redox state markers; MDA and SOD as well as apoptotic markers; BAX and BCL2). The results showed strong anti-murine ESC effect by increasing tumour necrosis and apoptosis (high caspase 3 and BAX with low BCL2) as well as decreasing angiogenesis (weak VEGF and iNOS) and by increasing oxidative stress (low SOD with high MDA). In addition, specific anti-T. gondii IgG was confirmed and high IFN-γ was detected. We concluded that ESAs could be used as an effective supplementary biotherapy in the treatment of cancer.

This study investigated whether miRNAs and cytokines could be markers of gestational and/or congenital toxoplasmosis (TX). A total of 172 clinical samples collected from women were investigated. For gestational TX, 63 plasmas from pregnant women were analysed: 44 with gestational TX (GT-PW), 11 with asymptomatic TX (AsT-PW) and 8 healthy pregnant women (H-PW). For controls, 68 plasmas: 34 healthy women (HW) and 34 with asymptomatic TX (AsT). For congenital TX, 41 amniotic fluid (AF) samples were tested: 29 with negative qPCR in AF and 12 with positive PCR. Nine miRNAs were assayed by qPCR in plasma and AF samples. IFN-γ, TNF-α and IL-10 detection in plasmas was performed by ELISA. Statistical analyses were determined by F-test and ROC curves. Among the 9 hsa-miRNAs studied, only hsa-miR-125b-5p was significantly expressed in the AsT-PW group. hsa-miR-144-3p was more expressed in the GT-PW group. In AF samples, hsa-miR-125b-5p was more expressed in 29 AF samples with Neg-qPCR and hsa-miR-144-3p in AF samples with Pos-qPCR. Pregnant women from the GT-PW group had lower IFN-γ, TNF-α, and IL-10 production than the other groups. The in silico analyses identified pathways for hsa-miR-144-3p and hsa-miR-125b-5p and were related to the pathogenesis and immune response in toxoplasmosis. These findings suggest that hsa-miR-125b-5p could be related to infection regulation and to be characterised as a potential marker for asymptomatic toxoplasmosis. On the other hand, the hsa-miR-144-3p could be related to the exacerbation of the infection since gestational and/or congenital TX groups expressed high expression of hsa-miR-144-3p and low expression of IFN-γ, TNF-α and IL-10.

Schistosome parasites are known to modulate host immune responses, which is achieved in part through the release of excretory/secretory (ES) products, including extracellular vesicles (EVs). During chronic schistosomiasis, increased regulatory responses are found, which include enhanced IL-10 production by B (Breg) cells. ES products from schistosome eggs are able to induce IL-10 production by B cells. However, since infection with male worms only (without egg production) also promotes IL-10 producing B cells, we here studied the stimulatory effects of adult worm ES and EVs on murine and human B cells. Worm ES increased IL-10 release by mouse splenic B cells; this activity was concentrated in defined size-separated fractions of adult worm ES. Interestingly, mass spectrometry of the fractions that induced the highest IL-10 response revealed an enrichment of EV-associated proteins. Indeed, highly purified adult worm EVs could interact with mouse splenic B cells, visualised by binding of a schistosome-specific tetraspanin (TSP2) targeting antibody. Furthermore, purified adult worm EVs induced IL-10 release in both mouse splenic and human peripheral blood B cells, suggesting that adult worm EVs can play a role in immune regulatory processes within their host.

Leishmania parasite adeptly evades the host's immune defences by infiltrating macrophages, exploiting apoptotic processes for further dissemination. Among the host's strategies to counter parasitic propagation, the pivotal role of B-cells, specifically B regulatory (Breg) cells, emerges. Recent evidence from in vitro and in vivo studies has thrust Breg cells into the spotlight, attributed to their IL-10 secretion and antigen presentation. The escalated IL-10 production coupled with decreased Th1 response provides a conducive milieu for parasitic proliferation within host cells. This abundance of IL-10, from Breg cells and other immune sources, impedes T cell differentiation into Th1, Th2 and Th17 subsets. Moreover, IL-10 obstructs CD8+ T cell differentiation into cytotoxic T cells, heightening the host's susceptibility to infections. Breg cells are also implicated in the production of IL-35, which in turn mediates the conversion of B cells into Breg and IL-35+ Breg cells and helps Leishmania to evade the immune response. Notably, recent data underscore the potential of B cell reprogramming via BTK and MEK inhibitors, offering a novel immunomodulation strategy. This approach presents a novel avenue for curbing Breg cells, potentially hindering prolonged BCR signalling. Although promising for Leishmania infection immunotherapy, a comprehensive understanding of IL-10-producing B cells' exact role demands further exploration. Developing targeted strategies to modulate Breg cell function could revolutionise Leishmania treatment, enhancing patient outcomes. Understanding Breg cells' role offers promising avenues for precise immunotherapy against this challenging infection.

