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Fulltext Host tissue reaction to Gnathostoma malaysiae (Nematoda: Gnathostomidae) in Rattus surifer Miller

Krishnasamy M, Palmieri JR, Oothuman P, Jeffery J

Southeast Asian J. Trop. Med. Public Health, 1993 Sep;24(3):489-93.
PMID: 8160058

The occurrence of adult Gnathostoma malaysiae in Rattus surifer and R. tiomanicus in Malaysia has been reported but there are no known reports on the host tissue reactions. This paper reports on the gross pathology caused by G. malaysiae in a red spiny forest rat, R. surifer and the tissue reactions caused. A tumor-like growth was located on the mid-stomach wall in a female rat captured in Gunung Bachock, Kelantan, Malaysia. This growth consisted of four tunnel-like structures containing sanguinopurulent fluid and leukocytes and this structure led into a central canal. The tissue surrounding the tumor was greatly inflamed and there was localized gastritis. The tunnel-like structure was surrounded by dense fibrotic tissue. The stomach wall was devoid of superficial epithelium and smooth muscle but mucinous glands were present. The midregion of the fibrotic scar contained eggs of G. malaysiae which had evoked a strong tissue reaction and were surrounded by pus. Blood vessels were empty, dilated and had undergone vasculitis and thrombosis.

Matched MeSH terms: Host-Parasite Interactions/immunology*
Fulltext IgM in human immunity to Plasmodium falciparum malaria

Boyle MJ, Chan JA, Handayuni I, Reiling L, Feng G, Hilton A, et al.

Sci Adv, 2019 09;5(9):eaax4489.
PMID: 31579826 DOI: 10.1126/sciadv.aax4489

Most studies on human immunity to malaria have focused on the roles of immunoglobulin G (IgG), whereas the roles of IgM remain undefined. Analyzing multiple human cohorts to assess the dynamics of malaria-specific IgM during experimentally induced and naturally acquired malaria, we identified IgM activity against blood-stage parasites. We found that merozoite-specific IgM appears rapidly in Plasmodium falciparum infection and is prominent during malaria in children and adults with lifetime exposure, together with IgG. Unexpectedly, IgM persisted for extended periods of time; we found no difference in decay of merozoite-specific IgM over time compared to that of IgG. IgM blocked merozoite invasion of red blood cells in a complement-dependent manner. IgM was also associated with significantly reduced risk of clinical malaria in a longitudinal cohort of children. These findings suggest that merozoite-specific IgM is an important functional and long-lived antibody response targeting blood-stage malaria parasites that contributes to malaria immunity.

Matched MeSH terms: Host-Parasite Interactions/immunology*
Effect of Brugia pahangi co-infection with Plasmodium berghei ANKA in gerbils (Meriones unguiculatus)

Junaid OQ, Vythilingam I, Khaw LT, Sivanandam S, Mahmud R

Parasitol Res, 2020 Apr;119(4):1301-1315.
PMID: 32179986 DOI: 10.1007/s00436-020-06632-4

Malaria and lymphatic filariasis (LF) are two leading and common mosquito-borne parasitic diseases worldwide. These two diseases are co-endemic in many tropical and sub-tropical regions and are known to share vectors. The interactions between malaria and filarial parasites are poorly understood. Thus, this study aimed at establishing the interactions that occur between Brugia pahangi and Plasmodium berghei ANKA (PbA) co-infection in gerbils. Briefly, the gerbils were matched according to age, sex, and weight and grouped into filarial-only infection, PbA-only infection, co-infection, and control group. The parasitemia, survival and clinical assessment of the gerbils were monitored for a period of 30 days post Plasmodium infection. The immune responses of gerbils to both mono and co-infection were monitored. Findings show that co-infected gerbils have higher survival rate than PbA-infected gerbils. Food and water consumption were significantly reduced in both PbA-infected and co-infected gerbils, although loss of body weight, hypothermia, and anemia were less severe in co-infected gerbils. Plasmodium-infected gerbils also suffered hypoglycemia, which was not observed in co-infected gerbils. Furthermore, gerbil cytokine responses to co-infection were significantly higher than PbA-only-infected gerbils, which is being suggested as a factor for their increased longevity. Co-infected gerbils had significantly elicited interleukin-4, interferon-gamma, and tumor necrotic factor at early stage of infection than PbA-infected gerbils. Findings from this study suggest that B. pahangi infection protect against severe anemia and hypoglycemia, which are manifestations of PbA infection.

