Abstract:Co-infection of malaria and intestinal parasites is widespread in sub-Saharan Africa and causes severe disease especially among the poorest populations. It has been shown that an intestinal parasite (helminth), mixed intestinal helminth or Plasmodium parasite infection in a human induces a wide range of cytokine responses, including anti-inflammatory, pro-inflammatory as well as regulatory cytokines. Although immunological interactions have been suggested to occur during a concurrent infection of helminths and… Show more
“…Interactions between the two parasites alter immune responses, thus influencing susceptibility to clinical malaria (92, 93). There are conflicting reports on the outcome of these interactions as some studies have reported enhanced severity (94, 95), others reduced severity (96, 97) yet others have revealed no association between helminth co-infection and malaria outcome (98, 99). These observations may be due to differences in the co-infecting helminth species (100), the host's level of immunity to P. falciparum (101) and differences in study design (91).…”
Section: Immunomodulation In Asymptomatic Malariamentioning
Malaria is still a significant public health burden in the tropics. Infection with malaria causing parasites results in a wide range of clinical disease presentations, from severe to uncomplicated or mild, and in the poorly understood asymptomatic infections. The complexity of asymptomatic infections is due to the intricate interplay between factors derived from the human host, parasite, and environment. Asymptomatic infections often go undetected and provide a silent natural reservoir that sustains malaria transmission. This creates a major obstacle for malaria control and elimination efforts. Numerous studies have tried to characterize asymptomatic infections, unanimously revealing that host immunity is the underlying factor in the maintenance of these infections and in the risk of developing febrile malaria infections. An in-depth understanding of how host immunity and parasite factors interact to cause malaria disease tolerance is thus required. This review primarily focuses on understanding anti-inflammatory and pro-inflammatory responses to asymptomatic infections in malaria endemic areas, to present the view that it is potentially the shift in host immunity toward an anti-inflammatory profile that maintains asymptomatic infections after multiple exposures to malaria. Conversely, symptomatic infections are skewed toward a pro-inflammatory immune profile. Moreover, we propose that these infections can be better interrogated using next generation sequencing technologies, in particular RNA sequencing (RNA-seq), to investigate the immune system using the transcriptome sampled during a clearly defined asymptomatic infection.
“…Interactions between the two parasites alter immune responses, thus influencing susceptibility to clinical malaria (92, 93). There are conflicting reports on the outcome of these interactions as some studies have reported enhanced severity (94, 95), others reduced severity (96, 97) yet others have revealed no association between helminth co-infection and malaria outcome (98, 99). These observations may be due to differences in the co-infecting helminth species (100), the host's level of immunity to P. falciparum (101) and differences in study design (91).…”
Section: Immunomodulation In Asymptomatic Malariamentioning
Malaria is still a significant public health burden in the tropics. Infection with malaria causing parasites results in a wide range of clinical disease presentations, from severe to uncomplicated or mild, and in the poorly understood asymptomatic infections. The complexity of asymptomatic infections is due to the intricate interplay between factors derived from the human host, parasite, and environment. Asymptomatic infections often go undetected and provide a silent natural reservoir that sustains malaria transmission. This creates a major obstacle for malaria control and elimination efforts. Numerous studies have tried to characterize asymptomatic infections, unanimously revealing that host immunity is the underlying factor in the maintenance of these infections and in the risk of developing febrile malaria infections. An in-depth understanding of how host immunity and parasite factors interact to cause malaria disease tolerance is thus required. This review primarily focuses on understanding anti-inflammatory and pro-inflammatory responses to asymptomatic infections in malaria endemic areas, to present the view that it is potentially the shift in host immunity toward an anti-inflammatory profile that maintains asymptomatic infections after multiple exposures to malaria. Conversely, symptomatic infections are skewed toward a pro-inflammatory immune profile. Moreover, we propose that these infections can be better interrogated using next generation sequencing technologies, in particular RNA sequencing (RNA-seq), to investigate the immune system using the transcriptome sampled during a clearly defined asymptomatic infection.