Chagas disease, caused by Trypanosoma cruzi, exhibits a wide clinical spectrum, which is influenced by the parasite's extensive genetic diversity. Growing evidence indicates that human infections are often multiclonal, involving a dynamic population of parasite clones, collectively termed the "cruziome". The immunological consequences of these mixed infections, particularly at the initial host-parasite interface, remain poorly characterised. This study aimed to investigate how single versus co-infection with phylogenetically distinct T. cruzi strains modulates the innate immune response of murine macrophages. RAW 264.7 macrophages were infected with T. cruzi strains from Discrete Typing Unit (DTU) I (G strain) or DTU II (Y strain), either individually or in combination (co-infection). Assays for cellular invasion and intracellular multiplication were performed. The production of key cytokines (IL-1β, IL-18, IL-6, IL-10, IL-12) and nitric oxide (NO) was quantified at 24 to 96 h post-infection. The Y strain displayed significantly higher invasion and replication rates and induced a potent pro-inflammatory response, characterised by elevated levels of IL-1β, IL-18, IL-12, and NO. The G strain elicited a more regulatory profile, with a progressive increase in IL-10 production at later time points and lower levels of inflammatory mediators. Co-infection resulted in a distinct, hybrid immune profile, marked by intermediate levels of both pro-inflammatory and regulatory cytokines and a moderated NO output. Co-infection with phylogenetically distinct T. cruzi strains generates a unique immunomodulatory environment that is not merely an additive effect of the individual strains. These findings provide in vitro evidence supporting the hypothesis that the composition of the infecting parasite population shapes the host immune response from the earliest stages of infection. This balanced interplay between pro-inflammatory and regulatory signals may contribute to the clinical heterogeneity observed in Chagas disease and underscores the need to consider parasite diversity in pathogenic and therapeutic studies.

Interleukins 33, 25, and thymic stromal lymphopoietin (TSLP) are core components of type two immune responses and have been studied extensively using helminth infection models. However, many questions remain regarding their cellular sources, their immune recipients, as well as how they shape immunity. Recent literature has demonstrated non-epithelial alarmin production, acting primarily on lymphoid effector cells, and has suggested a role for alarmins in licensing of effector function in tissues during immunity, in dissent with conceptions of classical alarmins as epithelium-derived, myeloid-targeting, and induced prior to adaptive responses. This review examines recent findings in alarmin helminth interactions at barrier sites and discusses the wider implications for how alarmin responses are conceptualised.

American tegumentary leishmaniasis (ATL) affects the skin and mucous membranes, with a spectrum shaped by Th1/Th2 responses. This study investigated inflammasome activation in correlation with macrophage subpopulations, tissue parasitism, and histological changes in cutaneous and mucocutaneous leishmaniasis. We assessed inflammasome activation, tissue parasitism, and macrophage populations by immunohistochemistry, correlating with histopathological alterations using 29 biopsies from cutaneous and mucocutaneous leishmaniasis. Cutaneous leishmaniasis showed higher parasite density and infected macrophages than mucocutaneous leishmaniasis skin and mucosal lesions (p < 0.05). CD68 and CD163 macrophages were more abundant in cutaneous leishmaniasis (p < 0.0001 and p < 0.05). Inflammasome markers IL-1β and IL-18 were significantly higher in cutaneous leishmaniasis (p < 0.05). In cutaneous leishmaniasis, CD68 macrophages correlated positively with inflammasome markers, whereas in mucocutaneous leishmaniasis, CD163 cells showed strong negative correlations with IL-1β and caspase-1. Parasite density correlated positively with inflammasome activation in cutaneous leishmaniasis but negatively in mucocutaneous leishmaniasis. Findings suggest that inflammasome activation plays different roles in ATL. In cutaneous leishmaniasis, inflammasomes contribute to the inflammatory response and parasite clearance, while in mucocutaneous leishmaniasis, they are less relevant, possibly due to a more defined immune response with minimal parasitism.

Naegleria fowleri is the etiological agent of primary amoebic meningoencephalitis (PAM), a lethal disease with a 97% mortality rate in humans. Currently, there is no vaccine that confers protection against N. fowleri. Recently, we reported that the synthetic membrane peptide (Smp145) was considered as a vaccine candidate, since it induced 60% protection in mice immunised and challenged with N. fowleri. The objective was to design in silico a vaccine based on the A1 domain of cholera toxin (CT), coupled to the Smp145 peptide of N. fowleri, and to evaluate its protective effect in a murine model of PAM. A bioinformatic design was performed with the Ser61Phe mutation in the active site of the A1 domain of CT (mCTA1), linked through a glycine linker to Smp145. Intraperitoneal immunisation with mCTA1-Smp145, followed by challenge with a lethal dose of N. fowleri, resulted in 60% protection, confirming its protective capacity as the most relevant finding. Furthermore, increased levels of IgA and IgG were observed in sera and nasal washes, which recognised antigenic bands of mCTA1-Smp145 and total extracts of N. fowleri. Overall, we propose mCTA1-Smp145 as a potential vaccine against N. fowleri, highlighting that its protective effect constitutes the main support for this proposal.