Matched MeSH terms: Host-Parasite Interactions/immunology
Fulltext Expression of Ascaris lumbricoides putative virulence-associated genes when infecting a human host

Mohd-Shaharuddin N, Lim YAL, Ngui R, Nathan S

Parasit Vectors, 2021 Mar 23;14(1):176.
PMID: 33757548 DOI: 10.1186/s13071-021-04680-y

BACKGROUND: Ascaris lumbricoides is the most common causative agent of soil-transmitted helminth infections worldwide, with an estimated 450 million people infected with this nematode globally. It is suggested that helminths are capable of evading and manipulating the host immune system through the release of a spectrum of worm proteins which underpins their long-term survival in the host. We hypothesise that the worm overexpresses these proteins when infecting adults compared to children to cirvumvent the more robust defence mechanisms of adults. However, little is known about the parasite's genes and encoded proteins involved during A. lumbricoides infection. Hence, this study was conducted to assess the expression profile of putative virulence-associated genes during an active infection of adults and children.
METHODS: In this study, quantitative PCR was performed to evaluate the expression profile of putative virulence-associated genes in A. lumbricoides isolated from infected children and adults. The study was initiated by collecting adult worms expelled from adults and children following anthelminthic treatment. High-quality RNA was successfully extracted from each of six adult worms expelled by three adults and three children, respectively. Eleven putative homologues of helminth virulence-associated genes reported in previous studies were selected, primers were designed and specific amplicons of A. lumbricoides genes were noted. The expression profiles of these putative virulence-associated genes in A. lumbricoides from infected adults were compared to those in A. lumbricoides from infected children.
RESULTS: The putative virulence-associated genes VENOM, CADHERIN and PEBP were significantly upregulated at 166-fold, 13-fold and fivefold, respectively, in adults compared to children. Conversely, the transcription of ABA-1 (fourfold), CATH-L (threefold) and INTEGRIN (twofold) was significantly suppressed in A. lumbricoides from infected adults.
CONCLUSIONS: On the basis of the expression profile of the putative virulence-associated genes, we propose that the encoded proteins have potential roles in evasion mechanisms, which could guide the development of therapeutic interventions.

Matched MeSH terms: Host-Parasite Interactions/immunology
Fulltext In vitro inhibition and reversal of Plasmodium falciparum cytoadherence to endothelium by monoclonal antibodies to ICAM-1 and CD36

Mustaffa KMF, Storm J, Whittaker M, Szestak T, Craig AG

Malar J, 2017 07 05;16(1):279.
PMID: 28679447 DOI: 10.1186/s12936-017-1930-9

BACKGROUND: Sequestration of parasitized red blood cells from the peripheral circulation during an infection with Plasmodium falciparum is caused by an interaction between the parasite protein PfEMP1 and receptors on the surface of host endothelial cells, known as cytoadherence. Several lines of evidence point to a link between the pathology of severe malaria and cytoadherence, therefore blocking adhesion receptors involved in this process could be a good target to inhibit pRBC sequestration and prevent disease. In a malaria endemic setting this is likely to be used as an adjunct therapy by reversing existing cytoadherence. Two well-characterized parasite lines plus three recently derived patient isolates were tested for their cytoadherence to purified receptors (CD36 and ICAM-1) as well as endothelial cells. Monoclonal antibodies against human CD36 and ICAM-1 were used to inhibit and reverse infected erythrocyte binding in static and flow-based adhesion assays.
RESULTS: Anti-ICAM-1 and CD36 monoclonal antibodies were able to inhibit and reverse P. falciparum binding of lab and recently adapted patient isolates in vitro. However, reversal of binding was incomplete and varied in its efficiency between parasite isolates.
CONCLUSIONS: The results show that, as a proof of concept, disturbing existing ligand-receptor interactions is possible and could have potential therapeutic value for severe malaria. The variation seen in the degree of reversing existing binding with different parasite isolates and the incomplete nature of reversal, despite the use of high affinity inhibitors, suggest that anti-adhesion approaches as adjunct therapies for severe malaria may not be effective, and the focus may need to be on inhibitory approaches such as vaccines.

Matched MeSH terms: Host-Parasite Interactions/immunology