“…However, it is crucial to consider the specific pathogen and the type of immune response elicited, as IL-4 can have both protective and detrimental effects depending on the context. High IL-4 levels have a significant impact on the modulation of effector elements that alter the physiology of the intestine, creating an unfavorable environment for worm parasites [ 108 , 109 ]. The administration of IL-4 from an external source can effectively treat persistent worm infections, whereas the use of IL-4 antagonists hinders the protective responses against such infections [ 110 , 111 ].…”
Interleukins (ILs) are signaling molecules that are crucial in regulating immune responses during infectious diseases. Pro-inflammatory ILs contribute to the activation and recruitment of immune cells, whereas anti-inflammatory ILs help to suppress excessive inflammation and promote tissue repair. Here, we provide a comprehensive overview of the role of pro-inflammatory and anti-inflammatory ILs in infectious diseases, with a focus on the mechanisms underlying their effects, their diagnostic and therapeutic potential, and emerging trends in IL-based therapies.
“…Studies on concomitant infections in humans suggest that A. lumbricoides infection may protect against cerebral malaria [10,11], while other studies suggest that children infected by Schistosoma mansoni may be more susceptible to P. falciparum infections and develop acute malaria episodes [12,13]. Also, it has been shown that the levels of TNF-α, IL-2, IL-10, IL-6 in Plasmodium-helminth co-infected individuals were significantly higher than the malaria-positive (MP) group [14] dampening the immune response to malaria. However, to our knowledge, no studies have been conducted regarding host immune responses to malaria in children co-infected with protozoan pathogens.…”
Section: Introductionmentioning
confidence: 99%
“…falciparum infections and develop acute malaria episodes [ 12 , 13 ]. Also, it has been shown that the levels of TNF-α, IL-2, IL-10, IL-6 in Plasmodium -helminth co-infected individuals were significantly higher than the malaria-positive (MP) group [ 14 ] dampening the immune response to malaria. However, to our knowledge, no studies have been conducted regarding host immune responses to malaria in children co-infected with protozoan pathogens.…”
Background
Co-infection with malaria and intestinal parasites is common in children in Africa and may affect their immune response to a malaria parasite infection. Prior studies suggest that co-infections may lead to increased susceptibility to malaria infection and disease severity; however, other studies have shown the reverse. Knowledge on how co-morbidities specifically affect the immune response to malaria antigens is limited. Therefore, this study sought to determine the prevalence of co-infection of malaria and intestinal parasites and its association with antibody levels to malaria merozoite antigens.
Methods
A cross sectional study was carried out in two villages with high transmission of malaria in Cameroon (Ngali II and Mfou) where mass drug administration (MDA) had been administered at ~6-month intervals (generally with albendazole or mebendazole). Children aged 1–15 years were enrolled after obtaining parental consent. A malaria rapid diagnostic test was used on site. Four (4) ml of peripheral blood was collected from each participant to determine Plasmodium falciparum infections by microscopy, haemoglobin levels and serology. Fresh stool samples were collected and examined by wet mount, Kato-Katz method and modified Ritchie concentration techniques. A Multiplex Analyte Platform assay was used to measure antibody levels.
Results
A total of 320 children were enrolled. The prevalence of malaria by blood smear was 76.3% (244/320) and prevalence of malaria and intestinal parasites was 16.9% (54/320). Malaria prevalence was highest in young children; whereas, intestinal parasites (IP+) were not present until after 3 years of age. All children positive for malaria had antibodies to MSP142, MSP2, MSP3 and EBA175. No difference in antibody levels in children with malaria-co infections compared to malaria alone were found, except for antibody levels to EBA-175 were higher in children co-infected with intestinal protozoa (p = 0.018), especially those with Entamoeba histolytica infections (p = 0.0026).
Conclusion
Antibody levels to EBA175 were significantly higher in children co-infected with malaria and E. histolytica compared to children infected with malaria alone. It is important to further investigate why and how the presence of these protozoans might modulate the immune response to malaria antigens.
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