Trypanothione reductase (TryR) is a unique and key redox protein of Leishmania donovani, the causative agent of visceral Leishmaniasis. In this work, we have developed a promising multiepitope vaccine using TryR. Multiple epitopes from TryR were identified using different bioinformatics tools to stimulate both humoral and cellular immune responses. An adjuvant was also included to enhance the antigen presentation and immune activation. Using bioinformatics tools, immunodominant T-cell and B-cell epitopes of TryR were predicted, and based on the findings, a chimeric multi-epitope vaccine construct was designed. The structural stability of the final construct was validated using different bioinformatics tools. Furthermore, a docking study was conducted with the human TLR4 receptor to assess the affinity of the multi-epitope construct. The Ramachandran plot analysis, Z score, and ERRAT support the stability of the multi-epitope vaccine candidate. Furthermore, in silico analysis showed that the multi-epitope vaccine candidate has high affinity with the human TLR4 receptor and has broad efficacy based on the population coverage. Immune stimulation confirmed the pro-inflammatory response with T- and B-cell activation.

Visceral leishmaniasis is a potentially fatal zoonosis with an increasing incidence. Most infected felines present the disease in its subclinical form and demonstrate greater resistance to parasitemia than dogs. However, the role of cellular immunity in felines is still poorly understood. This study measured serum levels of interleukin (IL)-12 and interferon-gamma (IFN-γ) in asymptomatic cats naturally infected with antibodies against Leishmania spp. and in uninfected cats. IL-12 and IFN-γ were measured in serum samples by ELISA. Parasite load quantification was performed on DNA from bone marrow samples using qPCR. Cats naturally infected by Leishmania spp. showed significantly higher serum levels of IL-12 and IFN-γ compared to control animals. IL-12 showed a positive correlation with IFN-γ suggesting a regulatory role of IL-12 in activating the Th1 immune response, which enhances macrophage function and promotes intracellular parasite elimination. Additionally, IL-12 showed a moderate negative correlation with parasite load, indicating a protective effect of IL-12 in feline leishmaniasis. These findings suggest that IL-12 and IFN-γ play critical roles in modulating the feline immune response against parasitic infection, possibly contributing to the control of parasite replication and in the prevention of clinical signs. The immune response observed in felines could be explored for future immunotherapeutic approaches, helping to mitigate the progression of leishmaniasis in cats and reducing the risk of transmission in endemic regions.

This study evaluated white turmeric (Curcuma zedoaria) as a sustainable feed additive alternative to common turmeric (C. longa) for enhancing disease resistance in Labeo rohita against Argulus siamensis infection. Juvenile L. rohita (15.8 ± 1.9 g) were divided into four treatment groups (n = 60 per group): (1) Control (commercial feed), (2) common turmeric-supplemented feed (1% w/w), (3) white turmeric-supplemented feed (1% w/w), and (4) combined turmeric-supplemented feed (0.5% common +0.5% white turmeric). Fish were fed experimental diets for 45 days before challenge with A. siamensis (10 parasites/fish), followed by 15 days of post-challenge monitoring (total experimental period: 60 days). Samples were collected on days 0, 15, 30, and 45 of the feeding phase, and on days 7 and 15 of the post-challenge phase. Results showed that turmeric supplementation significantly enhanced growth performance, haematological parameters (RBC, haemoglobin, haematocrit), immunological responses (lysozyme, respiratory burst, complement activities), and antioxidant status (SOD, CAT, MDA) compared to control. Post-challenge, turmeric-supplemented groups exhibited reduced parasite load and higher survival rates (Combined: 92%, common turmeric: 85%, White turmeric: 82%, Control: 68%). While common turmeric performed slightly better than white turmeric when used alone, the combined treatment showed superior efficacy in all parameters measured. These findings suggest that combining both turmeric species provides optimal benefits, while white turmeric can serve as a partial substitute for common turmeric in fish feed formulations when resource sustainability is a priority, thus helping to reduce competition with human food resources.

The severity of malaria is associated with low antioxidant availability and elevated free radical production, which induces oxidative damage in cerebral and pulmonary microcirculation. This can be mitigated by dietary antioxidants. We investigated the protective effects of lycopene (LYC) against oxidative changes induced by Plasmodium berghei (Pb). Mice were infected by intraperitoneal injection of 10 parasitized red blood cells and treated orally with LYC (3.11 mg/kg bw/day) or N-acetylcysteine (NAC, 62 mg/kg bw/day). Evaluations were conducted at 1-, 4-, 8- and 12-days post-infection. We measured thiobarbituric acid reactive substances (TBARS), antioxidant capacity by ABTS (AC-ABTS) and DPPH (AC-DPPH) inhibition, uric acid (UA) and nitric oxide (NO) in brain and lung tissues. Infection led to elevated TBARS, AC-ABTS, AC-DPPH, UA and NO, resulting in animal mortality. LYC significantly attenuated the infection-induced increases in TBARS, UA and NO levels compared to Pb (p < 0.0001) and NAC + Pb groups (p < 0.0001) normalising them to Sham levels. These findings highlight LYC's therapeutic potential against malaria-related oxidative stress.